All I Want for Christmas Is a Cure for This Damned Disease!

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I had a slight meltdown while serving as a semi-official MS patient advocate last week. Please let me explain…

I was invited to take part in a conference call organized by a significant multiple sclerosis consortium. The group is planning an MS conference which will take place over several days, with one of the days devoted to patients and patient education. My purpose on the call, along with several other patient advocates, was to help decide which seminar topics would be most interesting and useful for patient attendees of the planned meetings. In advance of the call I was supplied with a list of potential subjects and was told to be ready to choose which I thought should be included as part of the conference program.

As I perused the list, which included items such as "2018 MS Drug Pipeline" and "Mindfulness and MS", I found myself surprised and then increasingly angered by one glaring omission: there was no mention at all about the search for a potential cure for MS. This annoyed me to no end. After all, shouldn’t one of the primary goals of every MS Association, researcher, and neurologist be figuring out how to put themselves out of business by curing this damned disease? I thought it quite telling (and nauseating) that the planners of this MS conference hadn’t thought enough of this subject to even include it as part of the equation.

Despite assurances to myself that I would remain calm during the conference call, once it came my turn to speak I just couldn’t help myself. What began with my evenly pointing out that the prospect of a cure had somehow been overlooked quickly devolved into a sputtering, barely coherent chastisement of the entire MS medical establishment. Let’s not forget, the field of MS neurology was not so long ago considered a medical backwater, but has since been transformed into one of the biggest cash cows in all of modern medicine, all on the backs of outrageously expensive pharmaceutical products that may curtail disease activity but do absolutely nothing at all to cure MS.

Is this really where the MS status quo now resides? A place where we must accept that disease management is the best we’re going to get? Where patients struck with a hideous illness should be content or even grateful that the modern medical divinities have graced some of them with the ability to keep their potentially crippling malady in check for who knows how long? Where the torrents of cash generated by insanely priced drugs have so corrupted the MS establishment from top to bottom that the prospect of a cure seems unfit for conversation in polite company – why, for fear of spooking the goose that lays perpetual golden eggs? And what about those of us with progressive disease, who now have a whopping total of one approved drug that might, just might, slow the insidious decline of a subset of us by a less than dazzling 20%-25%? I readily admit that the disease modifying drugs currently available do dramatically improve the quality of life for many of the patients taking them– they also carry with them long lists of frightening and sometimes fatal side effects – but they do nothing at all towards stomping out MS. Forgive me for not genuflecting at the feet of the MS gods. How about this? Come up with a drug that cures my creeping paralysis and I’ll genuflect my ass off.

Some of the other patients on the conference call responded to my little tirade by saying that they’d given up hope for a cure in their lifetime. Though I do understand the frustration that lies at the root of this sentiment, to that I respectfully say “bullcrap”! Each of the top-selling MS drugs generates profits measured in billions of dollars per year; you’d think that some of that money might be spent looking for the cause of and then cure for multiple sclerosis. Instead, we have pharmaceutical companies devoting more money to marketing than to research (click here), and the funds that are spent on research are almost exclusively directed towards finding newer and better ways of manipulating the human immune system. NEWSFLASH TO MS RESEARCHERS: the aberrant immune response seen in MS patients is not the cause of the disease, it’s a symptom of some much deeper ill. Though the following analogy may be a bit of a stretch, treating MS by suppressing the immune system is like treating a broken leg with painkillers. It may make the patient feel better, but it doesn’t do a damned thing towards fixing the underlying problem.

At this point, you might rightfully ask, so, Mr. Smarty-Pants, if you’re so clever and smug and full of yourself, where would you suggest we start this quest for an MS cure? Well, I’m glad you asked. Even though I’m not a physician or researcher, I think I have a few good ideas. Here are just some of them:

• We’ve known for years that the Epstein-Barr virus is somehow implicated in the MS disease process. In fact, there seems to be such a close relationship between EBV and MS that some researchers have gone so far as to state that if a person doesn’t have EBV, they don’t have MS (click here). Certainly, EBV alone doesn’t cause MS, but in conjunction with specific genetic predispositions, it may just be the fire starter. We now have the ability to map patients’ genomes, so shouldn’t there be at least a few researchers laser-focused on understanding the interaction between EBV and patient genetic profiles in an attempt to get to the guts of the problem? At the very least, a comprehensive database of the genetics of MS patients should be started posthaste so that gene variants and epigenetic changes can be detected and identified.

