Tuesday, December 22, 2015

Candida's quorum sensing, farsenol, and Addison's disease

Microbes talk to each other by secreting compounds to each other.  These compounds have the ability to interfere with the host within whom the infection lives.  Candida secretes farnesol which is known to inhibit P450 enzymes.  This could explain the correlation of addison's disease and candida infections.

Polyglandular Autoimmune syndrome type one strongly associated with candida infections
http://emedicine.medscape.com/article/124183-clinical

Autoimmune thyroid and candida
http://www.ncbi.nlm.nih.gov/pubmed/9039290

Addison's disease has antibodies to 21-hydroxylase

21-hydroxylase is a p450 enzyme
https://en.wikipedia.org/wiki/21-Hydroxylase

Farnesol inhibits cytochromeP450
https://libres.uncg.edu/ir/uncg/f/G_Raner_Farnesol_2002.pdf

liver disease in PAI
http://www.ncbi.nlm.nih.gov/pubmed/9025859

Cytochrome p450 is a hepatic autoantigen in PAI
http://www.ncbi.nlm.nih.gov/pubmed/9141515

P450 antibodies different in PAI and idopathic addison's disease
http://www.jci.org/articles/view/116843

Farnesol is a quorum haulting Candida growth and is secreted by candida
http://aem.asm.org/content/68/11/5459.abstract
http://www.ncbi.nlm.nih.gov/pubmed/16420349

Lymphocytic colitis and polyglandular syndrome one in a patient
http://www.ncbi.nlm.nih.gov/pubmed/?term=microscopic+colitis+polyglandular

Lymphocytic colitis is associated with Candida
http://www.ncbi.nlm.nih.gov/pubmed/23314667

Polyglandular syndrome type two, more commonly found in adults has a strong association with 21-hydroxylase antibodies but not candida?

Could type 2 be different types of fungal infections that also use farnesol for quorum? Is it saccharomyces in the GI tract or candida in the vagina?

The idopathic addison's is associated with PAII
http://www.ncbi.nlm.nih.gov/pubmed/2333733

adult idopathic addison's major antibody is 21-hydroxylase
http://www.ncbi.nlm.nih.gov/pubmed/1511745
http://www.ncbi.nlm.nih.gov/pubmed/8959085

Microscopic colitis, addison's, and skin pigmentation
http://www.ncbi.nlm.nih.gov/pubmed/?term=microscopic+colitis+addison%27s

Patient with ?ulcerative colitis?, vitilgo, addison's (vitilgo is a  hypopigmentation skin disease)
http://www.ncbi.nlm.nih.gov/pubmed/25148815

Hyperpigmentation and PAII
http://www.ncbi.nlm.nih.gov/pubmed/25148815

Hypopigmentation is caused by malassezia (tinea vesicolor)
http://www.ncbi.nlm.nih.gov/pubmed/24320140

Microscopic colitis in woman has been found to have increased autoantibodies and anti-saccharomyces
http://www.ncbi.nlm.nih.gov/pubmed/23776613

note that saccharomyces is currently being used as a probiotic for c.diff
http://iai.asm.org/content/67/1/302.full

Collagenous colitis and addison's disease
http://www.ncbi.nlm.nih.gov/pubmed/9881910
http://www.ncbi.nlm.nih.gov/pubmed/2801683
https://www.jstage.jst.go.jp/article/endocrj1993/45/4/45_4_581/_article


Raynaud's is a mysterious vasodilation issue where when exposed to the cold the person has the opposite response to cold: instead of dilating the vessels of the fingers the blood vessels contract first in a vasospasm

p450 and vasodilation
http://www.ncbi.nlm.nih.gov/pubmed/17572144

Nitric oxide normally inhibits P450
http://www.ncbi.nlm.nih.gov/pubmed/9400024

When the body is exposed to cold temperatures nitric oxide triggers the blood vessels to contract.

What would happen if farsenal is constantly inhibiting p450 ?

Sclerodema and raynaud's
All scleroderma patients have secondary raynaud's....but not all raynaud's have scleroderma

Scloerodema and p450
http://www.ncbi.nlm.nih.gov/pubmed/11263781

How often is raynaud's with addison's disease?

Asthma and p450
http://www.ncbi.nlm.nih.gov/pubmed/15066132














Tuesday, December 15, 2015

Mesothelioma and co-carcinogenesis

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 Nobel prize for HPV work)  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2135410/

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen  inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.

Cancer cells can make unlimited copies because of the telomere modifications done by the virus. 

There are DNA polymerases and RNA polymerases. Think of DNA as the cookbook and RNA as recipes...one polymerase copies the entire cookbook, one makes repairs, and one polymerase copies just a recipe.

If the viral polymerases are inhibited by the carcinogen instead of the host's polymerase then the cancer "stem" cell could be created.  The host's polymerases have access to and can make unlimited copies.

In mesothelioma the carcinogen that has been linked is asbestos and the virus which has been linked is sv40.

Gangliosides are receptors to sv40
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC202381/

Ganglioside GM2 is increased in Mesothelioma 
http://www.ncbi.nlm.nih.gov/pubmed/25421609

sv40 induces mesothelioma
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1886912/

asbestos and mesothelioma
http://www.ncbi.nlm.nih.gov/pubmed/18671157

Asbestos inhibiting polymerases
http://www.ncbi.nlm.nih.gov/pubmed/21543585


Hashimoto's thyroid disease: cross-targeting of Candida and a flavivirus?

