Mycoplasma, Antibiotics and IC [Archive] - ICN Support Forum - Interstitial Cystitis, Overactive Bladder, Pelvic Floor Dysfunction

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icnmgrjill

08-09-2006, 07:57 AM

ICLori

08-09-2006, 08:21 AM

Thank you, Jill, this is very interesting! I had noticed that sometimes my symptoms lessen on antibiotics, but antibiotics never cured my IC...it's interesting to see a report where they used different antibiotics in sequence!

Blessings,
Lori

wombat

04-25-2007, 02:14 AM

Thanks for this posting. I've had constant bladder pain since Feb 2005. Still not formally diagnosed as having IC, but symptoms very similar. Was put on 3 lots of antibiotics in April of 2005 - doxycycline, metronidazole and amoxicillan. I was in very severe pain at the time and my symptoms did improve over a few days before getting worse again.

I've been looking for info on mycoplasma in relation to painful bladder conditions, but also in relation to fibromyalgia which I have as well and often occurs with bladder conditions such as IC. I can't help wondering if there is some kind of link that is not understood very well yet. Have found stuff on the net suggesting links between mycoplasma and fibromyalgia and mentioned it to my doctor the other day. She said it's interesting but seemed fairly doubtful about it. Still feel like there is some link between all these things. It would be great if connections were found leading to a direct treatment which could be applied to IC and related conditions. Can only hope.
:pray:

MarthaF

04-25-2007, 04:18 AM

Jill,

The response you cite from the UK website includes mention of the one study done in 2000 on the treatment of IC symptoms with antibiotics. If you read the whole article in the Journal of Urology detailing the study you see that they were unable to find any bacteria in the patients participating. But they decided to treat with antibiotics, in a scattershot approach, using 6 different ones sequentially for 3 weeks each. The answer on the UK site failed to say that 48% of the patients on antibiotics improved, which is better than the response from Elmiron.

But as someone who has spent much time investigating antibiotic treatment I want to point out that those of us who have had success know that the key is to find the bacteria possibly causing the problem and treating it with the right antibiotic for the right amount of time which can be several months. If we are dealing with bacteria in a biofilm, which is very possible, they are hard to detect and hard to treat. We know Scott Hultgren has found biofilm formation by E. coli, but other species are capable of protecting themselves via biofilms, too. There is a Japanese study showing Enterococci can form biofilms in human bladders and these can be polymicrobial. The U of MD study was not definitive in dismissing bacterial infection - they just weren't able to find bacteria.

It is possible for there to be other bacteria and viruses that cause urogenital symptoms, such as Mycoplasma hominis and Ureaplasma and Chlamydia, present. These are even harder to isolate than UTI bacteria, but if a patient does not respond to several months of the right antibiotic for a diagnosed bladder infection it is worth looking into testing for the other bugs. Some patients are being tested for Lyme Disease (Borrelia), especially if they have other symptoms.

We are finding the presence of UTI bacteria in the case of urogenital symptoms is one big part of the picture, but certainly other pathogens could be involved in addition. Testing is key and good testing is hard to find.

Martha F

ICNDonna

04-25-2007, 04:31 AM

Thank you for sharing this, Jill. It's very interesting to know.

Warm hugs,
Donna

jen74

04-25-2007, 05:01 AM

This is very interesting Jill. I do think that it is possible that there may be some kind of bacteria at a very microscopic level that our basic cultures just are not able to pick up that could be responsible for IC.

The other theory is, lets say there are some different bacteria at a micro level in everyones bladder normally. But take a person who has a slight problem with their immune system, then it becomes a problem. When we have an infection our bodies first response is to attack which is normal. But when our immune system is compromised even slightly, then the body seems to go haywire and starts attacking everything in sight,( even normally harmless bacteria). But our body see's this bacteria as being harmful and will continuosly attack that area trying to irradicate this bacteria which is always normally present in the baldder and usually harmless in the healthy individual without any immune system problems.

I guess what it boils down to is that right now, urology is still in the beginning stages of trying to learn all about IC and what could be causing it. As my gasrto doc said, Gastroenterologists are 30 years behind the anesthesiologists, and urologists are 30 years behind the gastroenterologists even. I agree with what L. Thomas said in one of the other posts, That they need to work harder on finding out how to calm the fire and then look into what started it. To many women are suffering with this pain day in and day out (myself), and need some kind of relief. And unfortunately, alot of people cannot tolerate alot of the side effects these meds have and it makes it even harder.

But all in all, I do think the bladder is the innocent bystander here. The doctors need to look at the BIG picture instead of just focusing on the bladder. Much more is involved I believe. That is just my 2 cents whatever it is worth :)
Jen

laura86846

12-20-2010, 12:48 PM

ureaplasma urealyticum was discovered in the urine of me and my fiancee this summer. my doc did a special test for this because of the sudden onset of my bladder symptoms after a miscarriage (no surgery/drugs given for it that couldve injured my bladder). I had the first uti of my life (e. coli) about 2 months before my IC began.

my urologist gave me hydroxyzine in case it gets very painful. a couple of months of antibiotics didn't knock it out. a few months on various types of antibiotics didnt knock it out. voiding symptoms were better but, alas... about to get an antibiotic sensitivity test on it to see where that goes. wish i had done that before taking the antibiotics so long. also need to get a swab to see if it's also present in my vagina and if inflammation is occuring because of it. alcohol bothers my bladder some. I will let you guys know about any interesting progress!

jeffmax

01-30-2011, 04:28 PM

I had read about the English study..

I have to mention that my homeopath does not believe in IC. She believes symptoms are caused my a low grade bladder infection that does not get completly eradicated over a long time. Therefore as time goes on nerve endings get messed up and pain commences. I am still researching and we will see. So far the natural route (ie. change of diet to eradicate my candida overgrowth from being on so many antibiotics) This means no sugar and no wheat in my diet and I have noticed a big improvement. I am still battleing with infections but I take sovereign silver and I have not had to do antibiotics. I eat as alkaline as possible. I was never an alcohol or cofee drinker even though I do miss my chocolate..

Good luck to everyone...

icadvice

04-11-2011, 06:14 PM

I had printed out a medical article:
"Interstitial Cystitis:
Definitions and Confusable Diseases
ESSIC Meeting 2005 Baden
Joop P van de Merwe and Jørgen Nordling"

And brought it to my gyno, because every place I've gone they always retest for bacteria and run the same urinalysis. And they always tell me "yes it covers every type of bacteria". The gyno I talked to said she didn't even know if there were tests for Mycoplasma or where she could get them..she said she might be able to order one to cover one type of it. I ended up having her prescribe me a Zpack just in case. After taking one month of Doxycycline and 3 grams total of Zpack I think it lessened the amount of urine I can hold from half a cup to 1/4th. I'm not 100% certain that maybe its not just a strain that is resistant to Zpack but more than likely I'm thinking I would have been cured with this treatment. Anyways I think it's best to get tested for everything that it could be which includes tests most doctors aren't aware of yet, because it helps to rule out the cause.

ICNDonna

04-12-2011, 02:41 AM

Jeffmax, be extremely cautious with ingesting silver. The side effects can be severe and permanent.
Donna

akh

04-15-2011, 04:58 PM

"A patient came requesting treatment for chronic interstitial cystitis - she had read that mycoplasma can be a causative agent and could be treated with doxycycline. Is there any evidence to support this?"

Read the UK Primary Care Question Answering Services response at:

http://www.clinicalanswers.nhs.uk/index.cfm?question=3615

I find it really, really interesting that mycoplasma infections are associated also with infection with a retrovirus named XMRV, which is being found as the cause of several autoimmune diseases from chronic fatigue syndrome to fibromyalgia to multiple sclerosis. It seems that now ITP is now on this list.

Here is a short introduction to the issue of the relation of XMRV to CFS and fibro: http://xmrv.me.uk/

I think this our silver bullet. Here are the articles on XMRV, mycoplasma and chronic fatigue/ME and their relation. The main thing XMRV does is infect immune cells and causes them to get confused and attack body tissue instead.

Watch this video and tell me what you think- does this sound like your IC symptoms?
http://www.youtube.com/watch?v=_TQzlL0nd6I&feature=player_embedded

Now back to XMRV and mycoplasma:

There is a correlation between the two. This article addresses this.

http://www.guptaprogramme.com/xmrv.asp

Here is a quote from the article: There are two broad aspects to the immune system, TH1 and TH2. TH1 involves Natural Killer (NK) cells whose job it is to identify and destroy viruses. The TH2 side of the immune system involves, amongst other things, antibodies which respond to threats. There is evidence in the literature that patients with ME/CFS are “TH2” biased, i.e. the TH2 aspect of the immune system is over-activated, causing suppression of the TH1 side and high levels of inflammatory cytokines; patients have lower Natural Killer (NK) cell immunity. This bias may mean that opportunistic viruses and bacterial infections can no longer be kept at bay effectively by the TH1 side of the system.

RNase L conducts a function of holding the virus at bay until NK cells are available to eradicate the pathogen, however even the RNase L’s ability to perform this function can be compromised over time if TH2 dominates for too long. RNase L dysfunction was also reported in the prostate cancer cases of XMRV, although later research has not found a genetic link. In ME/CFS, any suspected Rnase L deficiency many simply be due to chronic TH2 dominance. If TH2 dominates for too long, it can be hypothesised that viruses such as HHV-6, Epstein Barr Virus (EBV), CMV and Parvovirus B19 can flourish, as well as bacterial infections such as mycoplasma and chlamydia pneumonia.

A CFS forum discussion of the mycoplasma issue in this disease:
http://forums.phoenixrising.me/showthread.php?7013-You-aren-t-going-to-believe-this...Mycoplasma-Lo-XMRV/page6

Personally I'm betting that XMRV infection is the cause of IC too. The behavior of this virus explains nearly all of the symptoms of IC- it has been linked to chronic inflammation, it is responsive to hormones like cortisol and each day it seems they find this pathogen in the blood of more and more autoimmune diseases.

This would explain the co-morbidity of these diseases. The crazy thing is that XMRV was found by the Cleveland Clinic to be the cause of prostate cancer through the chronic inflammation created by XMRV.

http://my.clevelandclinic.org/urology/research/xmrv.aspx

What is even stranger is that prostatitis is mentioned by the ICA as being one of the conditions that occurs in tandem with IC:

http://www.ichelp.org/Page.aspx?pid=355

I posted this thread about my first ideas about a possibility of an IC and XMRV connection:
http://www.ic-network.com/forum/showthread.php?t=69293

It has been a few weeks and I'm drowning in information but the more I find, the more and more likely the idea there is a correlation makes sense. Of course all that needs to happen is we need some place like the Whittemore Peterson Institute to check the blood samples of IC patients for this virus.
:cat:

Snowden1

04-16-2011, 09:02 PM

akh

04-17-2011, 01:08 PM

I agree with you on this. I think that my IC began after I got a pelvic infection following a hysterectomy. I DO NOT think I would have this today if I had not gotten and infection. Also, most peope with IC seem to have several UTI's before finally getting IC. I do think there is a hidden bacteria or virus that is getting missed. Just like they thought stomach ulcers were from stress - they found otherwise - bacteria.

I couldn't open the link Jill posted. I would like to have read that.

Yes, I agree. Mine started with having my bladder stretched by being left sans bedpan for 10 hours after a rib fracture. Not fun, but right then my symptoms started. I too had mine start out with infections. What I'd wager is that the stretching and or the bacteria started that microscopic poring so common with IC bladders in me.

I think then what happened was this created a way for XMRV or something to infect the bladder wall. The fact is that XMRV infects tissue areas in people and what I think is going on is that each autoimmune disorder varies only by where the XMRV virus infects the tissue.

They have found a different retrovirus involved with lupus, juvenile rheumatoid arthritis, Sjogrens and Graves disease as well.

Here is information about this virus:
http://www.autoimmune.com/ADVAIntro.html
Autoimmune Disease Virus Assay (ADVA)

Researchers at Tulane Medical School have discovered a human retrovirus called the Human Intracisternal A-type Particle, or HIAP. It is the first A-type retrovirus to have been found in humans. Research data strongly suggests that this virus is the cause of four well-known autoimmune disorders. These disorders are lupus (systemic lupus erythematosus), Sjögren's syndrome, Graves' disease, and juvenile rheumatoid arthritis.

The Autoimmune Disease Virus Assay (ADVA) detects antibodies against HIAP. These antibodies appear in approximately 95% of patients with one or more of those four disorders but in fewer than 2% of healthy individuals. The Company believes that infection by this virus may produce the differing symptoms of the disorders in different patients because of genetic variations in the immune systems of the patients.

The published results of a study of an AIDS drug in Sjögren's patients suggest that anti-retroviral drugs may act against this virus.

The ADVA is covered by patents in the U.S. and other countries.

For more information about the HIAP-related disorders, see these pages:

I know some people here have Sjogrens and I have a friend who has this. I think this research is very important and for me, it explains things which otherwise are completely bizarre about IC. That quirky annoying virus causes its own unique mayhem.

It is likely this is the cause and it would be nice to not be beat up for our bodies acting in this way. From what I've read and heard, getting rid of XMRV is easier than getting rid of HIV. :cat:

akh

04-17-2011, 01:37 PM

Here is a link to the list from the WPI on autoimmune disorders officially linked to the presence of XMRV infection:

http://www.wpinstitute.org/xmrv/index.html

Overview

The spectrum of neuro-immune diseases including: Myalgic Encephalomyelitis (ME/CFS), Atypical MS, Fibromyalgia and Gulf War Syndrome, share common abnormalities in the innate immune response, which result in chronic immune activation and immune deficiency.

We have detected the retroviral infection XMRV in greater than 95% of the more than 200 ME/CFS, Fibromylagia, Atypical MS patients tested. The current working hypothesis is that XMRV infection of B, T, NK and other cells of the innate immune response causes chronic inflammation and immune deficiency resulting in an inability to mount an effective immune response to opportunistic infections. (See XMRV paper in Science.)

This discovery opens an entirely new avenue of Neuro-Immune Disease related research and our discovery has brought to this field world-renowned immunologists and retrovirologists building our team of collaborators to translate our discoveries into new treatments as soon as possible.

Because retroviruses are known to cause inflammatory diseases, neurological disease, immune deficiency and cancer, the discovery of XMRV has far reaching implications for the prevention and treatment of not only lymphoma, one of the potentially devastating complications of ME/CFS, but prostate cancer and perhaps many others.:angel:

akh

04-17-2011, 01:46 PM

XMRV is now also associated with leukemia, lymphoma and ITP
http://niceguidelines.blogspot.com/2011/03/xmrv-is-now-also-associated-with.html

Landish

04-17-2011, 07:54 PM

Yes, I agree. Mine started with having my bladder stretched by being left sans bedpan for 10 hours after a rib fracture. Not fun, but right then my symptoms started. I too had mine start out with infections. What I'd wager is that the stretching and or the bacteria started that microscopic poring so common with IC bladders in me.

Mine started with having my bladder stretched by being stuck in traffic for more than 5 hours. At that time I had severe kidney pain, I couldn't tolerate a slap on my back. A couple of days later the kidney pain was gone but my bladder never stopped hurting.

ems123

04-18-2011, 02:50 AM

Hi, I've just read her book cover to cover. She firmly believes in the low level bacterial infection causing IC. She has good advice on how to proceed and her arguments are very convincing. If you haven't read it already you really really must! It's called: The patients encyclopaedia of cystitis, sexual cystitis, Interstitial cystitis. A lot of uro doctors seem to agree with it. Read every page!

Landish

04-18-2011, 09:51 PM

Hi, I've just read her book cover to cover. She firmly believes in the low level bacterial infection causing IC.

