Monday, July 24, 2017

Updating the 16 medical hypotheses

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.  For example a flu virus inside of the pancreas and e.coli latching on to the outside could trigger type one diabetes.

4. Co-carcinogenesis: a virus and a carcinogen together cause cancer. Taking Rous’ hypothesis further, the carcinogen is a polymerase inhibitor which binds the viral polymerase with higher affinity. Thus the DNA methylation state has been changed but the virus is no longer viable.  DNA damage does not cause most cancers, the interaction of carcinogens and viruses do.  Further these 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 are ones that can cross the intestine or the blood brain barrier causing gluten sensitivity with the hole they leave behind. This explains the gluten sensitivity of Schizophernia from T.gondii, Celiac disease from e.coli, Tourettes from staph, and crohn’s from mycobacteria.

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 and 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 plasama membrane 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)

Friday, July 21, 2017

Is Dermographism urticaria caused by a spirochete infection?

Dermographism urticaria and spirochetes: can all 3 of these spirochete infections trigger dermographism by altering cortisol levels?

Lyme diseases' borrelia, the ulcer causing h.pylori, and leptospirosis (the spirochete of lakes)

H.pylori and dermographism urticaria
http://www.jtad.org/2009/3/jtad93301a.pdf
https://www.ncbi.nlm.nih.gov/pubmed/?term=dermographism+urticaria+h.pylori

Lyme's Borrelia spirochete and dermographism urticaria
http://www.healthy-skincare.com/lyme-disease-and-dermatographism-itching-hives.html

Dermographism....mast cells dysfunction?

If spirochetes make high levels of cortisol in the body over long periods of time would this then cause the mast cells to down regulate the receptors to the pool.

previous posts about spirochetes and cortisol
http://angelabiggs.blogspot.com/2016/07/spirochetes-and-high-cortisol.html

Normally mast cells decrease after cortisol applications and dermographism decreases
https://www.ncbi.nlm.nih.gov/pubmed/2597634

Leptospirosis, weil's disease, and rash
https://patient.info/health/leptospirosis-and-weils-disease

Can you have leptospirosis and not develop weil's disease?

doxcycline can kill spirochetes ?
https://en.wikipedia.org/wiki/Doxycycline

poison ivy allergy and spirochetes
http://angelabiggs.blogspot.com/2016/05/severe-poison-ivy-reactions-and.html

things that might kill spirochetes
http://angelabiggs.blogspot.com/2016/05/brassicaceae-mustards-mustard-flowers.html

Possums which eat ticks are immune to lyme disease. What does their immune system do to combat the Borrelia?


Tuesday, July 18, 2017

Can ISRIB rescue memories in Alzheimer's by returning mitochondrial movement?


Previous posts linked mitochondrial dysfunction with Alzheimer's disease: the mother's of  Down syndrome, diacetyl , and Herpes Zoster.
http://angelabiggs.blogspot.com/2017/06/alzheimers-and-dysfunctional.html

If the mitochondria cannot move down the nerve's axon to the synapse is memory blocked? Does blocking growth and metabolism prevent mitochondrial movement?

When cells are under stress it would be beneficial to slow not just metabolism but the generation of new mitochondrias.  The SESN2 genes are involved in mitochondria generation and slows metabolism.  Thus SESN2 protects the mitochondria under stress.

ISRIB stops the expression of SESN2 without inducing apoptosis the way P53 does. 

mitochondrial dysfunction and integrated stress response ISRIB 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4825760/

Under ER or mitochondrial stress ATF4 is expressed which increases SESN2 mitochondrial genes.

 ATF4 targets Nuclear genes involved in folding and assembly of proteins in the ER and ATF acts on mitochondrial genes involved with metabolism including protection against oxidative stress and regulation of apoptosis. 

Activation of p53 abolishes and reverses the earlier ATF4-mediated pro-survival stress response and induces apoptotic cell death.