Autoimmune cross-targeting hypothesis: a virus marks the inside of a cell while a larger infection marks the outside and the combination triggers autoimmune disease.  The immune system is instructed to destroy both the inside and the outside of the target.

For Hashimoto's does a flavivirus mark the inside while candida marks the outside?

Hashimoto's and viral infections

Hepatitis C (flavivirus)

note the the flavivirus dengue has been linked to the thyroid too

HPV B19

Family with genetic disorder linking Hashimoto's and Candida infections

Depression's SSRIs, the flu, and autism...can cross-targeting explain why only 50% get autism?


Autoimmune cross-targeting hypothesis: a virus marks the inside of a cell while a larger infection marks the outside and the combination triggers autoimmune disease.  The immune system is instructed to destroy both the inside and the outside of the target.


Low serotonin causes depression

Autism increased by 50% when antidepressant drugs are taken during pregnancy: Selective serotonin reuptake inhibitors specifically
http://www.sciencedaily.com/releases/2015/12/151214130227.htm

SSRIs bound to the outside of the frontal lobe nerves at the serotonin transporters

Testosterone increases the number of serotonin transporters
http://www.sciencedaily.com/releases/2015/01/150126083816.htm

This means more bound to the outside of the frontal lobe nerves increasing the change of the immune system attacking.

If we say that autism is an autoimmune disease caused by cross-targeting.

Autism and autoimmune antibodies to fetal brain
https://spectrumnews.org/news/researchers-flag-targets-of-autism-linked-antibodies/

 The flu virus which infects inside the frontal lobe nerves and RA which causes antibodies against the outside of frontal lobe nerves had been considered as the cause of birth autism on this blog.

Flu and autism
http://www.webmd.com/brain/autism/news/20121109/flu-pregnancy-autism

Frontal lobe and the flu
http://www.sciencedirect.com/science/article/pii/S0887899499001502

RA in mothers and autism
https://spectrumnews.org/news/large-study-links-autism-to-autoimmune-disease-in-mothers/

 (the vaccine triggered form of autism occurs on different parts of the brain according to this blog)

 However the amount of RA diagnosed has been decreasing and the amount of antidepressants prescribed has been increasing.

Could it be that SSRIs replace the outer infections of RA (mycoplasmas)? Did these babies born with autism from mothers taking SSRI get exposed to the flu? Is that why it is only 50% and not all?

Note that penicillin triggers autoimmune hemolytic anemia much the same way by coating the outside of the red blood cells.



Thursday, December 10, 2015

Not just the flu but flaviviruses and heptachlor could trigger Parkinson's through cross-targeting

Cross-targeting hypothesis suggests that simultaneous infections on one target triggers autoimmunity.  One infection on the outside of the target cell and one infection, like a virus, on the inside of the target.  

Target: substantia nigra neurons
Inside: swine flu, flavivirus, heptachlor
Outside: mycobacteras

parkinson's and melanoma
http://cebp.aacrjournals.org/content/16/6/1081.full
http://www.ncbi.nlm.nih.gov/pubmed/16718266?dopt=Abstract

Is this a shared virus between melanoma and parkinson's? Flaviviruses?

melanoma and flaviviruses
http://angelabiggs.blogspot.com/2015/09/skin-cancer-melanoma-and-melanocortin.html

Note that they are currently creating parkinson's disease mouse models with flaviviruses
http://www.ncbi.nlm.nih.gov/pubmed/17447419

prostate cancer, melanoma and parkinson's seem linked
http://www.neurologyreviews.com/specialty-focus/parkinson-s-disease/article/parkinson-s-disease-may-increase-risk-of-melanoma-or-prostate-cancer/87b6d2451e0f60eab67b5671d4128c70.html

chikyngunya virus and prostate cancer
http://www.hindawi.com/journals/criu/2015/120535/

hepatitis C which is a flavivirus has also been linked to risk of parkinson's
http://www.ncbi.nlm.nih.gov/pubmed/25608223

swine flu and parkinson's
http://www.ncbi.nlm.nih.gov/pubmed/23271861
http://www.ncbi.nlm.nih.gov/pubmed/21655265

Note that it only takes one virus to mark the inside.

Can heptachlor replace the virus in some cases? thus explaining the milk and parkinson's disease connection since milk has been found to be contaminated with heptachlor.  The inside of the cell has been marked as foreign and non self...a chemical instead of a virus.

Breast cancer and melamona cancers are increased in parkinson's patients
http://www.ncbi.nlm.nih.gov/pubmed/22278152

Does too much heptachlor leaves deposits in the breast and brain?

Heptachlor also deposits in the breast where it acts like a carcinogen with the  viruses: hpv or epstein barr

Bullous pemphigoid with breast cancer, psoriasis and parkinson's
 http://www.ncbi.nlm.nih.gov/pubmed/24791209

psoriasis and parkinon's connection

mycobacteria connections

ischemic stroke connected to high cholesterol and parkinson's

(evidence that mycobacterias are there)

Up until now I have said that cancer is caused by a carcinogen which inhibits a polymerase and a virus.  Obviously heptachlor and viruses can exist together in the substantia nigra neurons.  The reason these neurons die and do not become cancerous is because neurons cannot go through cell division because they lack centrioles. 

Tuesday, December 8, 2015

Mycobacterias possible connection to Type 2 diabetes and nonalcoholic fatty liver disease.

Title:
Mycobacterias possible connection to Type 2 diabetes and nonalcoholic fatty liver disease.