Helicobacter pylori causes a chronic low-level inflammation of the stomach lining and is strongly linked to the development of gastric ulcers.
H. pylori's is thought to have evolved to penetrate the mucoid lining of the stomach. Many bacteria can be found deep in the mucus.
In the past, it was believed stress and diet caused peptic ulcers. Today research shows that most ulcers develop as a result of infection with a bacterium called Helicobacter pylori.
Does this sound like IC ? Maybe it's a bacteria.

sshannon74074

04-23-2011, 04:37 AM

Akh,

Being such an optimist on XMRV as being the "smoking gun" and assuming you've done extensive research on getting tested for this virus, what have you found out because I am very interested.

I did do some research of my own and it seems there is a lot of non-conclusive data to support this theory. Believe me, I would love for this to be the answer.

sshannon74074

04-23-2011, 05:48 AM

Snowden1

04-23-2011, 08:03 AM

sshannon,

I just bought the book ems mentioned and am going to do some research. I haven't been tested for anything. Please keep me posted or pm me on your progress with this. If it works for you that would be wonderful. I also believe in that bacterial theory, but don't want to just throw a bunch of antibiotics at it until I know what antibiotic to use. There is the place you can get tested sending a sample to a lab in VA, but it seems either I don't do the test right or they make many mistakes. I don't know how to get a dr. to prescribe a long-term anti-biotic. I guess if you presented the data a dr. may listen.

ems123

04-25-2011, 07:38 AM

akh

04-26-2011, 11:36 AM

Mine started with having my bladder stretched by being stuck in traffic for more than 5 hours. At that time I had severe kidney pain, I couldn't tolerate a slap on my back. A couple of days later the kidney pain was gone but my bladder never stopped hurting.

Hey, wow!! That's like me!!! :dance: I've felt so alone in this. It is so hard to discuss IC as it is but when you tell people bladder stretching caused it, then people really start thinking head case.

This irks me, because in my case in a normal world, legal action would be the proper direction for me to follow since a hospital left me with no bedpan. The problem is that it would be a cold day in Hades before I'd ever win it.

This being said, my first nocturia- a-go-go flare up was caused by holding in while stuck on a bus for over an hour.

Best wishes for you!! :puppy:

akh

04-26-2011, 11:43 AM

Helicobacter pylori causes a chronic low-level inflammation of the stomach lining and is strongly linked to the development of gastric ulcers.
H. pylori's is thought to have evolved to penetrate the mucoid lining of the stomach. Many bacteria can be found deep in the mucus.
In the past, it was believed stress and diet caused peptic ulcers. Today research shows that most ulcers develop as a result of infection with a bacterium called Helicobacter pylori.
Does this sound like IC ? Maybe it's a bacteria.

I think the issue with XMRV is that its infection of the immune system sets patients who have it in their system for other attendant infections.

It is interesting that somewhere in this blog on CFS, the author mentions how the doctor which believed H-pylori was a problem wasn't taken seriously until let H-pylori create ulcers on himself:
http://cfschronicles.blogspot.com/
http://cfschronicles.blogspot.com/2010/09/its-virus-stupid.html

Here is the latest news from the Whittemore Peterson Institute: http://www.wpinstitute.org/news/news_current.html

akh

05-02-2011, 10:47 AM

akh

05-02-2011, 03:37 PM

For what it is worth, while I understand some skepticism, there seems to be plenty of worthwhile evidence to support XMRV is involved in the development of IC. I don't understand what the above poster meant by there being no evidence for what I assume to be XMRV infection in CFS/ME patients, fibromyalgia, Gulf War Syndrome and Atypical MS.

The studies are being attacked but the data linking XMRV infection to these disease keeps getting proven as solid. I do believe it is a delicate issue since it brings up the subject of sometimes willful neglect of millions of people sick with these diseases.

Share what I have? Certainly:
Reasons why an XMRV or related retroviral infection might be the cause of interstitial cystitis

1. Co-morbidity. Interstitial cystitis shares a co-morbidity of a number of autoimmune diseases
1. Autoimmune diseases which have co-morbidity to interstitial cystitis:
a. chronic fatigue syndrome
b. fibromyalgia
c. chronic prostatitis
d. Lupus
e. Sjogren’s syndrome
f. Pudential neuralgia
g. irritable bowel syndrome
h. endometriosis
Source:
The Interstitial Cystitis Association: http://www.ichelp.org/Page.aspx?pid=355

There is a general tendency for those sick with autoimmune disease to be sick with another autoimmune disease. There is no exclusivity in interstitial cystitis patients in the problem of autoimmune disease and co-morbidity.

Commonalities amongst Various Autoimmune Diseases

Studies conducted by the Whittemore Peterson Institute have found a gamma-retrovirus called XMRV (xenotropic murine leukemia-related virus) in a number of different autoimmune diseases. My hypothesis is that XMRV will be found with similar consistency in interstitial patients as well.

Small Adrenal Glands in Both Chronic Fatigue Syndrome and Interstitial Cystitis patients- both human and non-human.

1. Small Adrenal Glands in Cats with Feline Interstitial Cystitis.
a. Researcher on Feline Interstitial Cystitis, Tony Buffington finds IC felines have small adrenal glands.

Findings of Study:
“Conclusions: These results suggest that cats with FIC may have mild primary adrenal insufficiency. Decreased adrenal size has been observed in patients with chronic fatigue syndrome, which can be a co-morbid condition in some patients with IC. If these abnormalities are confirmed in humans with IC, hormone replacement therapy may be indicated in select patients”.

b. Source of this study:
“Small Adrenal Glands in Felines with Interstitial Cystitis.” Study conducted by Tony Buffington
Location of the study:
http://ckm.osu.edu/sitetool/sites/Indoorpetpublic/documents/hospital/indoorcat/westropp03.pdf

c. Another source’s summary of this study:
Painful Pelvic Disorder Linked to Small Adrenal Glands
http://www.tipna.org/forum/viewtopic.php?f=17&t=4873

3. Small or shrunken Adrenal Glands are common in Chronic Fatigue Patients.
• “Small adrenal glands in chronic fatigue syndrome: a preliminary computer tomography study.”
By: Scott LV, Teh J, Reznek R, Martin A, Sohaib A, Dinan TG. Source
Department of Psychiatry, Trinity College Dublin Medical School, St. James's, Hospital, Ireland.
• “Findings: The right and left adrenal gland bodies were reduced by over 50% in the CFS subjects indicative of significant adrenal atrophy in a group of CFS patients with abnormal endocrine parameters. This is the first study to use imaging methods to measure adrenal gland size in CFS. It is a limitation of this study that a selected CFS sample was employed. A future larger study would optimally employ an unselected cohort of CFS patients. This study has implications not only for the elucidation of CFS pathophysiology, but also for possible therapeutic strategies.”
C. Significance of the study in relation to XMRV and its effects on the adrenal glands: XMRV has the effect of deteriorating and shrinking the size of the adrenal glands in the bodies of patients with Chronic Fatigue Syndrome.

1. The CFIDS website shares in its data sheet on XMRV that the retrovirus goes to organs in the body which produce hormones. These range from the prostate, adrenal glands, thyroid. Source:

• Journal of Virology: “5 macaques were inoculated with XMRV intravenously. XMRV established a persistent chronic infection. XMRV gag was detected in tissues throughout, showed organ specific cell tropism: CD4 T cells in lymphoid organs including the gastrointestinallamina propria, alveolar macrophages in lung, and epithelial/interstitial cells in other organs, including the reproductive tract. Possible thyroid, adrenal glands, salivary glands and brain.”

Source: http://www.cfidsresearch.com/xmrv/
•
• From the article, “New Developments in XMRV from 1/19/11”

“In chimp studies the virus very quickly left the blood and went into reservoirs, lymph node, spleen, liver – maybe thyroid, sex organs, adrenal glands, salivary glands, brain.”

Location of article:
http://roosclues.blogspot.com/2011/01/new-developments-in-xmrv-11911.html
• Studies now indicate that XMRV travels not only prostate tissue to cause the inflammation which lead to prostate cancer as discovered by the Cleveland Clinic but also to both cervical and breast tissue. This would seem to indicate XMRV might be a causative factor in other cancers aside from prostate cancer where it was originally detected
• XMRV Global Action- Link to XMRV, Breast and Cervical Cancer now found:
http://www.facebook.com/notes/xmrv-global-action/dr-singhs-xmrv-patents-ground-shaking-revelations-on-xmrv-breast-cancer-prostate/472237776796
• Blog with further information on this:
. “Dr. Singh’s XMRV Patents: NOW BREAST CANCER?!!!”
http://bodyprinciple.wordpress.com/2010/11/26/dr-singhs-xmrv-patents-now-breast-cancer/

Significance of co-morbidity between various autoimmune conditions.

Chronic prostatitis is associated with interstitial cystitis in males which have IC. That is strange because there is a link between XMRV and chronic prostatitis. XMRV caused prostatitis has been found to cause prostate cancer.

Researchers at the Cleveland Clinic found in 2006 that inflammation of the prostate in prostate cancer patients was related to infection with a gamma retrovirus they named XMRV.
This was the first time this retrovirus had been found.

This correlation is made even more interesting by the fact that very few males suffer from interstitial cystitis.

2. XMRV Causes Inflammation

a. The Cleveland Clinic has proven XMRV as a cause of the inflammation which leads to prostate cancer in prostate cancer patients:
Sources:
“XMRV Infection Induces Host Genes that Regulate Inflammation and Cellular Physiology – Source: The Journal of Urology, Apr 2011 Supplement (#280)” http://www.prohealth.com/library/showarticle.cfm?libid=16024

“Conclusions from this study:
The chemokine IL-8 is one of the most highly induced genes in response to XMRV infection of prostate cancer cell line DU145. XMRV induction of the 30 host genes identified in this study suggests a profound effect of the virus on fundamental cellular physiology and inflammation. These findings could be relevant to the possible pathogenic effects on XMRV in prostate cancer.”

“XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors”

Study by Robert Schlaberg,a1 Daniel J. Choe,b Kristy R. Brown,a Harshwardhan M. Thaker,b and Ila R. Singhab2
Source:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739868/

“Abstract: Xenotropic murine leukemia virus–related virus (XMRV) was recently discovered in human prostate cancers and is the first gammaretrovirus known to infect humans. We found XMRV DNA in 6% and XMRV protein expression in 23% of prostate cancers. XMRV proteins were expressed primarily in malignant epithelial cells, suggesting that retroviral infection may be directly linked to tumorigenesis. XMRV infection was associated with prostate cancer, especially higher-grade cancers. We found XMRV infection to be independent of a common polymorphism in the RNASEL gene, unlike results previously reported. This finding increases the population at risk for XMRV infection from only those homozygous for the RNASEL variant to all individuals. Our observations provide evidence for an association of XMRV with malignant cells and with more aggressive tumors.”

Inflammation its role in interstitial cystitis: Interstitial cystitis is known for chronic and progressive inflammation of the bladder wall area, which is similar to the inflammation found in prostate cancer patients with XMRV infection present. As you may know, inflammation of the bladder wall is a characteristic symptom of interstitial cystitis. Inflammation in the bladder wall is progressive in interstitial cystitis, often to the point that the bladder increases physically in size in severe IC patients. In interstitial cystitis, the bladder becomes larger over time and loses volume until it decreases to the point it can only hold 250 ml of urine.

A. Mycoplasma infection is related to XMRV infection. I've noticed that many people here are betting on the idea that mycoplasma causes IC. These people are actually right! It seems mycoplasma is the gateway virus which allows infections like XMRV and HIV to take up hold in the immune system.

Mycoplasma infection is found to be associated with XMRV infection. The way it is supposed to be associated is that it is an initial infection with Mycoplasma which situates the human body to acquire other attendant infections, especially viruses which affect the immune system.

1. Mycoplasma and Chronic Fatigue Syndrome
“XMRV Virus Found in CFS Patients”
http://www.endfatigue.com/health_articles_f-n_2/Infections-xmrv_virus_found_in_cfs_patients.html

A study being conducted on CFS, XMRV infection and Mycoplasma:

“Mycoplasma Testing - Xenotropic Murine Leukemia - Related Virus (XMRV)”
http://www.clongen.com/index.php?option=com_phocagallery&view=category&id=456:xenotropic-murine-leukemia-related-virus-xmrv&Itemid=129

2. Gulf War Syndrome, XMRV infection and Mycoplasma
Patients with Gulf War Syndrome were found to be infected with XMRV by the WPI as well:
• http://www.wpinstitute.org/xmrv/index.html

• “Mycoplasma and Gulf War Syndrome; Antibiotics Recommended When Indicated for Treatment of Gulf War Illness/CFIDS/FMS,” By Prof. Garth L. Nicolson, The Institute for Molecular Medicine
http://weeksmd.com/?p=697+

• The following is a discussion of XMRV, Gulf War Syndrome and Chronic Fatigue Syndrome. Here the author is focusing on the commonalities of both diseases.

“Gulf War Illness and XMRV: GWI Implications.” By Nancy Klimas, RN, University of Miami”
http://www.va.gov/RAC-GWVI/docs/Minutes_and_Agendas/Minutes_Mar2010_AppendixA_Presentation03.pdf

Those studies have been attacked in various ways ranging from accusing the samples of being contaminated, to saying that even when XMRV is found in 95% percent of samples, there is no indication XMRV causes CFS. The problem seems to be a few professionals who have gotten comfortable with ignoring autoimmune disease.

I understand we get comfortable in thinking that it is just our weird female bodies or minds causing this disease. I'm not buying it though- and its more than just the truth that this hurts so horribly bad to be sick with this.

Beyond sharing this link which pins the origin of this medical bias where it actually comes from I'm going to be quiet about this. The facts in the end decide. After reading this link, the only thing which comes to mind for me is a huge issue of liability, but that is just my own opinion. Its facts which matter.

http://meactionuk.org.uk (http://meactionuk.org.uk)

ceebee

05-04-2011, 04:08 PM

AAAHHH, at last I have found fellow IC people who have shared similar experiences as myself. My IC was diagnosed in 97 after one infection after another. Then it vanished for 15 years, only to return after hitting early menopause and a barrage of infections that were never treated properly. I actually now have a urethral diverticula because of it. I am very interested in all this info, and thank you for your comment regarding "humans as spiritual beings" thank you.

ceebee

05-04-2011, 04:15 PM

ceebee

05-04-2011, 04:16 PM

My last reply was directed towards AKH. sorry.

ceebee

05-04-2011, 05:28 PM

What is the name of the Author and the book?

ceebee

05-04-2011, 05:33 PM

Landish

05-04-2011, 07:01 PM

The name of the book is Patients Encyclopedia of Urinary Tract Infection, Sexual Cystitis and Interstitial Cystitis: The international bible on self-help
by Angela Kilmartin

jeffmax

05-14-2011, 02:42 AM

So I read this book and it confirms why my change of diet (more alkaline) has
helped me so much. It is def. a lifestyle change and it takes a while for your cells to regenerate themselves. I know that antibiotics are not the answer since they give you yeast and these present with symptoms in themselves.
Candida overgrowth is a serious problem making your body more toxic and out of balance...feel free to e-mail me if anyone has questions or comments.

Good luck to every one but know that there IS light at the end of the tunnel.
I am proof of this.

ems123

05-15-2011, 07:16 AM

Yesterday I went to visit Angela Kilmartin (the author of the book I read- bacterial cystitis, sexual cystitis, interstitial cystitis...). I said I'd let you all know how I got on, as she's the one who talks about mycoplasma.

She said that I didn't seem to be in enough pain for mycoplasma but instead just thinks that bacteria from my anus is continuously getting into my bladder along an episiotomy child birth scar (the symptoms of inflammed bladder started shortly after child birth). She says that strict hygeine is the answer. Seems too good to be true but if this works I'll let you all know. Her book explains in much more detail and I continue to recommend it.

purpleviolet

05-15-2011, 09:55 AM

It really would be nice to have clarity.

Let us never mix up viruses and bacteria. However, I realize a bacteria could (the reverse is so when a viral cold leads to bacterial pneumonia) set one up for a virus. Antibiotics will not work on a virus.