SESN2 are  sestrins which hault growth under times of stress.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3858445/

ER stress, Memory loss,  and Alzheimer's:  the unfolded protein response (high ATF4)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3906588/

mice given ISRIB had reversed memory loss
https://www.ncbi.nlm.nih.gov/pubmed/23741617/

So my question is...can mitochondrias be visualized moving down axons in response to ISRIB.

2016 Alzheimer's and mitochondria review paper
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746252/




Wednesday, July 12, 2017

Zika, malaria drugs, and the ACTH receptor


Malaria drug protects against Zika infection
https://medicine.wustl.edu/news/malaria-drug-protects-fetuses-from-zika-infection/

This malaria drug is hydroxychloroquine.

Chloroquine causes an ACTH dump
https://www.ncbi.nlm.nih.gov/pubmed/6300682

Placenta is the origin of ACTH in pregnancy
https://www.nature.com/nature/journal/v254/n5501/abs/254620b0.html

ACTH could compete with the Zika virus for the ACTH receptor. Thus the protection by chloroquine could be by increasing the amount of ACTH.

Zika and ACTH receptors
http://angelabiggs.blogspot.com/2017/05/zika-acth-receptors-and-muscle-tightness.html
http://angelabiggs.blogspot.com/2017/06/updated-virus-families-bind-and-enter.html

Zika virus causes "old man syndrome" on the second day of the infection be due to the muscle tightness?  (my sister had Zika in Mexico and this is what she described happened on day 2)

My sister also mentioned that her feet felt like they were burning.

taking supplemental ACTH for "Cushing disease" can cause the burning sensation and a gait to the walk
http://www.ehealthme.com/ds/acth/burning-sensation/

For infants with zika virus they have seen increased pigment in the eyes
http://www.nbcnews.com/storyline/zika-virus-outbreak/babies-zika-linked-birth-defects-may-have-eye-trouble-too-n514876

High ACTH given to Zebra fish caused pigment a similar pigment increase.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4365489/


Friday, July 7, 2017

Does HPV5 use the Cannabinoid 2 receptor?

HPV5 and squamous skin cancer
http://onlinelibrary.wiley.com/doi/10.1111/j.1468-3083.2010.03713.x/abstract

squamous skin cancer over expresses CB2 receptors
https://www.ncbi.nlm.nih.gov/pubmed/20335147

which means that HPV5 uses the  CB2 receptor or CB1?

there is a bit of confusion because I had squamous linked to CB1 and basal linked to CB2

HPV16 for squamous and HPV18 for adenocarcinoma (basal cell)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2361088/

Previous post on HPV and Cannabinoid receptors
http://angelabiggs.blogspot.com/2016/08/cannabinoid-receptors-and-human.html

hpv16 and squamous (head and neck cancers)
http://clincancerres.aacrjournals.org/content/8/10/3187

CB2 receptor and head and neck
https://www.ncbi.nlm.nih.gov/pubmed/23601830

squamous clear cell carcinoma
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3687164/

Co-carcinogenesis hypothesis (Francis Peyton Rous) a virus and a carcinogen together cause cancer.

 My expansion on the hypothesis: It must be a nuclear virus.  (not all viruses enter the nucleus) The carcinogen and virus must be in the same cell's nucleus.  The receptor used by the virus to enter gives characteristics to the cancer. The triggered pathways are over expressed.

Cannabinoid one receptor and pancreatic cancer
http://www.ejcancer.com/article/S0959-8049(08)00810-1/pdf

HPV18 and pancreatic cancer
https://www.sciencedaily.com/releases/2012/07/120731151739.htm

so I might have had the HPV16 &18 viruses and cannabinoid receptors flipped

HPV18 : cb1 : basal cancer
HPV16: cb2: squamous

HPV18 and HPV16 with asbestos
https://www.ncbi.nlm.nih.gov/pubmed/24494324

Most breast cancer was asbestos chrysotile with HPV16

 "HPV-16 always co-exists with increased Chrysotile Asbestos deposits, and the outline of the breast cancer positive area is a relatively smooth and round or oval shape, and breast cancer with HPV-18 always co-exists with increased Tremolite Asbestos"

Most triple negative breast cancer are round and oval shaped
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4538191/





Thursday, July 6, 2017

HPV viruses that do not cause cancer

Previous post on HPV and Cannabinoid receptors
http://angelabiggs.blogspot.com/2016/08/cannabinoid-receptors-and-human.html

HPV16: CB1
HPV18: CB2

What receptors do the other non cancer HPV strains use if not Cannabinoid1 or cannabinoid2?