Abstract:
 Mycobacterias could cause disease when the cGMP they produce for quorum sensing interferes with the host's normal cGMP cellular systems.

https://www.researchgate.net/publication/270164235_Quorum_Sensing_and_Biofilm_Formation_in_Mycobacteria_Role_of_c-di-GMP_and_Methods_to_Study_This_Second_Messenger

Introduction:

Chron's, psoriasis, psoriatic arthritis, and parkinon's disease have all been associated with mycobacterias.  All 4 have also been associated with fatty acid liver disease and type 2 diabetes.

 The chemical reactions for type 2 diabetes and fatty acid liver disease are basically the same involving NO increasing cGMP levels.

Type 2 diabetes is when the pancreas makes insulin but the body's cells do not respond to insulin, a state called insulin resistance.  Normally when cells see insulin they produce NO which activates cGMP at the plasma membrane which stimulates the glucose transporter to import glucose into the cell.  The glucose transporter might be overloaded if mycobacterias are present and as a result shut down.

The same sort of NO/cGMP system functions in the liver for the break down of fatty acids.
http://www.ncbi.nlm.nih.gov/pubmed/12632570  If cGMP levels are constantly high this could cause the fatty acid liver disease.

Note that Nitric oxides role has been considered but that the reason for a disfunction at this step has not been found. http://www.ncbi.nlm.nih.gov/pubmed/24878261

Mycobacterias use cGMP for quorum sensing to communicate about the growth of the biofilm mycobacteria colony size.  It seems logical that a mycobacteria infection would cause cGMP pathways to become disrupted. This hypothesis paper analyzes mycobacterias cause as a possible cause of  cGMP linked diseases including type2 diabetes and fatty liver disease.

Hypothesis
Mycobacterias cause type 2 diabetes and nonalcoholic fatty liver disease by secreting cGMP into the bloodsteam of the host.

Evaluation of Hypothesis

Tuberculosis has a long history of association with type 2 diabetes and has recently been discovered to be linked to non alcoholic fatty liver disease.  Both type 2 diabetes and non alcoholic fatty liver disease can be connected to cGMP in their pathways of normal function.   Mycobacterias like tuberculosis use quorum sensing to communicate and the molecule they use is a type of cGMP. The hypothesis is that the cGMP made by the mycobacteria disrupts the normal cGMP processes of the host causing high cholesterol through fatty liver disease and insulin resistance by disrupting the glucose transporter.

Resveratrol, which has been shown to activate cGMP, has also been shown to decrease the amount of fat in the liver in cases of non alcoholic fatty liver disease.  Does the normal cGMP inside the cell down regulate if the mycobacteria has flooded the bloodstream with cGMP? Does fatty liver disease cause high cholesterol?

The glucose transporter of all of our cells has a plasma membrane cGMP stimulation that occurs after insulin raises NO levels in cells.  Is there less internal cGMP to turn the transporter on if bloodstream cGMP is high? Is this state what causes the insulin resistance of type 2 diabetes?

Both type 2 diabetes and nonalcoholic fatty liver disease has been connected to obesity.
However, Type 2 diabetes is not always associated with obesity because for obesity to be caused by the mycobacteria the immune system must be engaged and producing TNF-alpha.

 THF-alpha is part of the immune response against mycobacterial infections and separately TNF-alpha is how the host's body maintains the proper about of adipose tissue. If the immune system is over engaged for too long against mycobacterias the body would have unusually high leptin levels favoring more adipose tissue....obesity.

 If the host's immune system has chosen to calm down or doesn't fight the mycobacterias then high cholesterol and type 2 diabetes could exist without obesity because these are caused not by TNF-alpha but by the cGMP.  The cGMP from the mycobacteria can cause the fatty liver disease and type 2 diabetes in a person who would appear healthy and not obese.

The finding of high levels of alpha-synuclein in the blood of type 2 diabetes patients, parkinson's patients brains, and some Crohn's patients guts connect it to cGMP too. In fact cGMP was found to increase the levels of alpha-synuclein.

High cGMP could prevent the normal stimulation of glucose transport of cells and the breakdown of fatty acids while simultaneously dumping synuclein where the mycobacterias are growing because of the same cGMP.

Bipolar disorder has a strong association with type 2 diabetes too.  Could bipolar disorder be a cGMP disorder too? The SERT transporter which moves serotonin has been shown to be altered by cGMP levels. Or is bipolar a separate autoimmune disease triggered by the combination of mycobacterias and cmv virus?

Also note that Testosterone levels appear to be altered.
http://www.ncbi.nlm.nih.gov/pubmed/23797822?dopt=Abstract&holding=f1000,f1000m,isrctn







Wednesday, December 2, 2015

Heterocyclic Amines, cancer, and fire fighters...a co-carcinogenesis hypothesis


Firefighters are probably exposed the most to polycyclic aromatic hydrocarbon compounds.
http://www.ncbi.nlm.nih.gov/pubmed/24512044

Heterocyclic amines are from meat cooked at high temperatures.
Polycyclic aromatic hydrocarbons are from plant matter cooked at high temperatures.