I read here many times people temporarily improving on antibiotics (even me) - when no bacteria is supposedly present. Then I hear the reason someone gives - that antibiotics are anti-inflammatory. I never read that anywhere else. Can someone provide a believeable link on that?

I've felt better on Cipro and worse on Cipro - go figure!

I took a lot of antibiotics for sinus infections including zithromax and my IC did not go away.

That Kilmartin book if I remember correctly about cleaning up after a BM. Well you know the main thought is that bacteria creates a biofilm in the bladder and we are re-infecting from inside ourselves when we keep on getting infections.

Proven and not so proven chronic infection reducers - acupuncture (yes, proven!), cranberry powder capsules (my theory: blueberry capsules just as good!) , d-mannose (perhaps for some), forskolin ( ayurvadic herb proven to eject deep-seated bladder e-coli), probiotics ( I credit them for helping me to avoid infection), other herbs such a goldenseal ( cannot be taken long term - my herbal teacher claims high does have cured IC but I have not/will not subject myself). AND I believe somewhere I read Elmiron reduces infection rate but I have not researched that link

My brother has IC/prostitis symptoms, but not as bad as I do. So genetic disposition/ growing up in same environment (he has had infections, too) ?

I had infections followed by urethral dilations followed by IC --- so damaged by infection and by a surgical instrument which allowed something to take hold and damage the bladder lining, nerves and most importantly set up a cycle of inflammation and an aggravated nerve pathway to go straight to the brain!

So hard to have clarity. So hard to get doctors to think outside the box.:headbang:

sshannon74074

05-18-2011, 04:18 PM

just finished a round of z-pack and no luck. Seemed liked the first couple of days it was going to work but I got worse again.

akh

05-23-2011, 10:52 AM

Thank you immensely for sharing all that information. I absolutely agree with this study. How are you being treated now, may I ask? Do you see a specialist who agrees with this study? I know that my IC is connected to repeated bladder infections. The sad fact for me is that I can seem to get help here in Alberta, Canada. I may have to try Dr. Fenster in Vancouver. Thanks for all the info, really helpful. I did have urea plasma urea liticum in my early twenties but took a dose of tetracycline and it went away. I was recently re-tested again for the mycoplasma but my results were negative. I sincerely believe that pathogens literally dig holes in the lining of the bladder. That is just my two cents.

I'm not being treated. I reuse catheters just to be able to sleep. I guess since I qualify as the sickest of the sick- I have no urologist and my chances of getting decent treatment are nil- much less I think my odds of making it are nil as well, I have no trouble doing the necessary research to learn why my life has to end up this way.

I don't have a nice uro or even friends anymore because of ignorance about this disease. I met one woman with fibromylagia who had it as bad as me- and two women with CFS- in a homeless shelter too- because we all lost everything over ignorance about this disease.

Therefore finding answers is all I care about. I feel this as grossly unfair. I know I'm not alone. I had nearly all my possessions stolen after my car was broken into. The reason it was broken into was that night I was at the ER for a severe urinary, and kidney infection. My blood pressure was up to 215/144. I was not kept overnight at the hospital though I was missing days of sleep. This led me to forget to lock my car while I was moving out of state. My computer, everything was stolen. That's our lovely health care system in action. Now I have nothing and I feel like I have a gun to my head to sleep even while in severe IC pain because the consequences of showing any fatigue have been severe. Meanwhile, people think this is okay, that if doctors aren't sure what causes something then it is okay to flush us down the proverbial toilet.

Let me get one thing clear, however. I graduated college. I have severe, ulcerative IC. My IC is destroying my life. No, I'd say it has destroyed my life. I am looking at one miserable meaningless future. Therefore I want to know why the heck people just let this happen. I want to know what is wrong with my body.

Now that I've met people with other autoimmune diseases who've walked down this horrible path too, I feel angry and scared for all of us. When I learned that way doctors regard all these diseases is the same; we are just nutty women who aren't sick- even if we have friggin ulcers in our bladder,
I got online and got busy researching.

This whole drill ignoring diseases with identifiable physical symptoms raised red flags to me. Thankfully it has raised red flags in the minds of many people in the autoimmune community.

I Googled misogyny and medicine going on what my gut was telling me. It has paid off very well. This article (http://cfschronicles.blogspot.com/2011/02/what-independent-advocacy-means-to-me.html) is what brought everything together for me. It discussed disease advocacy and its faults and showed me many smart, successful women who'd be relegated to the scrap heap just because some doctor can say, "they are just hysterical nut jobs; and this okay because we can find no cause."

Better still it mentioned a cause for their disease. This is where I first learned of the WPI studies. I recommend following the CFS community to learn about the politics, issues and research in regards for this because it is highly likely it relates to IC.

I've learned that there is a slough of women's diseases which have been written off as mere fantasies from chronic lyme disease, to fibromyalgia, to Sjogren's syndrome.

I spent the free time I have now since I can't work to learn why I'm having to face the destruction of my life over a frackin' bladder disease.
Even the way it sounds to say it reeks of absurdity. Well I can say my efforts have paid off. I found my way into reading about the troubles people with chronic fatigue syndrome experience and the struggles they face with advocacy. Then I learned that there is a virus found to be the cause of their diseases and quite possibly ours. Again, we are looking at a virus which has a pathology that matches the symptoms of IC. It replicates in the presense of inflammation and hormones (http://paulacarnes.wordpress.com/2011/01/20/testing-negative-staying-positive/)
No one would help me because I looked messed up, stuttered and was a zombie from not sleeping for 3 days. I have no one to depend on. Everyone has abandoned me and not over much.

This is maybe why I am no fan of people telling me that this disease is some product of the emotional, female imagination. Believing that has only made me worse. As I said, having my bladder stretched started my IC. My symptoms onset immediately. This being said, I haven't believed it to be imaginary- that is when I'm not beaten down completely. Oh, I have believed I'm making a big deal out of nothing and this has led me to do things that are bad for IC to pretend I am like a normal person who doesn't have to pee all the time.

Gee, that has made my IC worse. I seem to get the crappiest urologists too since I'm using medicaid. I'm too sick to work now. I don't get love and support I get giggled at or feared when I'm sick and need help. Why? Because the credibility of those of us who are sick has been stolen. Why has it been? Apparently all it takes is a few doctors who are either working for a bias or want to establish a new running theory that women are hysterical, emotional and deficient in some way.

This is only a few doctors literally. Right now the main people fighting recognition of not just IC but other autoimmune disorders really are just a few people.

These people come from what is known as the Wessely school in Britain. The main person espousing the idea that we don't know when we are sick has been a man named Simon Wessely has been gunning to have not just all autoimmune disorders written of as psychosomatic, but Gulf War Syndrome, organophospate poisoning and other illnesses related to environmental disasters, and more.

Yes, I'm sure that this sounds like I've flown the coop, but this is unfortunately real. The chronic fatigue syndrome community, the Myalgic Encephalomyelitis (http://meactionuk.org.uk/)community, the fibromyalgia community, (http://www.dailystrength.org/c/Fibromyalgia/forum/917922-quack-doctor-abusive-doctor) the Gulf War Syndrome community (http://niceguidelines.blogspot.com/2008/10/professor-simon-wessely-gws-gulf-war.html).

Yes, Simon Wessely influences opinions on interstitial cystitis in the negative direction. It's all here:
http://www.investinme.org/Article-369%20Interstitial%20cystitis%20and%20Chronic%20Fatigue%20Syndrome.htm

http://www.bmj.com/content/339/bmj.b2707.extract

purpleviolet

05-24-2011, 10:09 PM

Have we heard of IC people with small adrenals? There are herbs for adrenal support, infact I'm starting on some soon.

I don't recall having flares with periods (I'm past that and I'm odd I guess)

My brother has some IC symptoms, so we caught the same virus or were susceptible to the virus due to genetics?

Long remissions. Why?

There are anti-virals, including some in Chinese herbs, so maybe that is a something to research?

Still this virus a possibility perhaps explaning the NO CURE it seems for many with IC.

THANKS for insights. It is amazing how urine can be so irritating AND most amazing that even after the bad urine is peed out the irritation remains unlike washing salt off a wound which brings immediate release. I feel as if the irritation has sunk into the nerves and they just don't calm down for days.

Landish

05-24-2011, 10:31 PM

akh

05-25-2011, 10:10 AM

If IC is a virus, sometimes, the viruses cause very mild or atypical symptoms during outbreaks. However, as neurotropic and neuroinvasive viruses, HSV-1 and -2 persist in the body by becoming latent and hiding from the immune system in the cell bodies of nerves. In an outbreak, the virus in a nerve cell becomes active and is transported via the nerve's axon to the skin, where virus replication and shedding occur and cause new sores.
They are capable of causing overt disease or remaining silent for many years only to be reactivated, maybe when a person goes into remission that means they no longer have signs.

Very good point. I haven't read much about HSV-1 and -2. That is worth knowing.

It strikes me how casually we as IC patients say that our IC is in remission; it never occurred to me until now that saying "you are in remission" is more often said about viral infections. I've been in remission from IC before and then I have symptoms again.

What is stranger is just by having sleeping pills which put me to sleep over my at the time, milder IC symptoms I ended a flare up. This was long before I was diagnosed but this and avoiding caffeine from much doomed trial and error, let to my remission.

Then in 2009, extreme brief stress triggered this second major flare up. All along I've been thinking that my body is crazy- rest healing injured bladder tissue makes no sense.

I'd given up and resigned myself to thinking the human body must be designed pretty pitifully for interstitial cystitis to be a natural reaction. The body stopping itself from sleeping to urinate all the time; I'd lost faith in my body and nature. More than looking for hope, I'm looking to make sense of all this. I plan to keep studying the virology/autoimmune disease stuff regardless if it solves the IC problem or not.

I'm learning all the suffering CFS, fibromyaglia, ME patients are enduring and it is heart breaking. A friend of mine has ITP which is a fatal autoimmune disease. We need answers. Thanks for your comment and the information. I'm done feeling powerless and I want to see if we can fight to understand this problem so we can get the cure WE ALL DESERVE!!!! :dance:

akh

05-26-2011, 03:38 PM

Here is what I'm working on

Theories on XMRV infection being involved with interstitial cystitis
“Replication of XMRV is stimulated by inflammation and hormones,” according to the article called “Testing Negative, Staying Positive,” by Paula Carnes.
http://paulacarnes.wordpress.com/2011/01/20/testing-negative-staying-positive/
Main processes involved with interstitial cystitis (IC):
According to a British medical journal article by Serge Marinkovic and others in 2009 et al; BMJ 8th August 2009:339:337-342)
“Increased permeability of the protective glycosaminoglycan lining of the bladder epithelium causes potassium (K) and toxins to leak into the mucosal interstitium, activating mast cells and generating an autoimmune response. Mast cells produce immune reactive chemicals, which in turn cause generalised bladder inflammation and bladder mucosal damage through the presence of tachykinins and cytokines. These further lead to the release of histamine, tumour necrosis factor, chymase, tryptase, and prostaglandins. Finally, inflammatory agents sensitise bladder neurones, producing pelvic and bladder pain….”
The mast cells create an autoimmune response. It is my theory that interstitial cystitis is an autoimmune disease and therefore worth testing for XMRV infection. I will explain my reasoning and demonstrate how this is proven by the etiology of the disease.
According to the BMJ article on IC, mast cells produce immune reactive chemicals which then cause generalized bladder inflammation and bladder mucosal damage through the presence of cytokines and tachykinins.
In the BMJ description of interstitial cystitis the release of histamine, tumor necrosis factor, chymase, tryptase and prostaglandins. These inflammatory agents sensitize the bladder neurons producing pelvic and bladder pain.
What is the cause of this response in the body of IC patients?
Bladder epithelial cells could be infected with XMRV. Urine might be confusing the immune system bringing an autoimmune response. It is also possible that XMRV infection is responsible for bringing about this autoimmune response.
What do bladder epithelium cells release? They release cytokines. What cell in particular releases cytokines? As you may know if you are familiar with interstitial cystitis, it is the mast cells that release cytokines.
Mast cells produce immune reactive chemicals which include cytokines and result in bladder inflammation and bladder mucosal damage particularly through the action of cytokines and tachykinins.
Where XMRV would fit in this process
It seems more than likely given the intensity of the inflammatory response of the body to urine, there may be more than just irritants creating the inflammatory response. Instead very could be XMRV, given its well documented link to causing chronic inflammation.
If XMRV increases replication in the presence irritants, then what is happening in the IC bladder in its reactions to these substances is the virus becoming active. IC flares are instigated by either irritating substances consumed by the IC patient, which then get excreted in the bladder. What is likely happening is more than the body being confused by urine, it may be XMRV rapidly replicating in the IC bladder when the virus is made active by the presence irritants.
Remember what research has found about the XMRV virus according to Carnes:
“Replication of XMRV is stimulated by inflammation and hormones.”

Furthermore, if XMRV begins to replicate when exposed to irritants, then irritants excreted in the IC bladder would cause the virus to enter the blood stream and infect more cells, or actually tissue. Tissue is what XMRV infects. XMRV only enters the bloodstream when stress or illness gives it the upper hand against the immune system.
The second fact supporting the theory of an XMRV infection in IC is that IC flares are also instigated by hormonal changes, including by cortisol, the stress hormone. Patients who are sick with Chronic Fatigue Syndrome, Myalgic Encephalomyelitis, and Fibromyalgia patients get flares in their symptoms during times of stress too. This is another reality which shows there may be common cause of all these conditions. What is known of XMRV thus far, can explain the process of flare ups very logically.

The findings of the Whittemore Peterson Institute studies indicate these patients test positive for XMRV to 95% of the time from latest studies.
Let’s say irritants like potassium trigger not a neurogenic bladder response but the replication of the XMRV retrovirus. This would explain the sheer intensity of the reaction of the bladder in an IC patient to irritating substances excreted in the bladder. The method of diet modification in symptom control could be explained scientifically with the XMRV theory, because by not consuming irritating substances like coffee, spices, caffeine and acidic foods would starve the XMRV virus.
Remember the old practice of using silver nitrate to destroy the cells of the bladder lining to force them to “grow back correctly?” This technique had only a 50% efficacy which to me seems to not fully support the theory that the cause of IC is bladder lining cells just behaving incorrectly and not excreting mucous to protect the bladder. Using the XMRV theory, what silver nitrate may actually do is destroy infected cells; not defective cells.
The efficacy of silver nitrate could be explained by how extensive XMRV infection is in the bladder wall. It seems unlikely that varied results such as what are found fully prove the theory that it is just defective cells that want to misbehave. Were the theory correct, silver nitrate should work %100 percent of the time, and not 50%.
The reaction of the mast cells in the bladder wall is said by IC researchers to release cytokines and tachykinins, which “further drive the release of histamine, tumor necrosis factor, chymase, tryptase, and prostaglandins… inflammatory agents sensitizing bladder neurons, producing pain.”
Like in prostate cancer, inflammation caused by either XMRV- or just urine (sic) leads to production of tumor necrosis factor.
It seems the next step in deciphering what is this is a response to urine or XMRV. Animal testing would seem the next step in trying to physically prove both of these theories. It also could be another virus or a bacterium causing this process too, but unlikely.
The theory of XMRV in interstitial cystitis is further supported by the responsiveness to IC symptom exacerbation by the presence of hormones. XMRV responsiveness to hormones is well documented.
XMRV replicates in the presence of hormones including androgens, cortisol, and estrogens. Judy Mikovits states in an interview:
“We know from work in the laboratories of Bob Silverman and Steven Goff from Columbia University that the retrovirus XMRV has what’s known as the cis-acting element, literally the on/off switch of the virus, two androgen and hormone responsive elements.”
“And that means that when that virus, when the on/off switch sees certain hormones, it can turn it on &/or off, so what you would want to do is have a balance of hormones and not spikes. And we really don’t know a lot of how exactly they control the expression of the virus or the reservoirs that might be involved given the hormone sensitivities or switch of the virus, but there is a hormone responsive element to the virus that we think will be critical in understanding how it might cause disease.”