Novel cannabinoid receptors are related ( TRPV )
https://www.ncbi.nlm.nih.gov/pubmed/15866316

transient receptor potential vanilloid TRPV is also known as the capsaicin receptor
https://en.wikipedia.org/wiki/TRPV1

These should be low risk cancer strains because the receptor does not cycle to the nucleus but because the receptor used is the capsaicin receptor this could explain why it feels hot.

90% of burning HPV genital  warts:
HPV 6 and HPV 11

As DNA viruses these must be moving into the mitochondria...TRPV1 are located on the mitochondria. Capsaicin induced increased mitochondrial calcium.
https://www.ncbi.nlm.nih.gov/pubmed/26010461

capsaicin and the treatment of moles and warts
https://www.google.com/patents/US20020006449

Can some warts look like moles?

pigmented warts
https://www.dailystrength.org/group/hpv/discussion/hpv-and-moles-again

HPV 16 and HPV 18 shuttle between the cytosol and the nucleus
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0075625

So are cannabinoid receptors at the plasma membrane or the nuclear membrane in the cytosol?

or do they come in using cannabinoid then use another group of receptors at the nucleus?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2190029/

peroxisome proliferator-activated receptors (PPARs, with three subtypes αβ (δ) and γ) ?








Wednesday, June 28, 2017

Comparing xanthomonas and spirochetes....and overlap of butyrolactones used as quorum?

Spirochetes look connected to vit C and cortisone levels
http://angelabiggs.blogspot.com/2016/06/does-hpylori-bind-to-sodium.html
http://angelabiggs.blogspot.com/2016/07/spirochetes-and-high-cortisol.html

Are they also connected weakly to butyrolactones?

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 Stenotrophomonas 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?

Do spirochetes like lyme diseases' Borrelia bacteria use butyrolactones too?  Maybe not continuously like Xanthomonas but at times? which is why vit C or vaccines can trigger the fibomyalgia like reactions in lyme disease patients?

Genes have been found to be shared between Xanthomonas and Borrelia.
https://www.ncbi.nlm.nih.gov/pubmed/?term=Borrelia+burgdorferi+Xanthomonas

Can is lyme disease a trigger of the same diseases as Xanthomonas? bone spurs, the fibromyalgia, pituitary tumors that GHB cause?

Xanthomonas are also called stenotrophomonas when they infect people

http://angelabiggs.blogspot.com/2015/11/stenotrophomonas-possible-connection-to.html

no pubmed ref connecting Borrelia to bone spurs but patient posts

"When I got Lyme symptoms last spring, I developed bone spurs in my right shoulder and knee almost over night. Recently I went off Banderol and Samento for 36 hours and had a bad herx.....joint pain, fatigue, depression, and I feel like I have developed bone spurs in my left shoulder. I get a popping noise when I put my arm behind my back, which I didn't have the day before. My upper and lower spine is also achy. I am not sure if the inflammation from Lyme has triggered an autoimmune disease. Has anyone else had this symptom? It seems to happen whenever I have a bad herx. I am detoxing with cucurmin, epsom salt baths, chorella, parsley, pinella, burbur, and sparga. Thanks for any advice."

fibromyalgia and borrelia
https://www.ncbi.nlm.nih.gov/pubmed/7573105


Collection of what might kill spirochetes http://angelabiggs.blogspot.com/2016/05/brassicaceae-mustards-mustard-flowers.html