Polycyclic aromatic hydrocarbon compound:
A compound built from two or more benzene rings. Sources of PAHs include fossil fuels and incomplete combustion of organic matter (in auto engines, incinerators, and even forest fires)." - National Research Council, 1994

Benzenes are carcinogens and inhibit polymerases.

https://books.google.com/books?id=sPgEDYgjlKAC&pg=PA203&lpg=PA203&dq=benzene+inhibits+polymerases&source=bl&ots=HQcY8V1E-H&sig=y7R938yWNDKgUc9xj91eIlUnDgQ&hl=en&sa=X&ved=0ahUKEwjLw5vjkb7JAhWCdx4KHRGoBOEQ6AEIPzAF#v=onepage&q=benzene%20inhibits%20polymerases&f=false

Lung cancer and leukemia from PAH
http://www.ncbi.nlm.nih.gov/pubmed/11293301
http://www.ncbi.nlm.nih.gov/pubmed/15833386

PAH has caused cancer in animals' lung, stomach, and skin.
Benzene goes into lung cells and migrates to the bone marrow. PAH is probably similar.

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 nobel prize)

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen with a benzene ring inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.

Cancer cells can make unlimited copies because of the telomere modifications. Co-carcinogenesis requires a virus and a carcinogen to start the cancer. The cancer tumor wears the entry receptor on the surface.

So what viruses infects bone marrow or lung tissue?

Respiratory syncytial virus infects lung, blood, and bone marrow....so does flaviviruses
We need a vaccine for these viruses to protect our firefighters.



Tuesday, December 1, 2015

The conundrum of high cholesterol, type2 diabetes, low testosterone, and fatty liver: is it from a mycobacteria's quorum cGMP?

Type 2 diabetes : the pancreas makes insulin but the body's cells do not respond to the insulin. 

Normally insulin from the pancreas stimulates the body's cells to produce NO which then activates cGMP which stimulates the glucose transporter to import glucose.  

Mycobacterias use cGMP for quorum sensing, communicating the growth of the biofilm mycobacteria colony.

If the body is infected with mycobacterias could the cGMP released by them disrupt the host's system causing the cells not to respond to insulin? cGMP does control the glucose transporter. Normally insulin raises NO which then triggers cGMP to turn on and import glucose at the transporter.

 High cholesterol tends to exist with Type 2 diabetes too.  Could cGMP be upsetting the liver which makes the cholesterol? Does high plasma cGMP cause nonalcoholic fatty liver disease? not the other way around? Fatty liver disease has been found statistically high with tuberculosis patients. 

Resveratrol has been shown to decrease fat deposits in the liver. Resveratrol has been shown to activate cGMP in cells. Has intracellular cGMP been suppressed because of the high plasma cGMP from mycobacterias?

Testosterone is made from cholesterol in the body. Why would testosterone be low when cholesterol is high? 

Testosterone is made in the testicles. The level of cGMP is critical for the proper function of males. Cholesterol is made into testosterone then the testosterone triggers cGMP.  cGMP is raised for reaction but then must go down. If cGMP is abnormally high it would make sense that the body would suppress testosterone production to keep internal cGMP lower?


Note that psoriasis has been associated with mycobacterias.  Psoriasis alone has been associated with a risk of fatty liver disease.

 Chron's has also been associated with fatty liver disease
http://www.ncbi.nlm.nih.gov/pubmed/16514570


Earlier post about mycobacterias:
http://angelabiggs.blogspot.com/2013/06/mycobacteria-diseases-psoriasis-chrons.html

References: 

mycobacteria's use and require cholesterol

 2013 Aug;9(8):479-93. doi: 10.1038/nrendo.2013.122. Epub 2013 Jun 25.

Testosterone and insulin resistance in the metabolic syndrome and T2DM in men.


http://www.ncbi.nlm.nih.gov/pubmed/23797822?dopt=Abstract&holding=f1000,f1000m,isrctn

Mycobacteria in host macrophage uses cholesterol
http://www.sciencedirect.com/science/article/pii/S1074552112000099


Quorum sensing and biofilm formation in mycobacteria: role of c-di-GMP and methods to study this second messenger.



Testosterone protects against type 2 diabetes in men


Testosterone and its precursors and metabolites enhance guanylate cyclase activity (progesterone/5a-dihydrotestosterone/pregnenolone/cyclic GMP) DAVID L. VESELY
http://www.pnas.org/content/76/7/3491.full.pdf


Insulin stimulates cGMP pathway in smooth muscle

non alcoholic fatty liver disease with type 2 diabetes...70% of those with type 2

Fatty liver disease with TB

mycobacteria and metabolic syndrome

Friday, November 20, 2015

The bacteria Stenotrophomonas possible connection to fibromyalgia and pituitary tumors.

Title  
Stenotrophomonas possible connection to fibromyalgia and pituitary tumors.

Abstract
Stenotrophomona infections could cause disease when the butyrolactones they produce convert to GHB in the human body.  This hypothesis suggests a common connection to strenotrophomona which explains the known overlap with the fibromyalgia, osteoarthritis, ovarian cysts, dyspnea,  osteophytes , and pituitary tumors.

Introduction
Xanthomona is the "black rot "bacteria that infects plants favoring nightshade plants. They use butyrolactones as signaling molecules between them.  One form of Xanthomonas has been found to infect the respiratory tract of people and is considered a new bacterial genus: Xanthomonas maltophilia was renamed Stenotrophomonas maltophilia.  Xanthomonas has been known to infect surgical bone equipment as well.  People with osteoarthritis have noticed sensitivities to nightshades which could reflect the origins of the bacteria. Further Stenotrophomonas maltophilia is unable to ferment lactose possibly causing sensitivities to lactose in people.   This hypothesis makes the assumption that stenotrophomonas infections of the body signal like the xanthomonas of plants and make butyrolactones which interfere with normal GABA signals.