XMRV theory holds because hormones and stress are known to trigger IC flares, indicating more than urine is involved. Previous theories on interstitial cystitis state that the hormonal fluctuations during menstruation determine the thickness of the mucosal lining of the bladder. This idea has furthered the meme that the disease of interstitial cystitis reflects some uncontrolled, quirky process unique to women’s bodies- even though men and cats get interstitial cystitis.
However, the thickness of the bladder lining is all that is determined by the presence of female hormones, and again this theory alone is insufficient to explain why the same process of stress causing symptom exacerbation also occurs in males (and felines) with interstitial cystitis. Were this true, men could not have stress induced flare ups in IC symptoms.
Speaking of one thing which is learned from males with interstitial cystitis is that prostatitis is a condition which is co- morbid to, or occurs with frequency in males diagnosed with IC.
Prostatitis is listed as a major co-morbid condition on the website for the Interstitial Cystitis Association. There is a definitive link between XMRV and prostatitis in men. Or more correctly, XMRV was first discovered in prostate cancer cell lines by researcher Robert Silverman at the Cleveland Clinic. XMRV is believed to create chronic inflammation in the prostate, (prostatitis), which leads to the growth of cancerous cells over time.
The reason XMRV is believed to infect the prostates of men is because the virus is drawn to organs in the body which create hormones and there are large amounts of androgens found in prostate tissue. Also subsequent studies have found a link with the virus in cervical and breast cancer in women.
XMRV research may prove the key in understanding the huge increase in breast and prostate cancer and may be the missing link to explain the epidemic of these conditions. It is also worth mentioning that XMRV was found to be present more often in males who were promiscuous, indicating viral transmission is the key factor behind these epidemics.
XMRV is found to replicate in the presence of hormones. Another reason it is found in the prostate is that the tendency of the virus is for it to travel to organs in the body which either produce or possess a high concentrations of hormones and hide there.
Studies were performed on chimpanzees which verify this fact. Carnes mentions in her article about the presentation by Dr. Judy Mikovits, the results of that study:
“In chimp studies, the virus very quickly left the blood and went into reservoirs, lymph nodes, spleen and liver- and maybe the thyroid, sex organs, adrenal glands, salivary glands and brain.”
Source: http://paulacarnes.wordpress.com/2011/01/20/testing-negative-staying-positive/

How XMRV modulates the human immune system to its own detriment; the etiology of autoimmune disease and explanation of the processes involved
A low count of natural killer (NK) cells is found in XMRV positive chronic fatigue syndrome (CFS) patients. XMRV is said to impair the functioning of NK cells. NK cells direct where the other cells in the immune system direct their attacks on pathogens that enter the body. It has been long known that NK cells in autoimmune disease get confused and direct the cells of the immune system to attack the body’s own tissue.
Current studies on XMRV’s role in reconfiguring the immune system are many in number. When Robert Silverman, Ph.D. sent his results on XMRV to Dr. Mikovits, it was because he found that RNaseL in the prostate cancer lines had been modified by the XMRV virus. RNaseL is an enzyme which is encoded by the RNaseL gene. This gene encodes part of the interferon-regulated 2-5A system which plays a role in the antiviral, antiproliferative role of interferons.
It was mutations in the gene, which Silverman discovered, which were found to predispose people to prostate cancer.
It seems that IC seems to bear the mark of XMRV infection. Included in the possibilities is that there is a link between anti-proliferative factor; the unique marker found in the urine of IC patients and the modifications in the RNaseL gene found in prostate cancer patients.
Another theory about XMRV and its role in in autoimmune disease is brought to us by Ashok Gutpa, M.A., MSc. In his article, “How XMRV retrovirus Findings may fit with Amygdala Hyperarousal Model for CFS/ME.”
REF: http://www.prohealth.com/library/showarticle.cfm?libid=14977
The first step is to understand exactly how the immune system works. The immune system is divided in concept between two parts which serve different functions: TH 1 and TH 2. TH 1 is the portion which involves NK cells whose job it is to identify viruses. It is the role of cells in the TH 2 branch to actually perform the work of destroying the pathogens invading the body.
A book on autoimmune disease likens each branch to units of a defending army. The TH 1 cells are the officers of the army, directing where the infantry should attack during an invasion/infection. NK cells are therefore cells which are responsible for organizing and ordering other cells like T-cells where to go and attack. In reality this attack is the TH 2 immune cells invading attacking cells and causing cell apoptosis.
In this way, both the TH 1 and TH 2 cells of the immune system must be normal and healthy to fulfill their role in defending the body. However, in autoimmune disease something goes wrong with the TH 1 cells, namely the Natural Killer cells. These commanding officers become confused in some way and order the body to attack its own cells. Now that XMRV research is coming to fruition, this process is being explained. In Gutpa’s article, he states that the TH 2 cells become over-activated and the TH 1 side is repressed.
Explained using the analogy from the autoimmune disease book, with XMRV infection in autoimmune disease the officers of the immune army get compromised, diminished and unable to give proper commands. This leaves the TH 2 side, the foot soldiers to continue fighting when they have no idea who the enemy is any more. This leads to friendly fire on the body itself, with damage being done to perfectly normal healthy cells and tissue.
Gutpa tells us if the TH 2 side dominates too long, its hypothesized that viruses such as HHV-6, Epstein-Barr Virus (EBV) and Parvovirus B can flourish; all diseases which have been found in CFS patients. The general idea is that XMRV infection destabilizes the immune system and it is the imbalances which wreak havoc.
In IC patients, if XMRV is involved to perform its typical immune system modifications, what could be happening therefore is the TH 2 cells are attacking bladder cells themselves, leading to the dysfunction and death of healthy bladder wall cells.
The dysfunction takes the form of the TH 2 side actually releasing far too many inflammatory cytokines.
Most IC patients may be familiar with the role cytokines play in our disease. It is the mast cells which secrete them. Most of the protocol for IC symptom control involves controlling the release of cytokines from mast cells. This is where some people have categorized IC as having to do with allergies as opposed to say being an autoimmune disease. While some researchers describe IC as an allergy because it induces the release of histamines, this idea is likely incorrect. The release of histamine simply triggers production of cytokines and other chemicals related to inflammatory responses. This is because it is the release of histamine which triggers the inflammatory response of the release of cytokines- the chemicals which modulate immune system responses. Cytokines refer to “immunomodulating” agents which are interferons and interleukins and also regulatory chemicals produced in the body.
Describing IC under the allergy model of medicine simply because IC symptoms involve unwarranted histamine release is a misnomer. While surely what is happening is an inappropriate response, much like nasal secretions of mucous are inappropriate for a pollen molecule, since pollen is not a virus like the cold virus, I believe leads researchers to look in the wrong direction to solve the IC puzzle.

Conditions Accompanying IC which Occur in Other Autoimmune Disease and Co-morbid Autoimmune Conditions
XMRV was found in animal studies involving the infection of chimpanzees with the virus, that the virus travels into reservoirs, lymph nodes, spleen and liver and maybe thyroid, sex organs, adrenal glands and salivary glands.
XMRV infecting the adrenal glands is an important issue in finding a link between XMRV and interstitial cystitis, because the shrunken adrenal glands of Chronic Fatigue Syndrome patients, which seem directly attributed to XMRV infection have been found in felines with interstitial cystitis.
The results of a study on felines with IC conducted by C.A. Buffington, Jodi L. Westropp, and Kristen A. Welk study were compiled in a work entitled, “Small Adrenal Glands in Cats with Interstitial Cystitis.” The results of this study were:
“Cats with FIC had significantly smaller glands when adrenal weight was normalized to body weight (3.2% _ 1.6% vs 6.5%_ 1.7%, p _0.0001, fig. 2). No correlation was found between serum cortisol and adrenal gland size at baseline, or 30 or 60 minutes (r2 _ 0.22, 0.08 and 0.11, respectively). The most significant finding in this study was the dramatic decrease in the size of the adrenal glands of cats with FIC.”

Research on human patients with Chronic Fatigue Syndrome found the exact same thing; human beings sick with CFS had adrenal glands just as significantly reduced in size as the felines with IC.
Multiple studies have found small adrenal glands in human CFS patients, in which adrenal gland sizes were reduced dramatically. The study, “Small Adrenal Glands in Chronic Fatigue Syndrome; a preliminary computer tomography study,” by Lucinda Scott, James Teh, Rodney Reznek, Aslam Sohaib and Timothy G. Dinn, found the adrenal glands in CFS patients he studied were reduced “in excess of 50% in both the right and left adrenals.”
The study mentions as well that the shrunken size of the adrenal gland let to “subtle under functioning of this gland. These results show that XMRV is therefore likely to infect adrenal glands and is also likely to account for their small size.

Shaelyn

05-26-2011, 05:58 PM

Doing some research on mycoplasma genitalium this morning. Wonder why I haven't run across this before since it seems I've been doing research for the last 4 yrs I've had this disease....duh. Also wondering why none of the doctors I've seen have even hinted on or explored this venue. Seems a very likely suspect to me. A bacteria that has no cell wall, is so small that normal detection methods do not apply. hmmm. Folks, this is not new stuff. Azithromycin is the antibiotic of choice. Who here has been specifically tested for mycoplasma genitalium? Who here has tested positive for this bacteria and taken Azithromycin? I know I'm going to make an appointment monday morning and get a prescription for Azithromycin. Oh by the way, please pardon the sarcasm I'm just getting sick and tired of this disease, incompetent doctors, and lack of research progress. Have a nice day:headbang:

I was tested and have it. I posted a thread on this but will briefly explain my doctors theory which is somewhat in-line with the XMRX theory as well. He believe that all autoimmune diseases are related in particular thyroid disease. He also believes as we all know by experience that we usually have more than one autoimmune disease. I have a mycoplasma and I am being treated with Doxycycline 100mg every other day for 1-2 years. He also has me taking adrenal supplements several times a day, as well as mostly T-3 as opposed to synthroid which only treats T-4. He has me on a host of other supplements including testosterone, estrogen, progesterone, and DHEA. When I got to him I felt like I was dying. 2008 was the worst year i ever had with IC pain. I started seeing him the end of 2008 I believe or the beginning of 2009, and I am a new person. I seriously thought I was dying when I got to him and had felt like that for years. Actually, I got progressively worse as time went on. As for the IC pain right now, the worst problem I seem to have is frequency which flares up here and there and interrupts my sleep. This will happen for a little while and then get better. I don't have the bladder pain I used to, but I still get flare ups or UTI like symptoms after sex. This really is the biggest problem I have right now. Interestingly regarding the standard UTI testing they do at clinics, their test won't show an infection however those OTC AZO urinary test strips will(at least the leukocytes or blood present). I am really interested in learning more about the XMRV theory, although I do believe the mycoplasma is part of the puzzle. I am getting immune to a lot of antibiotics so it's getting a little scary for me.

sshannon74074

05-28-2011, 11:29 AM

Is there a test for xmrv? Treatment? I asked my doctor about it and he's never heard of it which doesnt' suprise me.

akh

06-07-2011, 02:44 PM

Have we heard of IC people with small adrenals? There are herbs for adrenal support, infact I'm starting on some soon.

I have investigated this yet. I'll see if there are some studies.

My brother has some IC symptoms, so we caught the same virus or were susceptible to the virus due to genetics?

Yes, retroviruses embed themselves into the hosts genome.

Here is what Wikipedia says about retroviruses: (http://en.wikipedia.org/wiki/Retrovirus)
A retrovirus is an RNA virus that is duplicated in a host cell using the reverse transcriptase enzyme to produce DNA from its RNA genome. The DNA is then incorporated into the host's genome by an integrase enzyme. The virus thereafter replicates as part of the host cell's DNA. Retroviruses are enveloped viruses that belong to the viral family Retroviridae.When retroviruses have integrated their own genome into the germ line, their genome is passed on to a following generation.

There are only three known retroviruses to infect human beings: HIV, HTLV and XMRV. We already know about HIV. HTLV-1 is a human RNA retrovirus that causes T-cell leukemia and T-cell lymphoma in adults

Long remissions. Why?

It is believed that certain things like stress are needed to activate the virus to replicate. What Dr. Mikovits and others have found is that the virus remains most of the time in the tissue it has infected. That XMRV is fond of infecting tissue is a big red flag that this may be related to IC.

The center of our disease seems to involve bladder wall tissue. This also explains issues like fibromylagia. Fibro patients were found be as infected with XMRV as CFS/ME patients. In this case it infects muscle tissue. In CFS it is brain tissue.

What they are finding is that understanding the behavior of XMRV is crucial in identifying infection and its pathology. Dr. Mikovits has said that the negative studies on XMRV infection assume the virus to be in the blood most of the time. It isn't. It goes to tissue, mostly organ, and sets up a base there.

Yet what the animal studies on monkeys have shown is the the virus goes to certain places in the body, like the liver, the lymph nodes and establishes a base there.

There are times that XMRV is active; and times it is inactive and hiding out in tissue cells. It may get activated by a trigger. Research by Bob Silverman found that there are genes in the virus which are activated by hormones; that is "the hormones serve as an on/off switch."

From an interview with Dr. Mikovits (http://www.wellsphere.com/lyme-disease-article/me-cfs-xmrv-dr-mikovits/1010594):

I’d like to start with Judy and ask her a couple of questions having to do with how hormones might interact with XMRV, specifically androgens &/or estrogens, or even any other hormones. Judy, can you answer that?Judy – We know from work in the laboratories of Bob Silverman and Steven Goff from Columbia University that the retrovirus XMRV has what’s known as the cis-acting element, literally the on/off switch of the virus, two androgen and hormone responsive elements. And that means that when that virus, when the on/off switch sees certain hormones, it can turn it on &/or off, so what you would want to do is have a balance of hormones and not spikes.

There is an article in Virology Blog discusses goes into detail about what was learned from the macaques infected XMRV. Link:
http://www.virology.ws/2011/02/17/xmrv-infection-of-rhesus-macaques/

This is an excerpt from that article which helps explain the remission/flare up pendulum in XMRV infection:
Virus in the plasma fraction of blood was assayed by quantitative RT-PCR. Of three animals infected, virus was detected in one animal at day 4 and not after day 14; and in a second animal from days 14-20. The third animal did not develop detectable viremia. Proviral DNA was found in peripheral blood mononuclear cells (PBMC) of all three monkeys for 3-4 weeks, indicating successful infection. At one month post-infection proviral DNA was no longer detected. Plasma virus was again detected in one of the positive animals on day 291, 16 days after being immunized with a mixture of XMRV proteins. This means that viral DNA had been present in this animal but was not detected. XMRV was detected in CD4+ and CD8+ T cells and NK cells, but not in B cells or monocytes.

THANKS for insights. It is amazing how urine can be so irritating AND most amazing that even after the bad urine is peed out the irritation remains unlike washing salt off a wound which brings immediate release. I feel as if the irritation has sunk into the nerves and they just don't calm down for days.

Yes thanks for bringing THIS up! I mean really, you can't be finding things like say anti-proliferative factor (APF) in IC patients urine- you know the new urine test for IC- if the issue is just natural bladder inflammation. With APF, they can test for IC without performing a cystoscopy.

"An antiproliferative factor from interstitial cystitis
patients is a frizzled 8 protein-related sialoglycopeptide."
Susan K. Keay*†‡, Zoltan Szekely§, Thomas P. Conrads¶, Timothy D. Veenstra¶, Joseph J. Barchi, Jr., Chen-Ou Zhang*,
Kristopher R. Koch*, and Christopher J. Michejda§
Link to this study (you can read it for free): http://www.pnas.org/content/101/32/11803.full.pdf

About APF:

We have identified a glycosylated frizzledrelated
peptide inhibitor of cell proliferation that is secreted
specifically by bladder epithelial cells from patients with this
disorder. This antiproliferative factor (APF) profoundly inhibits
bladder cell proliferation by means of regulation of cell adhesion
protein and growth factor production.