• It’s been observed that HIV patients taking powerful antiretroviral drugs seem to develop MS in far lesser numbers than the general population (click here) and that HIV patients who already have MS often see their disease go into nearly complete remission once starting these drugs (click here). Again, why isn’t this a subject for intense scrutiny? Especially since one of the most commonly used anti-HIV drugs, AZT, has been shown to have anti-EBV properties (click here)? Please note, there was one trial of an anti-HIV drug, Raltegravir, on MS patients. This trial failed, but Raltegravir does not effect EBV.

• HSCT, the form of stem cell therapy that first eradicates an MS patient’s immune system with strong chemotherapy drugs and then reboots it via stem cell transplant has been shown to put properly selected multiple sclerosis patients into long-term remission (click here). Shouldn’t these patients be carefully tracked and tested to see just why this treatment can be so incredibly effective? Is it simply that their reconstituted immune systems are no longer autoreactive, or might there be some other reason? Does HSCT not only put MS into remission but actually cure it, with those patients who see a resumption in disease activity somehow developing MS anew after coming into contact with some environmental trigger? The fact is that Epstein-Barr virus, when dormant, resides in immune system B cells which are wiped out during the chemotherapy-induced eradication of patient’s immune systems at the start of the HSCT process. This means HSCT rids the body of EBV. Does this allow the genetic triggers of the disease to then reset, putting a halt to the autoimmune process? A shot in the dark, maybe, but one worth examining…
  
  
• Researchers at Harvard are currently studying the use of a century-old tuberculosis vaccine, called the BCG vaccine, to treat patients with type I diabetes, an autoimmune disease. They are reporting remarkable success, completely reversing the disease in some patients (click here). Apparently, the BCG vaccine works on both the immune system and on the genetic level, and thus could theoretically be of use not only in type I diabetes but across a broad spectrum of so-called autoimmune diseases. In fact, before the introduction of the MS disease-modifying drugs, there was promising research into the use of BCG to treat MS (click here), which seems to have been abandoned once money started rolling in from the first MS drugs. Why devote research monies to a 100-year-old vaccine that costs relative pennies when gazillions of dollars can be generated developing a never-ending stream of boutique drugs that profoundly alter the workings of the human immune system, the long-term ramifications of which are entirely unknown? As Deep Throat told Woodward and Bernstein, follow the money…

Okay, in the parlance of corporate speak, I’ve just spitballed a few ideas on which MS researchers devoted to finding a cure for the disease might focus their considerable brainpower. Of course, many of these ideas don’t have near-term blockbuster profit potential, so in the upside down world of pharmaceutical company driven medical research, they likely won’t get much attention. I’ve said it before, and I’ll say it again – capitalism is a wonderful system for creating wealth, but the marriage of capitalism and medicine is proving to be an unholy one. As long as profits take precedence over patients, as is currently the case, cures for any diseases will be rare beasts indeed.

MS organizations should never lose sight of the fact that their prime directive should be hastening their own demise by contributing to the effort to find a cure for the disease. The current status quo must not stand, and patients should not stand for it. I for one will not shut up about this topic, no matter how nuts it may make me seem to those less inclined to histrionics. If MS patients themselves don’t demand better, we will never get better, both figuratively and literally.

Oh, yeah, Happy Holidays!

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Since it is the season of giving, please allow me to recommend two MS nonprofits that are very worthy of your and your families’ and friends’ donations. I’m not suggesting the National Multiple Sclerosis Society, as, quite frankly, they have a vast contribution generating machine that sucks up lots of the cash that might be better directed at smaller MS organizations. Given the topic of this essay, I’m recommending two groups that are striving to find a cure for multiple sclerosis.

