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Viruses have been suggested as triggers for "auto-immune" diseases including MS. There has been mounting evidence that a virus such as EBV may make one more susceptible. The following research suggests that an initial virus may lay dormant in the CNS and then reactivated later by another virus. Just a theory, but might explain why this disease has been so difficult to crack.

Ian

http://www.jci.org/cgi/content/abstract/JCI27372v1

I like this theory. An article I posted a while ago suggested a similar idea. And as you say, it seems that the extra layer of complexity you get by throwing a second infection into the mix would help explain why it is so tough to figure out this disease.

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Well guys, here’s another limb on the hormone tree.

In considering whether infection with another virus reinitiates CNS infection later in life, I also wonder if “adrenopause”, when DHEA levels begin to fall in men and women, could also be a factor that might allow dormant viruses (or bacteria) in the CNS to become active later in life.

I’ve already posted the animal info about DHEA and the possibility it may protect against bacterial and viral infections.
This article describes adrenopause:

Intra-individual maximum concentrations of DHEA and DHEAS are achieved during the third decade, followed by a steady decline with advancing age…This decline has been termed “adrenopause”…The age-related decline in DHEA(s) levels show high interindividual variability…Adrenopause is independent of menopause and occurs in both sexes as a gradual process at similar ages.

Another take on adrenopause notes it is an imbalance between DHEA and cortisol secretion .

Several clinical signs might be related to the decline of DHEA secretion in aged people: ………..impairment of cognitive and affective performances, deterioration of immunocompetence are the most significant evidences……..

There has in fact been some research to suggest people with MS may have a dysfunction in DHEA and cortisol secretion .

A little OT, but the info on daclizumab peaked my interest in natural killer cells. It was recently reported that DHEAS effectively “corrected” two other “auto-immune” diseases by virtue of some impact on natural killer cells. Defect of a Sub Population of Natural Killer Cells in Graves’ Disease and Hashimoto’s Thyroiditis: Normalizing Effect of DHEAs

CONCLUSIONS: A functional defect of a subpopulation of NK immune cells, involving both NKCC and the secretory activity, was demonstrated in newly-diagnosed GD and HT patients. This defect can be reversed by a dose-dependent treatment with DHEAS.

At any rate, the hormone barker thinks low levels of DHEA in people with MS could be a contributing factor to the “re-emergence” of viral and/or bacterial infections later in life. If DHEA in fact affords some protection against viral and bacterial infections in humans (an unknown I think), DHEA levels start dropping during our 30’s (adrenopause and the “decade of diagnosis”) and DHEA is an immune modulator, it at least seems like DHEA could theoretically be considered as another factor that might contribute to the “re-emergence” of infections in people with MS in adulthood.

Just more speculation from the hormone corner…. Maybe the "real news" is that I posted something with an "auto-immune" spin.

Sharon

With my "obsession" in mind, please take my comments and questions in good humor.

It may all be as you propose--who knows? I wonder why scientists and drug companies collect information on the majority of MSers and throw out those cases that don't fit. Wouldn't it advance their work to look at the exceptions (and then work back to all the rest)?

My question here is why have all the pediatric cases of MS appeared? (To the extent that 6 pediatric MS clinics are being set up across the US.) Some of the children are as young as 2 years old! Not yet in the "decade of diagnosis!" Could it be a diet that promotes excess insulin production? Just a thought.

Here is one explanation of why kids get MS:

TORONTO - Researchers at The Hospital for Sick Children (Sick Kids) have shown an association between paediatric multiple sclerosis (MS) and the Epstein-Barr virus (EBV), indicating that exposure to the virus at a certain time in childhood may be an important environmental trigger for the development of MS.

This research is reported in the April 21, 2004 issue of JAMA (The Journal of the American Medical Association).

"Earlier studies suggested a relationship between childhood exposure to Epstein-Barr virus and the risk of developing MS. This is virtually impossible to quantify in adult MS patients, as nearly 90 per cent of the healthy adult population in Western countries has been exposed to EBV. In the paediatric patients, we can study viral exposures more easily, as children have fewer viral exposures due to their young age," said Dr. Brenda Banwell, the study's principal investigator, a Sick Kids neurologist and associate scientist, and an assistant professor in the Department of Paediatrics at the University of Toronto.