Hypothesis
Stenotrophomonas produce butyrolactones which  converts  to GHB in the human body. The GHB could trigger the immune system to develop antibodies to GABA.  If this occurs the immune system could confuse an immune attack against the bacteria stenotrophomonas with nerve endings. An immune attack at nerve endings could be the cause of fibromyalgia.  The GHB could if in high levels in the blood stream reach the pituitary and over stimulate it.  When the pituitary over produces hormones they cause ovarian cysts, dyspnea, and osteoarthritis.  High GHB could be the cause pituitary tumors.  This paper will analyze the areas of overlap and try to prove that stentrophomonas are there.

Evaluation of Hypothesis

Fibromyalgia, osteoarthritis, ovarian cysts, dyspnea, osteophytes, and pituitary tumors overlap but the reason why is unknown.  It is my contention that stenotrophomonas links them together.
Stenotrophomonas  is typically, historically been a respiratory or septic infection of immune compromised or cystic fibrosis patients.  Recently surgeries have resulted in cases of Strenotrophomona infection.  What happens in a person with a healthy, non suppressed immune system when they have Strenotrophomona?

If stenotrophomonas are in the body producing butyrolactones the body would converts these butyrolactones  into GHB, 4-hydroxybutanoic acid.

The GHB made by the bacteria over stimulates the pituitary causing an increase in growth hormone. (similar to acromegaly) Excess growth hormone alters bone metabolism which could be causing the osteoarthritis and bone spurs we see.

Patients with bone marrow or bone spur surgery have increasingly developed metastic cellulitis from stenotrophomona following surgery.   Follow up should be done on any surgery that resulted in an infection because it is likely that if the bacteria persists in the patient osteophytes and osteoarthritis could occur.

Osteophytes, bone spurs,  have strong associations with dyspnea or troubled breathing. ( Osteoarthritis has been associated with bone spurs and is very different from the bone spurs of psoriatic arthritis. )   Osteoarthritis has also been found to have high rates of dyspnea in the elderly.   Could dyspnea be the result of high GHB?  yes.

GHB acts as a central nervous system depressor.  

In fact GHB is also known as the narcotic date rape drug and  a woman who started giving this party drug version to herself on a daily basis for 2 years developed Crushing disease.  Crushing disease is a pituitary tumor that releases too much ACTH. 

GHB has a direct effect on the pituitary as a strong stimulator because it is so similar to GABA and binds the GABA receptors which are not just present at nerve endings  but are present on the pituitary gland.

Normally GABA stimulates the pituitary and is thought to alter hormone release but obviously long term over stimulation of the receptors causes Crushing disease tumors. 

Fibromyalgia has been associated with pituitary dysfunction and abnormal ACTH.   Fibromyalgia has also been associated with Osteoarthritis and lower back pain.  Osteoarthritis of the spine’s discs is believed to be the cause of lower back pain.  

Fibromyalgia has been linked to dyspnea and breathing issues.  Interestingly dyspnea has correlations with osteoarthritis and osteophytes which is the bone spurs.  The pituitary has also been associated with dyspnea.   Is dyspnea caused by GHB from stenotrophomonas?  Is fibromyalgia caused by GHB antibodies?

If the bacteria is secreting compounds that become GHB are there antibodies to GHB in fibromyalgia patients? GHB and GABA are such tiny molecules can antibodies be generated against them? How similar are they? How much cross reactivity exists? Does albumin bind to them and help to generate the antibodies by making it a larger compound? 

Fibromyalgia patients have been found with polycystic syndrome.  Pituitary tumors can produce high levels of FSH which cause ovary dysfunction specifically polycystic syndrome.

Erectile dysfunction can be caused in men with pituitary adenomas. 


The Date Rape drug is actually improperly used sleep aid medications which means long term prescribed use can also cause pituitary tumors, dyspnea,  osteoarthritis and the reproductive issues.  Xyrem is GHB.  Ambien is GABA.  No fibromyalgia would be triggered by medications because the immune system is not involved as it is in stenotrophomona infections .

This paper is still being written.

note that this bacteria does not like Chili peppers
http://www.ncbi.nlm.nih.gov/pubmed/27493606

Link to older post of references
http://angelabiggs.blogspot.com/2015/02/fibromyalgia-is-it-autoimmune-no-right.html

Chronic fatigue, fibromyalgia, and the pituitary
http://www.ncbi.nlm.nih.gov/pubmed/25832514
http://www.ncbi.nlm.nih.gov/pubmed/24959566
http://www.ncbi.nlm.nih.gov/pubmed/21946893

Monday, November 9, 2015

Carcinogens inhibit polymerases: reference links

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 Nobel prize for HPV work)  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2135410/

My co-carcinogenesis takes his further because carcinogens inhibit polymerases.

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen  inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.

Cancer cells can make unlimited copies because of the telomere modifications done by the virus. 

There are DNA polymerases and RNA polymerases. Think of DNA as the cookbook and RNA as recipes...one polymerase copies the entire cookbook, one makes repairs, and one polymerase copies just a recipe.

If the viral polymerases are inhibited by the carcinogen instead of the host's polymerase then the cancer "stem" cell could be created.  The host's polymerases have access to and can make unlimited copies.

Looking at breast cancer....the polymerase involved in DNA repair could the culprit.

Rous' hypothesis is Co-carcinogenesis which requires a virus and a carcinogen together to start the cancer.  My hypotheses are that the cancer tumor wears the virus' entry receptor on the surface and that the carcinogens must be polymerase inhibitors.