The first is the Tisch Multiple Sclerosis Research Center of New York (click here), which is currently in the process of building the largest stem cell laboratory devoted strictly to stem cells for MS, and will soon be starting the only FDA approved phase 2 stem cell trial on PwMS. In addition, the Tisch Center is involved in a wide range of groundbreaking research, from identifying MS biomarkers to understanding the root cause or causes of the disease, without an understanding of which there can be no cure.

My second pick is the Accelerated Cure Project (click here). The ACP is currently focused on the iConquerMS project, a crowdsourced database of information supplied by MS patients that will give researchers worldwide the opportunity to detect patterns and trends in the MS population that very well could provide the clues needed to come up with a cure for the disease. In addition to donating to the ACP, if you’re not already a participant in the iConquerMS project, I urge you to visit their website (click here) and start participating by answering some quick surveys. This is a patient-driven research effort and gives you a chance to join in the search for a cure.

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Finally, here’s a little Christmas present to my dear readers. The following clips are from the exquisite but little-known 1995 film “Smoke”, one of my faves.. Despite the fact that there are no explosions or car crashes, this one of my favorite scenes in all of filmdom, just one friend telling another a compelling Christmas story. Is the story true or made up, and does it matter? The scene features a masterful performance by the great Harvey Keitel playing opposite William Hurt, and touches on just about everything that makes Christmas and human beings such endlessly fascinating subjects.

Please watch both clips to get the full effect (I recommend viewing full-screen), as I couldn’t find a single clip that encompasses the entire sequence. As an added bonus, the sequence finale features one of my favorite Tom Waits songs, Innocent When You Dream. If you’re interested in watching Smoke in its entirety, it’s available for streaming on Amazon (click here). Enjoy!

How?

Given my tendencies towards intense introspection, I find it hard not to dwell on the “why’s” of my disease. Primary among these why’s is “why me?”, a question infused with self-pity that I know is best left unprovoked. I could quite easily drive myself half mad trying to figure all of the angles involved in this ultimately unanswerable query. If I’d made some different decisions in the past, might some alternate life path have avoided the Multiple Sclerosis landmine? Or would all roads eventually lead to Rome?

When I have allowed myself to stray down this tangled trail, a nasty battle always breaks out between my Buddhist and existential leanings, my inner Siddhartha calmly stating that there is no such thing as coincidence while my inner Jean-Paul Sartre screams back that life is nothing but an exercise in randomness. Nothing like a philosophical brouhaha roiling around inside the noggin to ruin what might have otherwise been a decent day. In the end, these thought kerfuffles inevitably lead me to counter the “why me?” conundrum with its other half, “why not me?”. This seems to temporarily satisfy both Siddhartha and Sartre, forcing them each to retreat back to their own little corners of my mind, where the Buddha sits in quiet meditation and Sartre drinks and smokes his brains out.

I have of late been giving more thought to the “how’s” of my illness, as in “how the frack did I get so sick!?!?”. Whereas the “why” question deals more with the metaphysics of the situation, the “how” is focused more on the nuts and bolts of the disease mechanism and the circumstances that led to my getting ground-up in its gears. At first glance the “how” might seem as insoluble a question as the “why”, but by sizing up what we know about the disease and matching it with the circumstances of my own life I think I’ve come up with a reasonably plausible explanation for how I got from point A to point B (and the B stands for “Blechh”).

It’s long been suspected that Multiple Sclerosis and other so-called autoimmune diseases have strong genetic components. As scientists have begun to unravel the human genome, more and more genes have been discovered that seem to play a role in the Multiple Sclerosis disease process (click here and here). While many patients might not be able to isolate their own genetic susceptibility without a complete mapping of their DNA, in my case the genetic connection is actually quite clear.