What APF mean for IC patients is more that we now have something to test for; it means that something unusual is happening with the cells of the bladder lining in IC patients. APF is a peptide inhibitor, which stops our bladder lining cells from healing and making mucous.

Again I cite the study on APF:
We previously reported the discovery of an antiproliferative factor (APF) peptide (5) that is made uniquely by bladder
epithelial cells from IC patients (6) and profoundly inhibits
normal bladder epithelial cell growth (7). Picomolar quantities
of HPLC-purified APF were able to induce several changes in
normal bladder epithelial cells in vitro, including significantly
decreased rates of proliferation (7) and decreased production of
a growth factor required for log-phase growth of bladder epithelial
cells (heparin-binding epidermal growth factor-like
growth factor, or HB-EGF) (6, 7). Microarray analysis indicated
that APF can also induce changes in the pattern of cellular gene expression toward a more differentiated phenotype (8). Identification
of this factor is therefore important for determining its
potential role in the pathogenesis of IC and establishing its utility
as a biomarker for this disease.

One thing that is really creepy about doing this research is how nicely everything is fitting into place with the theory of a link to XMRV and IC.
I've done many papers in my lifetime and never found anything like this. There are so many correlations that to just list them all is becoming a tedious task. Case in point:

I may learn about peptide inhibitors or any other IC specific issue and then cross reference it with a search on that chemical and XMRV research.

Last weekend I was reading about APF, do a search on XMRV and peptides and find this information about XMRV and peptides. :
Cheney – Okay. Why do you think peptide-T would actually inhibit XMRV? Is there a scientific basis for that? Or is just hoped that it will?Judy – Actually, no. On that note, Candice Pert who actually developed, discovered it and runs the company that has run clinical trials with peptide-T in HIV disease had actually, more than a decade ago, run a clinical trial in men with CFS and they saw improvement. And when our paper came out, she said – and I understand why now – she contacted me immediately and said, “We have an opportunity, we have some drug that is ready and certified by the FDA, so it’s a limited amount now, but we could run some small studies and actually follow XMRV. Peptide-T is known to interact with the monocyte, which is a cell type in your innateimmune response, that’s known to be infected in, and actually play a role in retroviral diseases. And as we mentioned, that was my PhD thesis. So, we actually had some sound scientific rationale to actually use peptide-T in this cohort with XMRV.

I'm sorry this is so much information but there is too much to process!

Landish

06-07-2011, 07:10 PM

. He believe that all autoimmune diseases are related in particular thyroid disease. He also has me taking adrenal supplements several times a day. He has me on a host of other supplements including testosterone, estrogen, progesterone, and DHEA.

Could you please tell me what adrenal supplements he recommended you?

akh

06-08-2011, 01:26 PM

I was tested and have it. I posted a thread on this but will briefly explain my doctors theory which is somewhat in-line with the XMRX theory as well. He believe that all autoimmune diseases are related in particular thyroid disease. He also believes as we all know by experience that we usually have more than one autoimmune disease. I have a mycoplasma and I am being treated with Doxycycline 100mg every other day for 1-2 years. He also has me taking adrenal supplements several times a day, as well as mostly T-3 as opposed to synthroid which only treats T-4. He has me on a host of other supplements including testosterone, estrogen, progesterone, and DHEA.

I'm glad you are doing well and have had the feeling that YES, your doctor is reading the same stuff that I am. I have a very deficient understanding of mycoplasma infections, but many people who discuss XMRV, invariably come back to discussion mycoplasma infection as opening the door for XMRV infection.

The idea is about basically that an initial mycoplasma infection is creating a door for retroviruses- including AIDS- to jump from animal hosts to infect humans. Specifically, people think that mycoplasma infections have created a gateway for viruses which specifically target the immune system.

Here's some links to discussion of mycoplasma and HIV: http://www.newton.dep.anl.gov/newton/askasci/1993/biology/bio057.htm

I do tend to do better briefly when on Cipro, and urologist gave me a long term prescription for Macrodantin. She said they didn't understand why it worked. I also remember that my IC started with a number of UTI's being diagnosed during the first 5 months.

What I think is that maybe none of these treatments are the silver bullet is because we could be infected with both mycoplasma and XMRV. some researchers are saying there is a link. I don't understand it well- there could be a whole chicken and egg scenario- what came first the XMRV or mycoplasma.

As for dealing with XMRV infection in the CFS patients it has been found in, there has been some success with AIDS drugs like Raltegravir. Here's the study about that: http://www.plosone.org/article/info:doi/10.1371/journal.pone.0009948

From what I do know, something changes in what is called the RNase L- a key immune system gene found in those prostate cancer patients first- when XMRV is present.

akh

06-08-2011, 03:01 PM

Have we heard of IC people with small adrenals?

Apparently we have- here: http://www.ic-network.com/forum/archive/index.php/t-8281.html

I'm sure you are familiar with them linking panic disorder with IC. I know someone with fibromyalgia. The research that looks for physical causes of this panic-autoimmune issue has linked it to the adrenal glands- which also happen to produce cortisol.

There was an actual study on IC patients adrenal glands and the production of cortisol:

http://www.ncbi.nlm.nih.gov/pubmed/11832727

The results:
Mean urinary or salivary cortisol did not differ in patients and controls. However, patients with interstitial cystitis and higher morning cortisol had significantly less pain and urgency, while those with higher urinary free cortisol reported less overall symptomatology (p <0.05).
Relationships with morning cortisol were also observed when controlling for co-morbid conditions known to be affected by the hypothalamic-pituitary-adrenal axis, such as fibromyalgia, chronic fatigue and rheumatoid arthritis. Patients with morning cortisol less than 12.5 nmol./l. were 12.8 times more likely to report high urinary urgency than those with values above this cutoff.

[/quote]

Again, we get into the issue that there is a relationship to CFS, fibromyalgia, rheumatoid arthritis, and interstitial cystitis. I could take it further and speak about relationship between IC cats, what Buffington found in the felines he studied and human beings. He found the IC cats to be more jumpy. I think we get many of the negative attributions with IC and emotional problems largely because of this side effect of abnormal cortisol production.

The way I figure it, it seems likely that this retrovirus and how it configures itself around hormones goes a long way in explaining this. Even still, if your adrenal glands are small, regardless of the cause, there is going to be a dysfunction in hormones- and this is about a physical cause still and not "emotional female" issues.

I am really interested in learning more about the XMRV theory, although I do believe the mycoplasma is part of the puzzle. I am getting immune to a lot of antibiotics so it's getting a little scary for me.

I'm so glad you found a doctor who tried this new technique and I remember discussing your remission. I think your doctor is really amazing. :cat:In my very, unlearned, neophyte opinion, I think this may entail dealing with mycoplasma AND XMRV. There is much talk of mycoplasma in CFS forums.

Sorry to hear you are struggling with the antibiotics. I'm glad you are interested in studying XMRV. There have been studies of successful treatments of XMRV using AIDS drugs. Raltegravir is the drug. Link to study:
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0009948

I am firm in my resolution to study this even if IC never fits into the picture with XMRV, and this is because I see now that people with CFS, or myaglic encephelomyelitis, fibromyalgia, and even lupus are struggling with the same issues we are. Those would be being left to suffer by doctors whom find our diseases as nothing more than psychosomatic bs, suffer pain like us, and even opt out for suicide like us.

The biggest gain I've received from reading about XMRV is realizing that even if our diseases have no connections, we are connected by the politics behind them, and the prejudices as well. I read here about people choosing IC treatments that cause kidney damage and do it willingly to get well- I would quite frankly. In that light, results or no results, I have to read about this because my body has IC, and so do people I know. I recall having no diagnosis for seven years and I recall meeting people who had IC for the first time at a support group. The fact that other people have it takes you out of hellish isolation but makes you see you are part of a much larger picture.

I'm browsing this CFS forum, which does indeed discuss mycoplasma as well as viruses: http://forums.phoenixrising.me/

What I'm seeing is that the issue of what causes our respective diseases is highly politicized, personally I'm not sure why save for some quack shrink in the UK with too much power in their government. Simon Wessely is that person's name he not only considers IC, CFS, fibro, IBS, as imagined diseases created by the emotionally unstable looking for secondary gains, says the exact same things about veterans with Gulf War Syndrome, people sick from an industrial chemical spill of aluminum sulfide in Camelford, Britain and people with cancer from cell phone use, and people who have illness from chronic exposure to organophosphate pesticides.

The most concise intro to what many call "Wessely Watching" is this ME/CFS website; http://meactionuk.org.uk
This website shares what Wessely has to say about IC too: http://www.meactionuk.org.uk/Interstitial_cystitis_and_Chronic_Fatigue_Syndrome.pdf

Every CFS forum, blog usually has something to say about him, so I recommend doing your own search.

It seems Wessely has ties to the insurance industry in Britain and has had a vested interest keeping ME/CFS patients written off as crazies to appease industry and government. He does indeed attack IC as 'imaginary" but it seems CFS/ME patients are his specialty. Oh, the things which keep us in the dark ages. Get reading on this one and you'll see a host of a bizarre cadre of gulf war vets, CFS patients, fibro-patients and chronic lyme disease patients and more.

This page shows what he looks like http://www.whale.to/v/wessely_h.html
:shake:

He does not believe in Gulf War Syndrome.

http://niceguidelines.blogspot.com/2011/01/professor-simon-wessely-does-not.html

Gulf War Veterans are not happy about this:
http://www.gulfwarvets.com/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=1;t=000240;p=0

BTW, the Whittemore Peterson Studies found Gulf War Veterans XMRV positive as well. This is where mycoplasma studies get intense and maybe political because the idea that damage to the body in someway opens the body up for mycoplasma infection, which in turn leads to immune system viruses.

http://lymeblog.com/modules.php?name=News&file=article&sid=376

I'm engrossed simultaneously in the effort to understand the convoluted politics behind this nightmare; of not just being sick but having someone amazingly cruel having the last word about my disease and others. Politics is never fun reading. This is why I don't read too much about mycoplasma, because as you can imagine, when it is attributed with AIDS and oh so much more, it leads me into reading about politics when I'm in the mood to do science. Seriously, I feel confused, disturbed, angry when I read about autoimmune disease and the politics. After reading more about Wessely it is just too hard to not feel like that! :cussing:

Worse I don't understand why this is happening- or how this can happen. CFS patients are more savvy about the politics behind these diseases and inaction from the Royal Medical Society and the CDC. There are things just too off the wall to think about now- or just too cruel and money biased. :confused:

Is there a test for xmrv? Treatment? I asked my doctor about it and he's never heard of it which doesnt' suprise me.
Yes- I will find it later. I am working to write a letter to request the WPI to start doing studies on us; the purpose of this research is THAT.

akh

06-08-2011, 03:22 PM

Is there a test for xmrv? Treatment? I asked my doctor about it and he's never heard of it which doesnt' suprise me.

Yes, I list the places which do it privately but expect to pay around $400. I am banking on drafting an intelligent letter explaining why testing should be done on IC patients. I think Dr. Mikovits might likely say yes at some point. She seems embroiled in defending the WPI's previous tests.

The WPI does seem to be testing autoimmune diseases across the board. A friend of mine has ITP- a fatal autoimmune condition where the body ceases platelet production. I just learned they found XMRV in ITP patients too:
http://niceguidelines.blogspot.com/2011/03/xmrv-is-now-also-associated-with.html

Places to get tested independently for a fee:
http://www.fibromyalgia-symptoms.org/xmrv-virus.html

http://www.xandxmrv.com/news/viral-immune-pathology-diagnostics-introduces-new-test-for-xmrv-patients-and-clinicians.php

It would be really great to see if it is even present in one of us. It would be more intriguing to test IC because Robert Silverman found the virus and also works with IC patients.

ems123

06-15-2011, 11:01 AM

akh

06-15-2011, 01:09 PM

AKH, Thank you so much for all of the time you have spent posting information on this subject. I have spent the evening reading everything and it makes good sense (although is so complex it's hard to take it all in!!). Tomorrow I'm going to London to have detailed tests done by a Dr Fred Lim who works at the London Clinic. Look him up if you get a chance. It's my first step in trying to find out if any mycobacteria etc. are present (as our UK NHS system wont do these detailed tests, so I'm going private). I'll let you know how I get on. I'm going to ask him about XMRV too, but it does seem that it's not as common in people in the uk (studies didn't find it in uk patients). I'm so sorry you are feeling so sick and lonely. I really hope you find a way of getting better soon xxx

You are more than welcome! Forgive the horrible writing and typos but I'm using a public computer these days and I can't read well from the screen- I usually have to print stuff out. I am glad to help. This past week I've seen enough from new material I'm reading to know I'm going in the right direction. I just have to become far more proficient in understanding this.

You are in Britain- that is nice. I am not that surprised they won't cover the cost of that. Testing for mycoplasma is a good idea. I think getting any tangible testing which starts isolating the physical components is important.

Unfortunately the technical things one has to learn to even make start in research is staggering. I found maybe one of the sources Shaelyn's doctor might have looked at regarding mycoplasma- on page 13 of this PDF it is mentioned: http://www.meactionuk.org.uk/magical-medicine.pdf

It may take months honestly before I could even begin to describe the relation of any of these infectious agents to each other, and the effects of them on the human body. Meanwhile I've discovered some really amazing things. I will have to spend time doing some serious work on this project but I have a feeling it is going to be worth it.

One fun thing I learned is that you can buy APF- Anti-proliferative factor- the key marker and maybe major part of IC symptom generation- online! I am sharing this to be funny more than anything else. If it is causing my IC symptoms I don't think I need any more of that stuff!! :toilet: Here's the link anyhow: http://www.peptanova.de/products/Carbohydrates-and-Conjugates/APF-Sialoglycopeptide.html.

Here is a detailed article about APF- http://www.pnas.org/content/101/32/11803.full.pdf+html

Meanwhile I have to do homework like understanding what a frizzled 8 Sialoglycopeptide is. What fun! I've got this to keep me busy indefinitely and 5 days before I see my uro. It's been a two month wait. At least this time I'm happy to say I understand enough about IC politics and medicine I'm prepared for the visit. I've just got to not act like I read about my disease that much or I'll fulfill the stereotypes. Now that I know where most of these ideas about IC come from I'll be far more prepared.

purpleviolet

06-15-2011, 10:35 PM

icadvice

06-20-2011, 02:15 PM

My question is Where to go to have a doctor who knows how to test for mycoplasma, xmrv, polymicrobial infections, and some of the other rare things they never offer you to test for..

I've traveled from doctor to doctor in my area, which results in the running the same tests over and over regardless of me telling what I've been tested for and my whole story about it having to be a bacteria/virus from intercourse. I didn't have the bladder pain until the first gyno told me to take diflucan but regardless I would like to test outside of what they offer. When I finally brought in an article about mycoplasma genetilium to my current gynocologist she had to look it up to see if they could even get a test for it.. and I can't remember which type she said they could order but it wasn't "genetilium" it was something else.. So I just feel a little lost and helpless finding someone who knows how to test outside whats normally taught or used.. and I lack the free time to research because the majority of time I'm at work..but then I'm almost always in pain so my life is centered around wanting to get better and solve this? Has anyone researched further than me and found a list of doctors that test for the unusual (at least in the states) I can't afford to travel overseas.

icadvice

06-20-2011, 02:20 PM

I must add in addition to reading a little about mycoplasma, and polymicrobial infections, I've also read some on L-form bacteria. I would love to find a doctor who knows how to test for these things.

ems123

06-20-2011, 09:27 PM

I've just been tested for all 4 types of ureaplasma in the uk. A doctor Fred Lim at The London Clinic can arrange it (I had to phone him as he doen't seem to respond to emails). It is a DNA test, where they look at the ureaplasma's DNA in urine and a high vaginal swab. Because it is a DNA test it doesn't matter if the ureaplasma are dead so the specimine can be posted as time delay doesn't matter. The STI clinic in london also allows you to post samples. This is all that I know about UK (as this is where I'm from) and it might not apply to you. I'm not advertising their services, just letting you know what I have happened to find out by searching the internet. Apparently this test is very hard to come by- I think there is only one place in the uk that does it.

icadvice

06-21-2011, 12:47 PM

Thank you Ems123 this helps me and anyone possible in that area who reads this post. I eventually plan to take a vacation to Europe for fun and if I don't find someone in the states I am definitely looking up that Dr.

akh

06-21-2011, 01:21 PM

I also posted under causes of IC about something called Plechner syndrome a controversial theory with a treatment developed by a veternarian for animals and perhaps people (cause taken up by an MD named Jefferies who has a book - Safe Uses of Cortisol). But why I put it here too is because the theory blames adrenal problems (like cats that have IC with small adrenals) for auto-immune diseases.
http://drplechner.com/article_dohavethissyndrome.php

Not sure how this relates to a virus or which would come first if there is a relationship.