Benzene inhibits polymerases
http://www.ncbi.nlm.nih.gov/pubmed/3381009
http://www.ncbi.nlm.nih.gov/pubmed/2926830
http://www.ncbi.nlm.nih.gov/pubmed/4006011 (mito but still a polymerase....needs to happen in the nucleus to cause cancer)

alcohol as a carcinogen in liver cancer
http://www.ncbi.nlm.nih.gov/pubmed/23101985

Alcohol inhibits polymerases
http://www.ncbi.nlm.nih.gov/pubmed/15585138

Aflatoxin inhibiting polymerases
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC244025/

Dioxin stimulates or inhibits RNA synthase depending on cell type?
http://www.ncbi.nlm.nih.gov/pubmed/7126257

Asbestos inhibiting polymerases
http://www.ncbi.nlm.nih.gov/pubmed/21543585

Aldehydes inhibiting polymerases
http://www.researchgate.net/publication/229290450_Differential_inactivation_of_DNA_polymerases__and__by_aldehyde_compounds

Formaldehyde inhibiting polymerases
http://link.springer.com/article/10.1007/BF01839520#page-1

Nitrates and nitrites inhibit viral polymerases

https://books.google.com/books?id=NW6m_TqbXWQC&pg=PA121&lpg=PA121&dq=nitrites+polymerase&source=bl&ots=q-JTD0FMD9&sig=LNVFbWXAzveE9SsQVPcnFpljhcQ&hl=en&sa=X&ved=0CD0Q6AEwBGoVChMIwJuOmdyDyQIVQ-9jCh3Mvwss#v=onepage&q=nitrites%20polymerase&f=false

nitrates, nitrities, nitric oxide connection
http://www.ncbi.nlm.nih.gov/pubmed/18167491

skin and nitric oxide
http://www.ncbi.nlm.nih.gov/pubmed/14615895
http://www.ncbi.nlm.nih.gov/pubmed/15275864

nitric oxide and nitrate  inhibiting polymerases
http://www.ncbi.nlm.nih.gov/pubmed/14642390

Antiviral acyclovir inhibits epstein barr polymerase (would only matter in breast or glial cells  because in nerves it would be in the mitochondria)
http://www.pnas.org/content/77/9/5163.full.pdf

special note: BRCA susceptibility genes in breast cancer are involved with DNA polymerases and DNA repair. the BRCA protein is promoted to areas of DNA damage.

http://www.shmu.edu.cn/courses/2010aut/20100925/20101101/yuxiaoli-Inhibition%20of__%20Poly(ADP-Ribose)%20Polymerase%20in%20Tumors%20from%20BRCA%20Mutation%20Carriers2009.pdf

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2917312/

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3078634/

So when a virus opens up the DNA and modifies the telomeres does the cell view that as DNA damage?

Curcumin derivatives have been found to be specific inhibitors of DNA repair polymerase.
http://cdn.intechopen.com/pdfs-wm/22183.pdf

Curcumin and cancer
http://www.ncbi.nlm.nih.gov/pubmed/26546056
http://www.ncbi.nlm.nih.gov/pubmed/26537958
 note that if you were healthy you might not want this because it inhibits DNA repair

Thursday, November 5, 2015

Metribuzin, herpes zoster, and glioma

Francis Peyton Rous' Co-carcinogenesis hypothesis: that a virus and a carcinogen together cause cancer. (1966 Nobel prize for HPV work)

What I surmise from his hypothesis:

A virus enters a cell through a receptor, opens up and alters host DNA telomeres. The carcinogen  inhibits the virus' polymerase because viral polymerases have stronger binding affinities than the host's.

Cancer cells can make unlimited copies because of the telomere modifications. Co-carcinogenesis requires a virus and a carcinogen to start the cancer. The cancer tumor wears the entry receptor on the surface.

RNA synthesis inhibited by metribuzin. Is this evidence of metriubuzin acting as a carcinogen inhibiting polymerases?

There are DNA polymerases and RNA polymerases. Think of DNA as the cookbook and RNA as recipes...one polymerase copies the entire cookbook, the other polymerase copies a recipe.

Here is the reference where metribuzin appears to inhibit RNA polymerases.

Use of Isolated Leaf Cells of A butilon theophrasti to Localize the Action of Two Aminotriazinone Herbicidal Derivatives
Knton K. Hatzios

If a virus is present I am suggesting that metribuzin would bind to the viral polymerase stronger.


 2005 Nov;62(11):786-92.

Agricultural pesticide use and risk of glioma in Nebraska, United States.


 2005 May 15;161(10):929-38.

History of chickenpox and shingles and prevalence of antibodies to varicella-zoster virus and three other herpesviruses among adults with glioma and controls.

Tuesday, November 3, 2015

Autoimmune cross-targeting of the adult brain and the overlaps with other mental illnesses

Autoimmune cross-targeting in the adult brain and overlaps with other brain disorders

Cross-targeting hypothesis suggests that simultaneous infections on one target triggers autoimmunity.  One infection on the outside of the target cell and one infection, like a virus, on the inside of the target.  could this apply to these diseases?

 Cotard's syndrome

Cotard's syndrome where the person thinks they have died and they are a zombie.  They have lost sensations, have migraines with auras, catatonic moments, and issues of self starvation. Might not be autoimmune.

The antiviral drug causes cotard's in people with kidney failure

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2151143/

http://www.independent.co.uk/news/science/reversing-walking-corpse-syndrome-cotards-syndrome-trigger-found-and-its-a-household-cold-sore-cream-8888670.html

or is it the drug itself causing renal failure?
http://www.shortlist.com/news/common-sore-cream-can-make-you-believe-you-are-dead



Does PDD overlap with Cotard's syndrome?