My mom developed gestational diabetes when she was pregnant with me, and unlike the vast majority of such cases, her illness did not resolve after I was born. Stranger still, her malady turned out to be type I diabetes, otherwise known as juvenile diabetes, by far the most serious form of the disease. Type I diabetes is thought to be caused by an autoimmune attack on the pancreas, leaving it unable to produce insulin. A shake of my mom’s family tree revealed that her grandfather and uncle also had type I diabetes, indicating that there is certainly a genetic trait for the disease being passed down from generation to generation. Research has shown that the children of diabetics have a 50% greater chance than the general population of developing some sort of autoimmune disease, and here I am with not only MS but also Hashimoto’s thyroiditis, an autoimmune disease that destroys the thyroid gland. It is also suspected that I’ve had an autoimmune attack on my pituitary gland, and for a while the doctors thought I had discoid lupus, an autoimmune disease that attacks the skin.

Of course, simply having the genetic predisposition to develop a disease doesn’t on its own guarantee that a person will get sick. Given my family history, it’s likely that many of my relatives share these same funky genes, and none of them, to my knowledge, have developed diabetes, Multiple Sclerosis, or any of the other usual suspects (lupus, rheumatoid arthritis, Crohn’s disease, etc.). Somewhere along the line something needs to trigger the genetic susceptibility for disease to take hold, in effect turning the “sick genes” on. In the case of MS, scientists have long focused on the Epstein-Barr virus (EBV), a member of the herpes virus family, as a likely disease trigger.

Epstein-Barr virus is the nasty bug responsible for mononucleosis, although most people infected with EBV never do develop Mono. Instead, the initial infection can manifest as a severe cold or flu, and a person can often be infected without having any symptoms at all. Once infected with EBV, the virus stays within a patient’s body for the rest of their lives. Infection with Epstein-Barr virus is so common that it’s estimated about 90% of the adult population harbors the virus. Astoundingly, though, it’s been found that 100% of MS patients are infected with EBV. That’s right, 100%. The correlation is so high that some researchers have stated that “people who are not infected with Epstein-Barr virus do not get MS” (click here).

Sure enough, blood tests have revealed that I am indeed infected with EBV. Of course, since the vast majority of adults are also infected with Epstein-Barr virus, the virus alone can’t be the cause of Multiple Sclerosis. In conjunction with a genetic susceptibility, though, the virus may be the thing that tips the scales between health and illness.

It’s interesting to note that in its dormant state, Epstein-Barr virus takes up residence within the immune system’s B cells. Just so happens that some of the MS disease modifying drugs destroy a patient’s B cells, thereby ridding the body of much of its EBV load as well. The interferon drugs (Rebif, Avonex, Betaseron, Plegridy) also happen to be very strong antivirals. Could it be that these drugs work, at least in part, not because of their immunosuppressive or immunomodulating properties, as is commonly believed, but because they are attacking EBV in the bodies of MS patients? Not a mainstream idea to be sure, but something I think worth considering.

Epstein-Barr virus isn’t the only infectious agent that has been linked to MS. The bacteria responsible for many sinus infections have been implicated in the disease as well (click here and here). I’ve suffered from sinus infections most of my life and had endoscopic sinus surgery in 2006 to try to eradicate the problem. Unfortunately, the surgery only helped temporarily, as my sinus problems reemerged soon afterwards. So I’m two for two when it comes to possible infectious triggers for Multiple Sclerosis.

Actually, make that three for three. Exposure to toxic molds and funguses have also been linked to neurologic and demyelinating diseases (click here), and back in the 1990s, when I was living in South Florida, I spent two years working in a building that was found to be riddled with toxic molds and bacteria. At the time I was employed by a startup company, and after a few months working in their very crowded offices the company moved into a larger building that had been empty for quite some time. The facility was in pretty bad shape, with wires dangling out of the decrepit ceiling panels and a musty smell hanging in the air. Simply walking into the place felt unhealthy.

After spending about a year and a half working within those walls it was revealed that upper management had been sitting on an environmental report which stated that the building was riddled with a smorgasbord of toxic microorganisms. The sons of bitches in the executive offices had kept the report hidden until one of their administrative assistants copied it and left it on the desks of several employees. Soon after, men in hazmat suits came and sectioned off parts of the building as they decontaminated the place section by section. In retrospect, my first weird symptoms started cropping up while I worked in that building, and last year when I was tested for exposure to toxic molds the results came back positive. Wonderful.