The research team found that 83 per cent of the paediatric MS patients showed evidence of a past EBV infection, compared with 42 per cent for the healthy control group. The paediatric MS patients also were less likely than the control subjects to have been exposed to herpes simplex virus. Epstein-Barr virus is very common and transmissible virus in the herpes family that causes infectious mononucleosis.

"We think the Epstein-Barr virus plays an important role in the development of MS, as the genetic code of the virus contains sequences that are identical to genetic sequences in the myelin basic protein, which is expressed in the brain, and destroyed in MS. It is conceivable that the immune system mounts a response to that genetic sequence in EBV, then sees it in myelin and targets it as well," added Dr. Banwell.

Multiple sclerosis (MS) is a disease of the brain, spinal cord, and optic nerves that can cause problems with muscle control and strength, vision, balance, sensation (such as numbness or tingling in your feet or hands), and mental functions such as thinking ( cognition) and moods.

The symptoms of MS are caused by inflammation of the central nervous system and the destruction of myelin, the protein coating that surrounds and protects nerve fibres (axons).

MS is believed to involve a complex interplay between environmental triggers (such as infections), genetic predisposition, and an abnormal autoimmune response. At least five per cent of all MS patients experience the onset of their disease before the age of 18. It is estimated that 50,000 Canadians have MS. Multiple sclerosis is the most prevalent in countries that are furthest from the equator, such as Canada, northern Europe, and Australia.

"We suspect that it is the sequence and timing of viral exposure and how this modifies an individual's immune response that is important," said Dr. Banwell. "Children with MS are the closest to the biological onset of the disease, which allows us to look at a whole host of causative factors that are very difficult to study in adults."

Other members of the research team included Dr. Suad Alotaibi (now at the Al-Sabah Hospital in Kuwait), and Julia Kennedy, Dr. Raymond Tellier, and Derek Stephens, all from The Hospital for Sick Children.

One of my neuros who is a big fan of EBV / MS says that there is similar data from research in Turkey i.e. that kids diagnosed with MS have a much higher incidence of infection with the EBV virus.


Ian

Ian--This is a completely plausible explanation, but why, in this material, would only 83% of the pediatric cases studied show signs of EBV? Shouldn't it be 100%? Maybe the real "cause" can be found more easily looking at the other 17%.

To quote this info: "It is estimated that 50,000 Canadians have MS. Multiple sclerosis is the most prevalent in countries that are furthest from the equator, such as Canada, northern Europe, and Australia."

This has always bothered me. MS is practically non-existent among the Eskimos and Lapps--far from the equator--Why? Why aren't researchers looking there? The prevalence of MS is much greater in Massachusetts--closer to the equator.

I think my frustration is building with this crummy disease, and I have reached the point that I need to vent! I count on you all to be understanding.

Lyndacarol,

I don't know why they didn't find EBV in the other 17%. And if EBV is the trigger / cause - it may only be the cause in some people. Other viruses or bacteria may play a role.

In mid-May an EBV / MS think tank is taking place, run by the UK MS Society and one of the top MS doctors / researchers at the Institute of Neurology. The event is bringing together the top dogs in the MS world (UK and Europe) and I think the data being presented will be very interesting. I was invited, but will be in the US with work (very near to you Sharon). I have asked to be copied in on the results and will post here.

I suppose, if EBV is the trigger / cause in some / most cases of MS, what does it do? Does it stay in the system and reactivate? Does it affect one's hormones etc etc? Lots of unanswered questions - but don't fret they must be getting nearer to an answer.

Ian

Thank you for your calm head and for my math correction--another sure sign that I didn't have control for a while.

It is most unfortunate that you will not be able to attend that May event; I respect your abilities greatly--you would be a real asset there! I appreciate all you contribute to this website. And your calming influence.

Lyndacarol,

I qualified as an accountant before moving to a much more interesting job, so find it hard not to correct numbers (sorry).

Please don't regard me as a calming influence - the digital clock radio that I smashed a few weeks after dx and the metal bathroom cabinet that no longer shuts are not signs of a calm person.