Cerebellum and catatonia
http://www.researchgate.net/publication/21102475_Cerebellar_atrophy_and_catatonia

PDD catatonic
http://u2pea.free.fr/resources/Lorazepam,-fluoxetine-and-packing-therapy-in-an-adolescent-with-pervasive.pdf

Are these autoimmune issues of the Cerebellum? ataxia, migraine with aura, self starvation, sensory issues. Midlife migraine with aura had higher rates of cerebellum brain lesions later in life

Does Cotard overlap with the sutterella/campylobacteria form of autism? Or is this some other infection at the cerebellum.

Cotard also overlaps depression and schizophrenia: T.gondii has been linked to schizophrenia. Is a parasite involved with cotard?

a parasite of birds called Trichomonas gallinae
http://www.michigan.gov/dnr/0,4570,7-153-10370_12150_12220-27288--,00.html

In people trichomonas vaginalis has been identified as a sexually tramsmitted disease
http://www.ashasexualhealth.org/stdsstis/trichomoniasis/

Has anyone heard of trichomonas with cotard's? Does this occur through the kidney or the cerebellum?

The drooling, the fetid odor, the behavior match...please start testing for this.

Is it the trichomonas infecting the kidney causing the symptoms by damaging the kidney? Not autoimmunity? Does the CMMG go to the cerebellum?

Note that trichomonas has a PNP that works in reverse.  Could this mean that the parasite makes something that acts like CMMG?

Capgray's syndrome

Capgray's where they think their loved ones are an imposter
has lewy body dementia similar to PD

Capgray is linked with hypothyroidism (fungal involvement?)
The condition has prosopagnosia which is impaired facial recognition? 

Strong overlap with Asperger's where the person is unable to recognize facial expressions and Fregoly syndrome where unfamiliar people are thought to be familiar. These diseases are also linked to hypothyroidism.

Asperger's is an issue of the amygdala

 2005 May 1;57(9):991-8.

Functional disconnectivity of the medial temporal lobe in Asperger's syndrome.

Abstract

BACKGROUND:

Autistic spectrum disorders (ASD) are neurodevelopmental conditions that may be caused by abnormal connectivity between brainregions constituting neurocognitive networks for specific aspects of social cognition.

METHODS:

We used three-way multidimensional scaling of regionally parcellated functional magnetic resonance imaging (fMRI) data to explore the hypothesis of abnormal functional connectivity in people with ASD. Thirteen high-functioning individuals with Asperger's syndrome and 13 healthy volunteers were scanned during incidental processing of fearful facial expressions.

RESULTS:

Using permutation tests for inference, we found evidence for significant abnormality of functional integration of amygdala and parahippocampal gyrus (p < .05, false discovery rate [FDR] corrected) in people with Asperger's syndrome. There were less salient abnormalities in functional connectivity of anterior cingulate, inferior occipital, and inferior frontal cortex, but there was no significant difference between groups in whole brain functional connectivity.

Is capgray a fungal infection of a brain region?

 1987 Jan;150:117-21.

Brain imaging in a case of Capgras' syndrome.

Abstract

A patient developed Capgras' syndrome as part of an interictal psychosis of epilepsy; magnetic resonance imaging revealed bilateral subcortical lesions in occipitotemporal and frontal regions. These findings have implications for the postulated association between Capgras' syndrome and neuropsychological deficits, in particular prosopagnosia.


Geschwind Syndrome

Geschwind Syndrome involves the temporal lobe and has hyper religiosity "they feel god". Appears to be linked with temporal lobe epilepsy.

Van Gogh had Geschwind?
Khoshbin asserts that the painter suffered from a type of epilepsy that affects the temporal lobe of the brain. Geschwind had observed a syndrome he called interictal (i.e., between seizures) personality disorder, associated with temporal lobe epilepsy, that includes hypergraphia, hyper-religiosity, unstable sexual behavior, intermittent aggressiveness, and "stickiness" (i.e., clinging behavior).

Epilepsy and whopping cough bacteria
http://www.forbes.com/sites/tarahaelle/2015/11/03/surprise-link-between-epilepsy-and-whooping-cough-whats-the-connection/

DTP vaccine and sudden infant death syndrome
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1647245/

 2007 May;4(5):e180.

Association of human herpesvirus-6B with mesial temporal lobe epilepsy.




Alien hand is from frontal lobe lesions therefor it is not autoimmune. Having said that it could be the reason that the frontal lobe form of autism which is the RA and flu form created in pregnancy. Looking now to see if it is the form of autism with the arm flapping and uncontrolled movements.


 1989 Apr;46(4):456-9.

The alien hand syndrome. Clinical and postmortem findings.

Abstract

Two patients had automatonlike movements of their left hands and arms (alien hand syndrome) following damage to the brain. Autopsy findings in one patient demonstrated gunshot wound damage to the medial frontal white matter bilaterally, as well as the corpus callosum, right basal ganglia, internal capsule, and thalamus. The other patient had a ruptured anterior communicating aneurysm, with subsequent resection of the right frontal gyrus rectus. We postulate that this syndrome is due to the combination of a partial callosectomy and mesial frontal lesions.