Thanks; this may turn out to be helpful later on. Understanding the processes involved in these diseases is very helpful, since we are just beginning to learn about the viral and bacterial components likely to be involved.

I've been doing some intense reading on the processes involved with these diseases, and it seems this is less about proving a theory but letting the pieces fall into place. I've had to read in detail about the processes happening in IC- this is really turning into a project!!

Oh, the macaque study where monkeys were infected with the virus show XMRV travels to and infects the adrenals, thyroid- basically your hormone producing organs.

Apparently they have found "XMRV in Fibromyalgia, Atypical Multiple Sclerosis, Gulf War Syndrome, Autism, Chronic Lyme and other neuro-immune disorders."
http://www.codiagnostics.com/XMRV/index2.php

purpleviolet

06-22-2011, 09:48 AM

I am a bit confused about cortisol. This is the study

Diurnal cortisol variations and symptoms in patients with interstitial cystitis.

Lutgendorf SK, Kreder KJ, Rothrock NE, Hoffman A, Kirschbaum C, Sternberg EM, Zimmerman MB, Ratliff TL.

Source

Department of Psychology, University of Iowa, Iowa City, Iowa, USA.

Abstract

PURPOSE:

Little attention has focused on systemic factors that may allow a state of chronic bladder inflammation to be established and maintained in interstitial cystitis cases. Abnormalities of the hypothalamic-pituitary-adrenal feedback system result in poorer regulation of the inflammatory response and are present in many chronic inflammatory and pain conditions, of which some have high co-morbidity with interstitial cystitis.

MATERIALS AND METHODS:

A total of 48 patients with interstitial cystitis and 35 healthy, age matched controls collected 24-hour urine samples and 3 days of salivary samples at 7 to 8 a.m., 4 to 5 p.m. and 8 to 9 p.m. for cortisol analysis. In addition, they completed a concurrent symptom questionnaire. Prospective symptom diaries also were completed in the month before sampling.

RESULTS:

Mean urinary or salivary cortisol did not differ in patients and controls. However, patients with interstitial cystitis and higher morning cortisol had significantly less pain and urgency, while those with higher urinary free cortisol reported less overall symptomatology (p <0.05).

SO: HIGH CORTISOL = LESS PAIN (the WHILE is a little confusing and I don't get the FREE part in the second part of the sentence but it also seems to say HIGH CORTISOL = LESS PAIN)

Relationships with morning cortisol were also observed when controlling for co-morbid conditions known to be affected by the hypothalamic-pituitary-adrenal axis, such as fibromyalgia, chronic fatigue and rheumatoid arthritis. Patients with morning cortisol less than 12.5 nmol./l. were 12.8 times more likely to report high urinary urgency than those with values above this cutoff.

SO: LOW CORTISOL = MORE FREQUENCY (PAIN?)

CONCLUSIONS:

These findings imply that regulation of the hypothalamic-pituitary-adrenal axis may be associated with interstitial cystitis symptomatology and there may be different diurnal hypothalamic-pituitary-adrenal patterns in patients with interstitial cystitis who do and do not have co-morbid conditions. These findings may have treatment implications for patients with interstitial cystitis who have early morning cortisol deficiencies.

Comment in
J Urol. 2002 Nov;168(5):2132.

PMID: 11832727 [PubMed - indexed for MEDLINE]

SO: MORE CORTISOL IS GOOD?

Now read this - if they can determine the level of cortisol in people research groups and apparently norepinephrine as stated below and in CATS why can't our doctors test ALL OF US for this. I don't hear of that being done by urologist. WHY NOT?

Here is cat study that is quoted all over the place

Painful Pelvic Disorder Linked to Small Adrenal Glands
Friday November 10, 2006 (0103 PST)

ISLAMABAD: In experiments with cats, researchers found the animals who suffered from interstitial cystitis had smaller adrenal glands than those without the condition.
The finding could lead to new treatments for the chronic, painful pelvic disorder that affects more than 700,000 people in the United States, 90 percent of them women.

Interstitial cystitis is a chronic inflammatory condition of the bladder wall. Symptoms include urinary urgency and frequency, difficulty urinating, minimal urine output and pain in the bladder and/or the urethra that is temporarily relieved by voiding. In some patients, pain may radiate to the genitals, rectal area and thighs.

"In cats that have interstitial cystitis, which appears to be the same in cats as in humans, two of the four zones of their adrenal glands are unusually small," says lead researcher Dr. Tony Buffington, a professor of veterinary clinical sciences at Ohio State University.

In their study, Buffington and his colleagues compared the adrenal glands of 13 cats that had interstitial cystitis with eight cats that did not have the disorder.

The adrenal glands of the cats with interstitial cystitis were about half the size of the adrenals in the normal cats, according to the report in the December issue of the Journal of Urology. The adrenal glands sit next to the kidneys and produce hormones that, among other things, help regulate heart rate and blood pressure.

The researchers found that when cats were injected with the stress-inducing compound adrenocorticotropic hormone, those with interstitial cystitis produced lower levels of the stress hormone cortisol, which is produced in the adrenals.

Under normal conditions, the functioning of the adrenal glands in cats with interstitial cystitis appears normal, Buffington says. "It is only under stress that it is abnormal," he adds.

Buffington believes this finding indicates that while there may not be adrenal insufficiency under normal circumstances, there may well be an insufficiency in adrenal reserve during periods of stress.

Interstitial cystitis worsens with stress, Buffington notes. The combination of increased stress and decreased adrenal response may be the reason why, he adds.

These findings may offer a new direction to studying interstitial cystitis in humans that can eventually lead to new treatments, Buffington says.

"Preliminary findings in humans suggest that the same abnormalities in adrenal function may be present in women when the disease is flaring up, but not when the disease is in a quiet state," he notes.

Small adrenal glands may be an underlying risk factor for interstitial cystitis, Buffington speculates.

Interstitial cystitis is a complex disorder and the abnormalities that underlie it are very subtle, Buffington says. These new findings may shed light on the causes of the condition and lead the way to new treatments, he adds.

Dr. Richard Bercik, associate director of urogynecology at Yale University, says that "physicians and lay people need to realize the connection between stress and interstitial cystitis."

"It is not just that stress exacerbates symptoms but also that other diseases associated with stress disorders, for example chronic fatigue syndrome, irritable bowel disease, fibromyalgia, endometriosis, chronic pelvic pain, anxiety, obsessive compulsive disorder, depression, neuralgia, temporomandibular joint (jaw joint) disease, phobias, all can possibly interface with interstitial cystitis," he adds.

Bercik advises that patients with these disorders are at higher risk for interstitial cystitis and should be screened for it.

This study will lead to similar testing in human interstitial cystitis patients, Bercik says. "We know that interstitial cystitis patients have higher norepinephrine levels in the urine, and interstitial cystitis patients with low cortisol in urine tend to have more symptoms."

"These may be two different subgroups, but both point to an altered immune/inflammatory response, which http://integrativeexchange.com/profiles/blogs/its-time-to-rethink-adrenal is regulated by the hypothalamic-pituitary-adrenal system," he notes

AND WOW I JUST FOUND THIS LINK WHICH I WONT PASTE IN BUT A MUST READ
http://integrativeexchange.com/profiles/blogs/its-time-to-rethink-adrenal

and the comment by Wendy Cohen (yea Wendy)

and they seem to be studying this in MAPP (of which I am a participant but they don't tell me nadda = I just log symptoms and they got my DNA, blood, etc, but I WON'T be told anything)
http://ir.uiowa.edu/icru/SURF2011/SocialSciences/3/

AND THESE SYMPTOMS SOUND LIKE ME (and probably lots of people without IC)
http://www.myadrenalfatigue.com/adrenal-fatigue-symptoms

BUT there is TONS out there on adrenal fatigue which most doctors don't acknowledge and I've also read that it is very TRICKY this adrenal thing and herbs and other adrenal tonics can stimulate the wrong way or too much (even though I love herbs) just there is a caution here AND why aren't our traditional doctors looking at this. (my naturopath has an inkling and started me on some stuff but I don't know where that is heading)

WHICH CAME FIRST THE CHICKEN OR THE EGG - IC OR ADRENAL PROBLEMS
??????????????????????????????????????????????

akh

06-22-2011, 02:13 PM

I am a bit confused about cortisol. This is the study

Diurnal cortisol variations and symptoms in patients with interstitial cystitis.

Lutgendorf SK, Kreder KJ, Rothrock NE, Hoffman A, Kirschbaum C, Sternberg EM, Zimmerman MB, Ratliff TL.

I read that article. I found it interesting. I wouldn't get confused by varying cortisol levels. I think issues like when the virus is active would probably explain the difference in morning levels of cortisol in IC patients vs. normal people.

The virus is activated by hormones and we are just learning about what XMRV does. Surely, we have strange issues like nocturia and the instance of panic attacks in CFS and fibromyalgia is being linked to XMRV's utilization of hormones, particularly cortisol.

This snippet of an interview with Mikovits explains XMRV & cortisol:
http://www.xandxmrv.com/news/interview-with-judy-mikovits-and-annette-whittemore-about-xmrv.php

Correct. It’s a simple retrovirus which means its expression, the On or Off, is controlled by, and we’ve just learned this, its unpublished data, by just 3 things, the response to Hormones, the response to Inflammatory Cytokines, its called an NF-Kapa B element. So Cortisol, the Stress Hormone turns on the Virus very rapidly and continues to have it expressed. So do Inflammatory events as caused by other Pathogens and so do Hormones like Androgens and Progestins also make sense with regard to Inflammatory Prostate Cancer and the disease being more prevalent in women.

Tony Buffington found in his IC cats some very interesting things, like a more dramatic response to stress. He fully factors this in as hormonal, and being the result of shrunken adrenals varying their cortisol output. However, he said that under non-stressful events the cortisol levels measured the same as normal cats without the disease.

I think the important thing to understand is that cortisol is produced by the adrenal glands. The adrenal glands deteriorate in CFS and IC for some reason. In both IC cats and CFS human beings the adrenal glands shrink to about 50% their normal size.

Tony Buffington, the veterinary researcher has done the most work with hormones and interstitial cystitis- the IC blood test which just came out was his pet project, no pun intended.

Buffington thinks that IC is mainly a hormonal and neurological condition. I think he's right. Strangely so is ME/CFS. He has a nice diagram in this PDF showing how he understands IC:
http://ckm.osu.edu/sitetool/sites/Indoorpetpublic/documents/hospital/indoorcat/vcna041.pdf

What I'm using to prove the link between IC and XMRV is largely the result of what he learned with his blood tests. Buffington found that tryptophan in IC patients wasn't processed normally and instead was broken down into kynurenine.

This has been the tipping point where it seems promising there is a link. First of all, I heard of these two hormones being important in fibromyaglia. Second, a simple search into tryptophan and kynurenine in CFS reveals these two hormones to be important there- and linked to the immune system.

Here is one article showing that- and strangely a link to mycoplasma:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC127654/

Again, if you want to help I will appreciate it. Pretty much I think there is indeed a link between IC, XMRV and mycoplasma. It is going to take a while to write what I want to write because there is a match in XMRV infection traits, CFS infection traits, and IC traits. I'll keep you posted.

The method of healing IC used by Shaelyn's uro included adrenal support with treating mycoplasma infection. You need normal cortisol levels to at least avoid problems experienced under stress. FYI, it is only under stress that IC feline's and human's adrenals fail to function normally.

I mean if XMRV is infecting the adrenal glands it is likely in some way changing when and how they operate. We have nocturia and fibromyalgia patients have insomnia. This isn't a scientific opinion- just my guess, but I think the cortisol issue is about the virus activating the hormone in some way to serve its own needs. It's on/off switch for replicating depends on hormones including cortisol.

If you used anything for say, a food supply, chances are if you were a pathogen, you'd probably figure a way to make sure your supply meets your needs. I'm guessing that maybe virus behavior has much to do with WHEN certain things like flares or lack of sleep occur.

On the first night of my first flare up, when I had to go every 5 minutes I asked myself this one question: what is wrong with my body that it would engage in an activity that is harmful if not down right dangerous for me.
I won't begin to discuss lack of sleep and how much I've lost in my life because of it. Worse, it is ultimately fatal. Look up "fatal familial insomnia" if you have questions about lack of sleep being very dangerous.

The one thing that struck me about research tying so many bizarre autoimmune disorders to a virus, is that it makes more sense something external, something that has nothing to do with the human body- would cause a reaction so detrimental to survival.

It isn't "wishful thinking" to tie it to this. For me it feels like the missing link. You need to understand since my ulceration was diagnosed I've been unwilling to read much about IC. This has because when you learn the ulcers come back, your quality of life will be worse than end stage renal failure, if you are a rational thinking person, looking at this can be overwhelming.

I can't sleep more than 20 minutes at a time now. I have a disease where I do have to also live in fear of not being treated or helped. As to why or how my own body would do this to me for the heck of it--- I haven't had an answer for this since the day this disease started for me in 1998.

I am also a died in the wool skeptic, I'm educated and I know when to keep my mouth shut about an idea- like when there is no evidence to support it.

I wouldn't be posting if I didn't think I've encountered something very, very important. This is more than to help me. What astounds me was when I met someone with fibro this winter and they knew all about severe sleep loss. They only had fibro- this means no restroom visits and more.

Also, I think that since nearly all autoimmune diseases have similar things which are inherent to them- like mitral valve prolapse, low blood pressure, low body temperature--- it seems that, yes, they are connected.

Okay, we've only known about XMRV since 2006. Worse still, our diseases are politicized, moreso in Britain. Still, given all the misery that has been caused over glib dismissal of autoimmune disease- and even deaths which are common with ME/CFS- and the high suicide rate in CFS/ME, IC which unfortunately backs up every lie ever told about the "unreality" of these diseases, I'm not surprised so many studies out to attack the viral research happen.

akh

06-23-2011, 03:00 PM

WHICH CAME FIRST THE CHICKEN OR THE EGG - IC OR ADRENAL PROBLEMS

Personally I don't know why exactly testing for cortisol hasn't fit into their equation on diagnosing IC. Maybe the levels of cortisol can be influenced by other things. Or maybe they aren't intersted in testing for this to diagnose IC. But what you should know is that the blood test for interstitial cystitis was developed recently but Tony Buffington. I was more amazed to find that the test for IC matches a test for fibromyaliga. Fibro and CFS patients have this odd problem of breaking down tryptophan to kynurenine. This is important stuff to know, because this ties in with the immune system and factors related to infection, both mycoplasma and xmrv:

Chemical In Blood May Explain Susceptibility To Bladder Pain

Follow-up studies of the chemicals that appeared in blood samples suggest that the way tryptophan, an essential amino acid, is processed in cats and humans with interstitial cystitis ultimately could affect the way signals are transmitted in the brain. The results, while preliminary, suggest that the disease is not just a malfunction of the bladder, but might instead have origins in the central nervous system, researchers say.