I hope some of my postings are useful, some of the time.

Ian

I like your thinking, Ian. It would be nice to get to the bottom of this conundrum regarding the implication of certain viruses or bacteria in MS. There has often been speculation of a linkage between Herpes HHV6 or EBV and MS. In Bangkok recently, I saw a US trained Thai neuro who said that MS might result from one of 6000 viruses! So, please keep up your good work in this area.
Regards,
Phil.

The UK MS Society held a conference last weekend and the various presentations will be posted in due course. I came across the following on another MS website:

"I went to the MS Life Convention in Manchester over the weekend and attended a lecture by Prof Alistair Compton about genetics. It's not proven to be genetic i.e. your child has less that 0.5% risk of being diagnosed with MS if you have MS.

There was a woman in the audience who had 4 children, 3 of them have been diagnosed with MS (I can't remember if she had MS though!). Professor Compton said it was purely co-incidental that three out of four of her children had been diagnosed with MS.

I think there is a risk that if a family member has MS then you have that gene but it needs to be activated in some way e.g. they think that having Glandular Fever (EBV) might be a trigger".



I find it hard to believe that having 3 of your 4 children diagnosed with MS is purely coincidental. I assume they would all have the same genetic susceptibility, and if a virus was the trigger, then it is likely that your children would infect each other. Again, EBV suggested as the possible trigger.


Ian

I have before me an article from the Chicago Tribune, January 5, 2003. It tells about an epidemiological study planned (It must be done by now, though I have not seen the outcome.) for PawPaw, Illinois (tiny agricultural town of 850 near Rockford) where Harold Ikeler's family has been targeted by MS--his wife died of it, all three of his daughters have it, and five grandchildren have it!

At the time of the article and for the study, a resident had tracked down 14 current and former residents with the disease. (Kind of shoots the usual estimates of one case for every 1,000 people, doesn't it?)

I wrote to Harold some time ago with my suspicion of insulin, even suggesting the fasting test (Are you surprised?). I never heard if his family followed up; I assume not.

In my opinion, this cannot be coincidence! IMO, of course, the problem lies in the pancreas--either a diet (or chronic inflammation) that promotes insulin production, or a genetic weakness in the organ, or maybe a pancreas damaged by virus or bacterium.

This family/town would be a PRIME target for researchers, it seems to me! Where are they?

Hi Everyone

We now have an EBV, insulin, DHEA duel. Just kidding. Backing up a bit in the thread, Lynda Carol asked:

My question here is why have all the pediatric cases of MS appeared?

Hopefully they're studying this to try and better understand the disease. But, hormone barker would also like to note that the low DHEA and high cortisol ratio I referenced earlier may also be seen in fairly young children as indicated in this abstract on major depression in 8 to 16 year olds. Thus, the presence of a high cortisol/low DHEA ratio is a possibility in some children.

Lynda Carol--just for you , a couple of abstracts on DHEA. The first is that "hyperglycaemia decreases circulating DHEA levels in healthy men" and the second that DHEA improves glucose-induced insulin secretion

The present results suggest that DHEA may be a promising drug to prevent diabetes during aging.

Now, unfortunately, I don't have a clue if those are consistent or inconsistent with your ideas about insulin and MS.

I'm glad to see you're advocating Lynda Carol. Take care.

Ian--we'll get together sometime.

Sharon

Sharon,

Ian--we'll get together sometime.

How many times do I have to tell you - I'm happily married and young enough to be your son.


Love

Ian

Sharon--there is no real "duel" here, as you know; we just have "inquiring minds" and I enjoy the exchange of ideas! And I appreciate the emotional support when I experienced a recent "meltdown."

To your second abstract and your comment: "Now, unfortunately, I don't have a clue if those are consistent or inconsistent with your ideas about insulin and MS," I can only point to the title wording, "increases beta-cell mass and improves...insulin secretion," and think this is not what I want to do if I think there is too much insulin there to begin with. I wish I were a scientist; then there would be a CHANCE I might understand!

Since I'm not, I can only continue to stumble around in the dark and keep looking. For me, there is no other option.