Autism and movement disorders at birth
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC25000/

Monday, November 2, 2015

Attempting to connect amyloid to mitochondria movement (still writing)

Alzheimer's disease appears to be a dysfunction of the neurons's mitochondria.  The hallmark of Alzheimer's disease is the formation of amyloid plaques building up in the brain.  I had suggested previously that I thought the normal function of this amyloid protein was one of growth.  This post is a collection of links looking at what is currently known today and I am trying to piece together the mitochondria, amyloid, and this neuron growth notion into a feasible hypothesis that explains Alzheimer's.

First we know that agent orange, diacetyl (butter flavoring), and herpes which all damage the mitochondria cause amyloid plaque build up.

Diacetyl causes amyloid
http://www.ncbi.nlm.nih.gov/pubmed/22731744
Herpes causes amyloid
http://www.ncbi.nlm.nih.gov/pubmed/17980964
agent orange causes amyloid
http://www.publichealth.va.gov/exposures/agentorange/conditions/al_amyloidosis.asp

If you look at the full length protein before it is clipped it is found in the mitochondria and plasma membrane, specifically associated with calcium channels.

app in the mitochondria.
http://www.ncbi.nlm.nih.gov/pubmed/19544621
http://www.ncbi.nlm.nih.gov/pubmed/17911214
http://www.ncbi.nlm.nih.gov/pubmed/16943564

In alzheimer's you can see the app build up in the calcium channels

http://www.jneurosci.org/content/26/35/9057.full.pdf
Accumulation of Amyloid Precursor Protein in the Mitochondrial Import Channels of Human Alzheimer’s Disease Brain Is Associated with Mitochondrial Dysfunction

So here is what I am thinking: The app goes to the calcium channels, increases the calcium, turning up the mitochondria.  The mitochondria then moves down the nerve.  If you imagine the mitochondria as a little car that has to move down to where the nerve is growing or needing ATP at the tip of the nerve.

We already know that NO stops the mitochondria from moving
http://www.ncbi.nlm.nih.gov/pubmed/?term=mitochondria+moving+nitric

 2006 May;97(3):724-36. Epub 2006 Apr 5.

Nitric oxide impairs mitochondrial movement in cortical neurons during hypoxia.


The mitochondria has it's own NO synthase.  
For fireflies NO turns off the mitochondria which turns off the fireflies light. 

NO turns the mito off....does Calcium turn it on? since muscles are driven by Calcium released from the ER it would be logical calcium might trigger the mitochondria too. 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1819417/
 interacts directly with the Calcium channels and controls if and when the channels are at the membrane. Hypoxia increases  . This is the L-type channel of the plasma membrane, what about the mitochondria's calcium channels, are they increased?

Is Aβ the calling card of the mitochondria asking it to move down the neuron? increase the calcium channels thus increasing the calcium thus increasing the ATP?

http://www.sciencedirect.com/science/article/pii/S000527280900036X

Mitochondrial calcium as a key regulator of mitochondrial ATP production in mammalian cells


The mitochondria's Calcium uniporter and app
http://www.ncbi.nlm.nih.gov/pubmed/23982146

 2013 Dec;27(12):4776-89. doi: 10.1096/fj.13-234765. Epub 2013 Aug 27.

Mitochondrial dysfunction and calcium deregulation by the RanBP9-cofilin pathway.


The mitochondrial calcium uniporter: mice can live and die without it.


http://www.ncbi.nlm.nih.gov/pubmed/19544621
APP and myitochondrial dysfunction


 2007 Dec 18;429(2-3):95-100. Epub 2007 Oct 13.

Herpes simplex virus infection causes cellular beta-amyloid accumulation and secretase upregulation.




 2005 Aug 18;5:48.

Herpes simplex virus interferes with amyloid precursor protein processing.


 2015 Oct 21;5:15444. doi: 10.1038/srep15444.

Herpes Simplex Virus type-1 infection induces synaptic dysfunction in cultured cortical neurons via GSK-3 activation and intraneuronal amyloid-β protein accumulation.



Herpes viruses take over the mitochondrias transport and travel down the nerve.  Blocking calcium stopped the viral spread from one nerve to another
http://www.princeton.edu/main/news/archive/S33/79/51K43/


 1991 Feb;28(2):192-9.

Nerve growth factor-induced increase in calcium uptake by PC12 cells.


Lysine as a treatment for Alzheimer's because it helps herpes infections


 1996 Jul;67(1):98-104.

Nerve growth factor and ras regulate beta-amyloid precursor protein gene expression in PC12 cells.




 2015;2015:787805. doi: 10.1155/2015/787805. Epub 2015 Jun 28.

Calcium Channel Blockers, Progression to Dementia, and Effects on Amyloid Beta Peptide Production.


amyloid beta treated (extra added to ) neurons have mitochondrias that don't move to the synapse and the synapse degrades
http://www.sciencedirect.com/science/article/pii/S0925443911000202


The genetics of Alzheimer's involves APOE.  (Allen Rose who discovered APOE believes the mitochondria is central to Alzheimer's)

I am trying to remember: omega fats  are in the inner mitochondrial membrane.  Vitamin E stabilizes the omega fats just as cholesterol does for the plasma membranes....APOE are fatty acid carriers. Does this fit with the mitochondrial hypothesis that the fluidity of the inner mitochondria is poor.  The mitochondrias do not function well? Imagine that you want more omega fats and you want it to be slick and fast. 

http://www.ncbi.nlm.nih.gov/pubmed/25333200
 2014 Oct 20;6(10):4452-71. doi: 10.3390/nu6104452.

Fatty acid metabolism in carriers of apolipoprotein E epsilon 4 allele: is it contributing to higher risk of cognitive decline and coronary heart disease?