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

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

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.

Occup Environ Med. 2005 Nov;62(11):786-92.

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

Lee WJ1, Colt JS, Heineman EF, McComb R, Weisenburger DD, Lijinsky W, Ward MH.

Am J Epidemiol. 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.

Wrensch M1, Weinberg A, Wiencke J, Miike R, Sison J, Wiemels J, Barger G, DeLorenze G, Aldape K, Kelsey K.

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

Biol Psychiatry. 2005 May 1;57(9):991-8.

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

Welchew DE1, Ashwin C, Berkouk K, Salvador R, Suckling J, Baron-Cohen S, Bullmore E.

Author information

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?

Br J Psychiatry. 1987 Jan;150:117-21.

Brain imaging in a case of Capgras' syndrome.

Lewis SW1.

Author information

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/

PLoS Med. 2007 May;4(5):e180.

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

Fotheringham J1, Donati D, Akhyani N, Fogdell-Hahn A, Vortmeyer A, Heiss JD, Williams E, Weinstein S, Bruce DA, Gaillard WD, Sato S, Theodore WH,Jacobson S.

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.

Arch Neurol. 1989 Apr;46(4):456-9.

The alien hand syndrome. Clinical and postmortem findings.

Banks G1, Short P, Martinez J, Latchaw R, Ratcliff G, Boller F.

Author information

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/

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

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

Nitric oxide impairs mitochondrial movement in cortical neurons during hypoxia.

Zanelli SA1, Trimmer PA, Solenski NJ.

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/
Aβ interacts directly with the Calcium channels and controls if and when the channels are at the membrane. Hypoxia increases Aβ . 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

• Elinor J. Griffiths^a, b, , , 
• Guy A. Rutter^c

The mitochondria's Calcium uniporter and app

http://www.ncbi.nlm.nih.gov/pubmed/23982146

FASEB J. 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.

Roh SE1, Woo JA, Lakshmana MK, Uhlar C, Ankala V, Boggess T, Liu T, Hong YH, Mook-Jung I, Kim SJ, Kang DE.

• Abstract
J Mol Cell Cardiol. 2015 Jan;78:46-53. doi: 10.1016/j.yjmcc.2014.10.013. Epub 2014 Nov 4.

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

Harrington JL1, Murphy E2

http://www.ncbi.nlm.nih.gov/pubmed/19544621

APP and myitochondrial dysfunction

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

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

Wozniak MA1, Itzhaki RF, Shipley SJ, Dobson CB.

BMC Microbiol. 2005 Aug 18;5:48.

Herpes simplex virus interferes with amyloid precursor protein processing.

Shipley SJ1, Parkin ET, Itzhaki RF, Dobson CB.

Sci Rep. 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.

Piacentini R1, Li Puma DD1, Ripoli C1, Elena Marcocci M2, De Chiara G3, Garaci E4, Teresa Palamara A2,4, Grassi C1,4.

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/

J Neurosci Res. 1991 Feb;28(2):192-9.

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

Nikodijevic B1, Guroff G.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2987503/

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

J Neurochem. 1996 Jul;67(1):98-104.

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

Cosgaya JM1, Latasa MJ, Pascual A.

http://www.ncbi.nlm.nih.gov/pubmed/26221415

Oxid Med Cell Longev. 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.

Lovell MA1, Abner E2, Kryscio R3, Xu L4, Fister SX5, Lynn BC1.

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

Nutrients. 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?

Chouinard-Watkins R1, Plourde M2.

Examining liver cancer using the co-carcinogenesis hypothesis

Liver cancer

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.

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

Hepatitis viruses as the triggers: means there should be at least 3 types of liver cancer (hepatomas)

Hepatitis A is an enterovirus
Hepatitis B is a polyomavirus
Hepatitis C is a flavivirus

hepatitis B as a polyomavirus would use serotonin  receptors
http://www.ncbi.nlm.nih.gov/pubmed/23087410

Hepatocellular carcinoma and hepatitis B
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047495/
http://www.medscape.com/viewarticle/709167
http://www.ncbi.nlm.nih.gov/pubmed/19702903

hepatitis C as a flavivirus would use the melanocortin receptors
http://www.meduniwien.ac.at/Hans-und-Blanca-Moser-Stiftung/images/projekt_krenbek.pdf

Hepatitis C and heptoblastoma
http://www.ncbi.nlm.nih.gov/pubmed/19207587

Angiosacrcoma is a liver cancer of the liver's blood vessels

Angiosarcoma has arsenic as the carcinogen.
http://link.springer.com/article/10.1186%2F1471-230X-11-142

hepatitis A as an enterovirus would use the acetylcholine receptors
http://english.sibs.cas.cn/ns/es/201409/t20140930_128798.html

as a cytosolic RNA virus...enteroviruses would not cause cancer.

these receptors are located in the blood vessels of the liver
https://en.wikipedia.org/wiki/Muscarinic_acetylcholine_receptor