The researchers then determined the chemical structures within those molecular profiles, which showed that blood from cats with the syndrome contained at least 20 percent more tryptophan and kynurenine than did samples from healthy cats. Kynurenine is a brain compound produced when tryptophan breaks down in the body. An elevated level of kynurenine suggests that tryptophan is being diverted from its conversion into a chemical responsible for sending signals in the brain.:cat:

http://www.sciencedaily.com/releases/2009/06/090615144323.htm

Relationship between interferon-gamma, indoleamine 2,3-dioxygenase, and tryptophan catabolism.
Taylor MW, Feng GS.
Source

Department of Biology, Indiana University, Bloomington 47405.
Abstract

Interferons have been shown to be potential anti-cancer agents and to inhibit tumor cell growth in culture. The in vivo mechanism of the anti-proliferative effect may be direct or indirect through the immune system; however, in vitro a primary mechanism of cytotoxicity is through the depletion of tryptophan. In particular, interferon-gamma (IFN-gamma) induces an enzyme of tryptophan catabolism, indoleamine 2,3-dioxygenase (IDO), which is responsible for conversion of tryptophan and other indole derivatives to kynurenine. The inhibitory effect of interferon on many intracellular parasites such as Toxoplasma gondii and Chlamydia trachomatis is by the same mechanism. Elevated kynurenine levels have been found in humans in a number of diseases and after interferon treatment, and the enzyme is induced in rodents after administration of interferon inducers, or influenza virus. IDO induction also occurs in vivo during rejection of allogeneic tumors, indicating a possible role for this enzyme in the tumor rejection process. The gene for IDO has been cloned and shown to be differentially regulated by IFN-alpha and IFN-gamma. IDO induction has been correlated with induction of GTP-cyclohydrolase, the key enzyme in pteridine biosynthesis. A direct role for IDO in pteridine synthesis has not been shown, and this parallel induction may reflect coordinate regulation of genes induced by IFN-gamma. A possible role for IDO in O2-radical scavenging and in inflammation is discussed.
http://www.ncbi.nlm.nih.gov/pubmed/1907934

Role of Indoleamine-2,3-Dioxygenase in Alpha/Beta and Gamma
Interferon-Mediated Antiviral Effects against Herpes Simplex
Virus Infections
O. Adams,1 K. Besken,2 C. Oberdo¨rfer,2 C. R. MacKenzie,2 O. Takikawa,3 and W. Da¨ubener2*

Two distinct but functionally overlapping types of IFNs are
known: alpha/beta IFNs (IFN-/), which include some species
of IFN- and a single IFN-, and IFN- (36). Within the
last decades several IFN-induced effector mechanisms for the
control of viruses have been described. These include the expression
of double-stranded RNA-dependent protein kinase
(22), Mx proteins (19), 2-5 oligoadenylate synthase, and
RNase L (15). The most prominent IFN-inducible antimicrobial
effector mechanism for the control of parasitic, bacterial,
and viral growth in murine cells is NO production by the
inducible isoform of nitric oxide synthase (iNOS) (4). However,
there are only few studies showing an antimicrobial effect
mediated by the induction of NO in human cells. In contrast
there are abundant published data showing antibacterial and
antiparasitic effects mediated by the induction of indoleamine-
2,3-dioxygenase (IDO) in human cells (3, 7, 27, 33).
http://jvi.asm.org/cgi/reprint/78/5/2632.pdf

Indoleamine 2,3-dioxygenase overexpression causes
kynurenine-modification of proteins, fiber cell apoptosis
and cataract formation in the mouse lens
http://ko.cwru.edu/docs/publications/Mailankot1.pdf

Maneesh Mailankot1, Magdalena M Staniszewska1, Heather Butler2, Moonkyung H Caprara2

Indoleamine 2,3-dioxygenase (IDO) is the first enzyme in the kynurenine pathway. The kynurenines formed in this
pathway chemically modify proteins and cause apoptosis in cells. Evidence suggests that kynurenines and their
protein modifications are involved in cataract formation, but this has yet to be directly demonstrated. We generated
transgenic (Tg) mouse lines that overexpress human IDO in the lens. Homozygous Tg (homTg) lenses had higher IDO
immunoreactivity,B4.5 times greater IDO mRNA, andB8 times higher IDO activity compared to lenses from hemizygous
Tg (hemTg) animals. The kynurenine content was threefold higher in homTg than in hemTg but was not detected in
wild-type (Wt) lenses. Kynurenine modifications were B2.6 times greater in homTg than in hemTg or Wt. HomTg lenses
had vacuoles in the epithelium and cortical fiber cells. Kynurenine modifications coincided with apoptosis in the
secondary fiber cells of homTg lenses.

This should give you some introduction, albeit complicated to the new places the IC blood test can take us to. I'm having this feeling that some connections just aren't being made with this new research in all these areas. Maybe the fun of being delegated to the circular file in terms of regard for our illnesses gives us the chance to discover the connections ourselves. I'm having fun with this either way.

Fitting XMRV into this equation? It has been done, but I have much more to read.
Here's an interesting snippet from a very long article. Before you read this, know that tumor necrosis factor, prostaglandins, apoptosis, cytokines, and large amounts of nitrous oxide in the body are all associated with interstitial cystitis. Refer to that BMG article I first showed and by all means, do your own searches. There is too, too much information to share. I have no idea where this is going specifically but I know for sure it is going somewhere!

I'm even finding links between erractic tryptophan catabolism or processing and mycoplasma. I'm also finding links to these chemicals and bladder cancer.

This is just one facet of many, many interesting things I've found which may help with IC from just working with the concept of all autoimmune diseases having a pathogen as a cause and of all autoimmune diseases being related. I think that's a sufficient enough of an umbrella to cover what the core concept is behind the research.

Even though I'm reluctant to embark on reading about this now, but I'm figuring there's a link between XMRV and mycoplasma. Anyhow, I'm sharing just a few tidbits of what I'm looking up. Trust me, there are so many other things to share. Eventually I'll share the rest. I'm just learning the basics now.

Immune Function is the Ultimate Key to Autism, Alzheimer’s, HIV/AIDS, Asthma, Allergies, Arthritis, Diabetes, Cancer and even Heart Disease

Dr Jeff Bradstreet, MD, MD(H), FAAFP

http://drbradstreet.org/2011/03/29/immune-function-is-the-ultimate-key-to-autism-alzheimers-hivaids-asthma-allergies-arthritis-diabetes-cancer-and-even-heart-disease/

Caption: Microglia are the primary recipients of peripheral inflammatory signals as they reach the brain. Activated microglia initiate an inflammatory cascade by releasing cytokines, chemokines, prostaglandins and reactive nitrogen and oxygen species (RNS and ROS, respectively). Bi-directional exchanges between microglia and astroglia amplify inflammatory signals within the central nervous system (CNS). Cytokines including interleukin (IL)-1, IL-6, tumor necrosis (TNF)-alpha and interferon (IFN)-gamma induce indoleamine 2,3 dioxygenase (IDO), the enzyme responsible for degrading tryptophan, the primary precursor of serotonin (5-HT), into kynurenine, which is eventually metabolized into quinolinic acid (QUIN), a potent NMDA agonist and stimulator of glutamate (Glu) release. Multiple astrocytic functions are compromised due to the excessive exposure to cytokines, prostaglandins, QUIN and RNS/ROS, ultimately leading to downregulation of glutamate transporters, impaired glutamate reuptake, excessive glutamate release and compromised synthesis and release of neurotrophic factors. Oligodendroglia suffer damage due to toxic overexposure to cytokines such as TNF-alpha, and diminished neurotrophic support, both of which promote apoptosis and demyelination. Copious amounts of glutamate are released from astrocytes in the vicinity of extrasynaptic NMDA receptors, whose activation leads to inhibition of BDNF synthesis. Excessive NMDA activation, caused by QUIN and D-serine, is compounded by diminished glutamate reuptake by astrocytes and oligodendroglia. NMDA-mediated excitotoxicity, combined with a consequent decline in neurotrophic support, and an increase in oxidative stress, synergistically disrupts neural plasticity and induces apoptosis (cell death).

purpleviolet

06-24-2011, 05:18 AM

The funny thing is I took this as a supplement for sleep and it did not increase my IC symptoms as I recall even though I thought it would. It did not do much of anything.

akh

06-24-2011, 11:50 AM

The funny thing is I took this as a supplement for sleep and it did not increase my IC symptoms as I recall even though I thought it would. It did not do much of anything.

I used to take it for sleep too. One time it did start a bad flare up but it was mixed with the sleep medication I took at the time. Potassium is supposed to be a big player in IC symptoms and a flare up causer, too. I can still eat bananas and potatoes. There is something wrong in the IC bladder, where it can't absorb and diffuse potassium molecules.

As for the cortisol/adrenal supplementation-- even the CFS people can't agree on a broad regimen which works.

Here are some links to how CFS, fibro and other patients supplement cortisone:
http://www.endfatigue.com/health_articles_f-n/Hormones-adrenal_problems_in_cfs.html

http://forums.phoenixrising.me/archive/index.php/t-785.html

http://www.medhelp.org/posts/Fibromyalgia---CFS/XMRV-and-hydrocortisone/show/1356480

nener63

07-03-2011, 05:11 AM

I went to my Gynocologist for my yearly papsmear. He gave me an antibiotic for a bacterial infection. I can't remember the name of it. It was a cream I inserted into my vagina for five days. While taking the antibiotic I wa in alot of pain and could not get out of bed. But, a day or so after taking it I started feeling better. I was so excited !!! That lasted about two weeks. I called my physician and he put me on another round of the same antibiotic. As of right now I feel so much better. I know this won't last long but, I'll take advantage of of every minute I can feel good. Hopefully, it won't be long until they find out more to help us. At least the physicians are trying. I feel mine are doing the best they can with the knowledge they have about this disease.

akh

07-05-2011, 03:07 PM

I don't have much time right now. I'm going to post some interesting links and let people review them for now.

This article is about mycoplasma and the indoleamine 2,3 (IDO pathway. This is what is most certainly amiss in IC patients because a dysfunction IDO pathway is what the IC blood test detects. Tryptophan is being broken down into kynurenine and not serotonin. This study happens to be about exactly that.

l-Tryptophan-l-Kynurenine Pathway Metabolism Accelerated by Toxoplasma gondii Infection Is Abolished in Gamma Interferon-Gene-Deficient Mice: Cross-Regulation between Inducible Nitric Oxide Synthase and Indoleamine-2,3-Dioxygenase
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC127656/

Personally I don't think mycoplasma tells the whole story and this is why. Essentially what precipitates the IDO pathway is gamma interferon.

Gamma interferon is important in XMRV infection in CFS/ME and FMS patients.

I know mycoplasma relates to this and I'll share more about this:Here is another article about gamma interferon, IDO and mycoplasma:
http://www.ncbi.nlm.nih.gov/pubmed/1907934

The IDO pathway has a link to gamma interferon;
Relationship between interferon-gamma, indoleamine 2,3-dioxygenase, and tryptophan catabolism
http://www.fasebj.org/content/5/11/2516.abstract
\
Gamma interferon abnormalities has a link to XMRV, ME, CFS
IFN-γ induced IDO and WRS expression in microglia is differentially regulated by IL-4
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2486430/

There are others who attribute abnormal IDO pathway activity to chlamydia: Tryptophan depletion as a mechanism of gamma interferon-mediated chlamydial persistence
http://www.cpnhelp.org/tryptophan_depletion_as_a

All the same I think that the source is viral and because gamma interferon rests at the source, I'd say I'm about 99% sure this is the result of the genetic mutations caused by XMRV.

The main reason is that I'm finding all sorts of coincidences.
I discovered something very interesting about gamma interferon. Apparently it binds with the glycosaminoglycan heparin sulfate in the body. I didn't have too look through any complicated articles either. I found this on the article about gamma interferon (IFN-y) on Wikipedia:

Interferon-gamma (http://en.wikipedia.org/wiki/Interferon-gamma)

See also: Interferon-gamma receptor
Cellular responses to IFN-γ are activated through its interaction with a heterodimeric receptor consisting of Interferon gamma receptor 1 (IFNGR1) and Interferon gamma receptor 2 (IFNGR2). IFN-γ binding to the receptor activates the JAK-STAT pathway. IFN-γ also binds to the glycosaminoglycan heparan sulfate (HS) at the cell surface. However, in contrast to many other heparan sulfate binding proteins, where binding promotes biological activity, the binding of IFN-γ to HS inhibits its biological activity.[7]

The structural models shown in figures 1-3 for IFN-γ[1] are all shortened at their C-termini by 17 amino acids. Full length IFN-γ is 143 amino acids long, the models are 126 amino acids long. Affinity for heparan sulfate resides solely within the deleted sequence of 17 amino acids.[8] Within this sequence of 17 amino acids lie two clusters of basic amino acids termed D1 and D2, respectively. Heparan sulfate interacts with both of these clusters.[9] In the absence of heparan sulfate the presence of the D1 sequence increases the rate at which IFN-γ-receptor complexes form.[7] Interactions between the D1 cluster of amino acids and the receptor may be the first step in complex formation. By binding to D1 HS may compete with the receptor and prevent active receptor complexes from forming.

I don't have the link with me, but I know some doctors treat IC by giving heparin injections instead of instillations.

I've been lost in finding amazing stuff related to the ATP, IC and XMRV.

For starters, there is abnormalties regarding ATP in IC bladders:

Augmented extracellular ATP signaling in bladder urothelial cells from patients with interstitial cystitis.
http://cystitis.researchtoday.net/archive/2/12/84.htm

XMRV has been found in the receptors which bind to ATP- receptors called ABC's. This list here has data on where in the body XMRV has and hasn't been found. http://precedings.nature.com/documents/4669/version/1/files/npre20104669-1.pdf

purpleviolet

07-07-2011, 05:43 AM

Hi AKH,

Great work! Can you summerize all this is in lay terms what you think this all means? Anything we can do about it? Thanks

akh

08-01-2011, 12:30 PM

Hi AKH,

Great work! Can you summerize all this is in lay terms what you think this all means? Anything we can do about it? Thanks

I can summarize this by saying there is little doubt in my mind that all autoimmune diseases are linked. I hope my typos from limited computer time and limited sleep hasn't silenced this topic. I sort of would like the ability to post a new thread.

I've been pretty busy because I've got working theories I have to flesh out. The amount of information I'm reading and still have to read is staggering. Here's a thesis I'm working with now. As for controversy regarding viral research, I don't have time for this; more importantly, Antiproliferative factor in interstitial cystitis has been isolated as being the result of gene p53- gene p53 is a gene linked to cancers, and both environmental and viral factors have been found to alter p53.
http://www.ncbi.nlm.nih.gov/pubmed/17628545

p53 is an amazing gene: http://news.bbc.co.uk/2/hi/health/7861474.stm

Meanwhile, here's my new thesis:

Notes on IC and ATP

Studies have shown that when bladder epithelial cells are stretched they release ATP. In the bladders of people with interstitial cystitis, more extracellular ATP is released than in control patients.

Quote: (BMJ August 8th, 2009: 339:337-342)
“(IC bladder uroepithelial cells released significantly higher concentrations of ATP (adenosine triphosphate) than control biopsies suggesting that ATP plays an important role in this syndrome. An investigation of cultured bladder epithelial cells showed that such cells have an abnormal, much higher concentration of ATP. This higher concentration of ATP decreases the ability of the bladder wall to conduct (channel) potassium ions which again indicates impaired potassium ion conduction is part of the pathology of interstitial cystitis.”

Studies on ME/CFS have shown deficient “ion channelopathy to be part of the pathology of ME/CFS. Some studies about ME/CFS and potassium conduction attribute this flaw to abnormal mitochondrial gene expression.

The BMJ article cited says studies on IC showing ATP increase and changes in potassium conduction as also resulting from abnormal gene expression.

I suggest the issue of ATP, potassium ion channelopathy as being the result of XMRV. Idiosyncratic production of ATP and its components such as purinergic receptors, ATP- binding cassettes (ABCs) and or ABC transporters is well documented in many other autoimmune diseases and can be fully attributed to the source of most IC symptoms.

I hypothesize these abnormalities are the result the presence of XMRV in interstitial cystitis, and occur through many different mechanisms, including viral mimicry and others.

The hypothesis that XMRV likely cause of significantly high release of ATP in bladder urothelial cells is supported by observed defects in ATP-binding cassette transporters, where XMRV viral mimicry of proteins is likely to have occurred..

About ATP Binding Cassettes
“ATP-binding cassette transporters are members of a protein superfamily that is one of the largest and oldest proteins.
ABC transporters are transmembrane proteins that utilize the energy of adenosine triphosphate (ATP) hydrolysis to carry out certain biological processes including the translocation of various substrates across membranes and non-transport related processes such as translation of RNA and DNA repair. ABC’s transport a wide variety of substrates across extra and intracellular membranes, including metabolic products, lipids and sterols, and drugs. Proteins are classified as ABC transporters based on the sequence and organization of their ATP-binding cassette (ABC) domain(s). ABC transporters are involved in tumor resistance, cystic fibrosis, bacterial multi drug resistance and a range of other inherited human diseases.”

One of these diseases is Pseudoxanthoma Elasticum (PXE), “a hereditary connective tissue disease in which proteoglycans have altered properties.” In pseudoxanthoma elasticum there are abnormalities which show some relevance to interstitial cystitis. Both diseases show a relationship with sulfated glycosaminoglycans. The only difference is that in PXE, an inherited genetic defect in an ATP-binding cassette transporter identified as ABCC6/MRP6

The idea that ABCC6/MRP6 is the cause of PXE was tested in 2003 in Italy.
Proteoglycan metabolism in PXE was studied by Francesca Maccari, Dealba Gheduzzi and Nicola Vopi at the University of Modena, in Modena, Italy.

In this study, the researchers measured sulfated glycosaminoglycans in the urine of people with PXE, people carrying the disease and healthy controls. Sulfated glycosaminoglycans are what compose the mucosal lining of the human bladder, known as the GAG layer. The GAG layer is deficient in IC patients because the bladder epithelial cells which secrete GAG become compromised and cease to serve their function.

The glycosaminoglycans this study on PXE tested for were chondriotin sulfate disaccharide and heparan sulfate disaccharide. Note also that to treat interstitial cystitis, heparin sulfate is instilled into the bladder to augment the defective GAG layer. In Canada and elsewhere outside the U.S., chondriotin sulfate has been used with even better results than heparin sulfate as a “bladder instillation,” to help IC patients in those places.

In PXE 34% less of the polysaccharides were detected in the urine of PXE individuals, than controls or unaffected carriers of the genetic defect.

It is worth noting that the commonality between IC and PXE patients may extend beyond glycosaminoglycans being abnormally low. On the revealing of the genome for XMRV, a comparison of what human proteins the XMRV retrovirus “mimics” finds a link between the virus and ABC transporters.

A retrovirus is different from normal viruses. Normal viruses only have their DNA transcribed into RNA in the host, and the RNA is then translated into a protein. A retrovirus functions in a different way, which more adeptly inserts its genome into human DNA. Retroviruses have their RNA reverse-transcribed into DNA, which is then “integrated into the host’s genome and then undergoes the usual transcription and translation processes to express the genes carried by the virus.

How this relates to the issue of XMRV and autoimmune diseases, its speculated that XMRV creates proteins which mimic those in the human body. The idea is that the fake DNA created by the virus initiates a response from the human immune system. Some believe that the human immune system becomes confused from the retroviral proteins which mimic its own proteins. This leads to the unending attack from the body on its own tissue.

There is an ATP-binding cassette associated with the viral mimicry of XMRV infection. It is called ABCC9:

It is known as EAW96452.1. This is an ATP-binding cassette of the subfamily C (CFTR/MRP), member 9, isoform ABCC9. XMRV GAG- PRO-POL was found to mimic the natural properties of this ABC.

Note that ABCC6 in PXE where altered levels of glycosaminoglycans is very closely related to ABCC9. Both of these ATP-binding cassettes are of the subfamily MRP.

However, a link between this possibly compromised ATP binding cassette know as ABCC9 and interstitial cystitis goes further than its proximity in nature to ABCC6.
Here is what the genome mapping project says about ABCC9

“ABC proteins transport various molecules across extra and intra cellular membranes. ABC genes are divided into seven distinct subfamilies (ABC1, MDR/TAP, MRP, ALD, OABP, GCN20, White). This protein is a member of the MRP subfamily which is involved in multi-drug resistance. This protein is thought to form ATP sensitive potassium channels in cardiac, skeletal and vascular and non-vascular smooth muscle. Protein structure suggests a role as the drug-binding channel modulating subunit of the extra pancreatic ATP-sensitive potassium channels. Mutations in this gene are associated in cardiomyopathy dilated type 10. Alternative splicing results in multiple transcript variants.”

Now we go back to the idea the BMJ article expressed; the idea that come IC pain comes from inability for the bladder epithelial cells in IC patients to channel potassium ions. Also issues involving dysfunctional bladder smooth muscle activity parallel a possible defect in ABCC9 as a causative agent in IC symptoms. Bladder spasms and pelvic floor muscle issues become clearer when the idea of viral mimicry of ABCC9, or other ABCs.

Potassium channeling function by ABCC9 also alludes to the co-morbidity of mitral valve prolapse in interstitial cystitis patients. This too is another trait common to both IC and CFS/ME. Furthermore, defective cassette binders have been linked to the lack of energy proliferation in the bodies of CFS patients. Potassium channeling has also been linked to the pain of fibromyalgia.

The studies of Dr. Light bind the idea that a defect in receptors in the muscle fiber of fibromyalgia patients—receptors which detect levels of ATP used or not used by the body which is part of the role which ABCs and or ATP sensors like purinergic receptors play in the pathology of that disease.

This makes good enough sense to me. Looking at the many studies which show the prevalence of extracellular ATP in both human and feline IC patients, and furthermore, studies which demonstrate a clear link between extracellular ATP and pain in the human bladders, I have a good feeling about the stability of my hypothesis.

Studies regarding extracellular ATP causing pain in human bladders go far beyond IC research. There was a study performed in Sweden demonstrating that extracellular ATP and the purinergic receptors P2Y are responsible for the inflammatory response in human bladders exposed to the E coli bacteria. Or to put in simple terms, ATP and purinergic receptors which bind to ATP are responsible for the pain and inflammation in the common urinary tract infection.

Bladder stretching itself also causes the bladder epithelial cells to excrete ATP. Studies have ranged from hypothesizing that extracellular ATP serves a role as a signaling mechanism in the human body, where its release upon stretching the human bladder generates the feeling and urge to “go.” I blame the inability of ABC transporters to serve their role in transporting substrates through intra and extracellular membranes as being part of why some substances irritate IC bladders and cause no sensation of pain in people with normal bladder tissue.

I attribute the experience of interstitial cystitis as being largely dependent upon defective ATP-binding cassette behavior.

I suggest exercise works as an IC therapy because it uses up the extracellular ATP.

I will show proof for my argument in referring to a study which show that extracellular ATP is responsible for other IC anomalies, including the defect where tryptophan in IC patients is broken down into kynurenine over serotonin and melatonin. The indoleamine 2,3, dioxygenase pathway is the formal name for the modification of tryptophan into various other chemicals.

There is a study proving that extracellular ATP effects the maturation of human dendritic cells (immune cells), affecting the indoleamine pathway.

“Extracellular adenosine triphosphate affects the maturation of human dendritic cells, mainly by inhibiting T-helper (Th 1) cytokines, promoting Th2 cytokines and modulating the expression of costimulatory molecules. In this study we report that adenosine triphosphate can induce immunosuppression through its own action on DCs, defining a new role for extracellular nucleotides. Microarray analysis of ATP-stimulated human DCs revealed an inter alia a drastic up-regulation of 2 genes encoding mediators involved in immunosuppression: thrombospondin-1 and indoleamine 2,3 –dioxygenase.

Hypothesis 2

It is possible that bladder stretching in interstitial cystitis is the result of when the bladder is distended, abnormal ATP release and possibly more abnormalities enable the glycosaminoglycans heparin sulfate to allow viruses, bacteria or mycoplasma to penetrate the blood brain barrier.

It is known that bladder stretching causes cells to release ATP. This is one way physical changes alone can alter bladder surface biochemistry.

Furthermore, the amounts of extracellular ATP becomes more prevalent upon mechanical stretch can be reduced by chemicals already present in the bladder. In a study by Sun Y and Chai TC at the Division of Urology at the University of Maryland School of Medicine, both heparin sulfate and dimethyl sulphoxide (DMSO) reduce the higher levels of stretch activated ATP release in the bladders of people with interstitial cystitis.

The idea supported by the results of this study is that bladder epithelial cells (bladder urothelial cells or BUCs) are able to detect levels of ATP and rely upon ATP as a chemical messenger of sorts.

Here are links to ATP and IC correlations:
http://ajpcell.physiology.org/content/290/1/C27.full
http://www.plosone.org/article/info%...l.pone.0018704

BTW, if the doctors are going to use depression being a little co-morbid as a way to relegate us to the medical communities circular file, so to speak, they need to do their homework first. Depression relates to a modified indoleamine pathway (IDO). IDO is the techie term for IC patients processing trytophan differently- making it into kynurenine and not serotonin. This modified IDO pathway behavior is the result of modified ATP/ABC/purinergic issues: Extracellular ATP, too, modifies the IDO pathway: http://bloodjournal.hematologylibrary.org/content/106/12/3860.full.pdf

This information is the tip of the iceberg of a mountain of research I'm doing. I'm getting my own computer working again after losing everything to being so tired I didn't lock my car when I was moving out of state. The computers here time me out very fast and it has made it hard to edit. I hope to have mine running at the end of the week. Also I can actually type my notes now with a computer in my possession again.

BTW, the CFS people have great information on XMRV and ATP because they are figuring modified ATP binding and processing is at the core of ME symptoms. Purinergic receptors are being sited as the cause of fibro pain by Dr. Light- a pain researcher. He has the best theories on fibromylagia I've seen and some great new ones about CFS.

Forgive typos, and lack of source citing; I must go and well the call of this thing interferes with things too: :toilet:

akh

08-09-2011, 09:57 PM

I know the description I gave is very detailed. Forgive that. Lack of time combined with the sad truth there isn't any easy way to describe biochemistry. I'm still learning it.

I also have the wifi up and running so I can put in the time write clearly and explain what I'm finding in a way that makes sense to all of us

The latest IC research has found that gene p53 which is designed to trigger cancerous cells to die when it finds them also triggers bladder lining cells to die in the bladders of IC patients!

Yes, I know we don't have cancer. For some reason this gene that detects damaged DNA and is programmed to hunt down cells that have it dislikes our bladder cells. I know this is strange. I like a good mystery, especially when it gets closer to discovery WHY IC even happens! :bow:

Here's the study:
p53 Mediates interstitial cystitis antiproliferative factor (APF)-induced growth inhibition of human urothelial cells
Jayoung Kim,ab Susan K. Keay,c Jordan D. Dimitrakov,ab and Michael R. Freemanab*
aThe Urological Diseases Research Center, Children’s Hospital Boston, Boston, MA 02115, USA
bDepartments of Surgery, Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1939966/

I don't know how widely this study has been circulated yet but this study has discovered that a gene important to cancer, p53 is found to control Antiproliferative Factor in IC bladders.

p53 causes cells in the body to destroy themselves, and also stops cells from growing. The reason it does this is to stop cancer cells and other bad cells from replicating and destroying the body. in cancer, the p53 gene is found often to be damaged and in fewer numbers.

This makes it possible for cancer cells to replicate aggressively. p53 is a gene exists to rescue the body from cancer cells. It detects abnormal DNA and initiate the destruction of bad cells.

In interstitial cystitis the reverse happens- p53 levels are increased which causes the cells in the bladder to be destroyed- cells which don't have cancer. Antiproliferative Factor is a substance found only in IC bladders and it is mediated by p53.

Now understanding this, there is a good chance research can find a way to stop the process. The finding that p53 is the cause of missing IC bladder epithelial cells is a very important discovery.

More importantly, p53 has been widely researched for its role in stopping cancer. We understand this gene very well as a result.

p53 is activated when it finds damaged DNA. It also repairs DNA.

This may means that there is damaged DNA in the bladder cells of IC patients. Things which damage DNA are things like radiation, toxins and retroviruses also alter DNA.

Regardless of where this leads, this study identifies the exact gene causing bladder cells to die and not grow in IC.

p53's innate functions as an anti-cancer gene oddly match the pathology of IC.

Learning why p53 does this in IC patients is the next step. The p53 discovery narrows the search dramatically. There are only a few things which trigger it.

Treatments? I don't know. Most research on p53 has been on getting cancer patients to make more of it. In IC the exact opposite is the case- p53 is mediating an attack on bladder cells which aren't cancerous. p53 levels would have to be reduced to treat IC.

Basic reading about p53 you can do on line shows it can be controlled

Mdm2 is the name of the gene and a protein it makes which serves the sole purpose of controlling p53 levels. Mdm2 description on Wikipedia (http://en.wikipedia.org/wiki/Mdm2),

I learned this from a very nice, simple article about p53: http://www.bioinformatics.org/p53/introduction.html

I haven't started digging for studies about p53 and viruses but this graphic I found might go a long way to show there is a link between p53 and retrovirus infections.

This could very well idea that XMRV could be involved in IC. p53 plays a role in DNA transcription and it also detects damaged DNA.

A retrovirus alters human DNA.

A retrovirus infection is different because actually mixes its genes our human DNA. DNA stands for deoxyribosenucleic acid. A retrovirus only has ribonucleic acid (RNA). It is the simplest life form. A retrovirus induced genetic alteration could trigger a response from p53.

Endogenous retroviruses are ones that can actually be inherited from generation to generation.

Research has found that the human genome is riddled with genes from ancient retroviruses that infected our ancestors. Most all of this viral DNA causes no symptoms.

This is testimony to how well retroviruses tangle themselves into our genetic imprint. Maybe enough to trigger a wary cancer gene looking for DNA changes? Hmm.

p53 and the retrovirus which causes leukemia (http://www.google.com/imgres?q=p53+retrovirus+mouse&um=1&hl=en&client=firefox-a&rls=org.mozilla:en-US:official&biw=1024&bih=629&tbm=isch&tbnid=9Xst5jQClxd6iM:&imgrefurl=http://www.fhcrc.org/science/education/courses/cancer_course/basic/molecular/accumulation.html&docid=uWYg0HpO14Y1fM&w=358&h=614&ei=jjlCTrSYHbHfsQKVqJmpCQ&zoom=1&iact=hc&vpx=421&vpy=76&dur=562&hovh=153&hovw=89&tx=63&ty=136&page=4&tbnh=153&tbnw=89&start=44&ndsp=15&ved=1t:429,r:2,s:44)

akh

08-20-2011, 04:45 PM

Toxoplasma gondii is the Latin name for mycoplasma, btw.

Parasite Uses the Power of Attraction to Trick Rats Into Becoming Cat Food

ScienceDaily (Aug. 20, 2011) — When a male rat senses the presence of a fetching female rat, a certain region of his brain lights up with neural activity, in anticipation of romance. Now Stanford University researchers have discovered that in male rats infected with the parasite Toxoplasma, the same region responds just as strongly to the odor of cat urine....

Sapolsky's group previously determined that although the parasite infects the entire brain, it shows a preference for a region of the brain called the amygdala, which is associated with various emotional states. Once in the brain, the parasite forms cysts around itself, in which it essentially lies dormant...

Read the rest at: http://www.sciencedaily.com/releases/2011/08/110819141519.htm

Another unrelated post:

I hear people are using colloidal silver instillations and these work amazingly well: http://forums.phoenixrising.me/showthread.php?5299-Interstitial-Cystitis&p=87054&viewfull=1#post87054

Has anyone else heard of colloidal silver instillations? Maybe this relates to why silver nitrate worked? Any thoughts?

vanilla

08-23-2011, 06:35 AM

Colloidal silver turns human skin blue and it's irreversible.