Stress is another factor that has been linked to MS and similar diseases. Many MS patients report their first symptoms after periods of acute stress, and it’s been demonstrated that stress can bring on relapses in those patients suffering from Relapsing Remitting Multiple Sclerosis (click here). Though I’d always been neurotic and prone to worry, my years in South Florida were especially filled with stress, both of the acute type brought on by upsetting life events, and long-term simmering stress engendered by living in a place where I always felt like a stranger in a strange land.

My periods of acute stress were almost always initiated by the breakup of romantic relationships, which I inevitably took much harder than was even remotely reasonable. Losing a long-term girlfriend more often than not sent me into a period of prolonged psychological agony, during which I’d lose weight, sleep, and sense of self for months and months at a time. Yes, I know it’s hard to believe that any woman would leave a fella as oozing with charm as me, but lo and behold, there were a few who unceremoniously gave me the gate. And when they did, I imploded. Seems I had an incredible knack for zeroing in on precisely the women who would be most toxic to me and then fall for them, hard. I believe the accepted psychological term for a person who habitually engages in such behavior is “jackass”.

Soon after one breakup in 1997 I suffered from incredibly severe headaches for about three weeks, super intense searing headaches that emanated from the base of my skull and left me damn near completely debilitated. Now my MRI images reveal my one big juicy MS lesion at the very top of my spine right beneath my brainstem, precisely at the spot from which those headaches seemed to radiate. Could it be that those headaches of old were somehow involved in the formation of the lesion that is at the root of my current neurological mess?

The latter five or six years of my stay in South Florida found me enmeshed in a kind of simmering, low-level stress brought on by trying to be someone I wasn’t. I spent that time working in extremely corporate environments, shirt and tie type places that I found to be soul stifling. Though I had creative jobs within those organizations, the stress of trying to conform with corporate culture took its toll. I had once sworn I would never join the 9-to-5 workaday world, but there I was, sending myself off to prison each and every day.

Though I made several very close friends in Florida and was never wanting for a social life, I always felt somewhat alien there, my aesthetics and values simply at odds with the place and most of its inhabitants. Still, for reasons I can’t fully explain, I remained living in a place I couldn’t stand while working at jobs I hated until one final romantic breakup mercifully sent me packing back to New York, where I rediscovered the me that I’d almost forgotten existed. And then, just a few years later, the beast that had been showing glimpses of itself for years finally reared its ugly head, and I was diagnosed with MS.

There then is the “how” of my disease, as best as I can figure. Genetic predisposition? Check. Exposure to infectious triggers? Check. Periods of stress, both acute and long-term? Check. Now, if only there was some way to uncheck some of those boxes. Researchers are just starting to try to figure out how to address the genetic aspects of disease, and many biotech startups are attempting to develop gene therapies for a variety of illnesses. Scientists are working on vaccines for Epstein-Barr virus, but the work still seems to be in its early stages (click here). And though life will never be free of stress, individuals can learn techniques such as mindfulness and meditation that can help them make better life choices and reduce the impact of stress on their existence.

I wish I could say that figuring out how I got sick brings with it some sort of gratification. I suppose that on a purely intellectual level fitting the puzzle pieces together into a somewhat coherent picture is a teensy weensy bit satisfying. Then again, all of my conjecture may be completely wrong, my illness due more to the evil eye put on me by a Gypsy beggar I once crossed than to the elements identified by my keen analytical powers. Perhaps it was my destiny to wind up the Wheelchair Kamikaze, and no matter what choices I made, all roads would’ve converged at point B (as in B, for “Barf”). Okay, I’d better stop this thought train before Siddhartha and Sartre square off and pelt each other with rocks and garbage in the deepest recesses of my brain pan…

Bits and Pieces: Autumn Equinox Edition (also Tysabri, MS and HIV,viruses, relapse rates, misdiagnoses, diet, and asinine research)

Personification of Autumn (Currier & Ives lithograph, 1871) (Photo credit: Wikipedia)

Well, according to the full scale replica of Stonehenge that I have sitting in my living room (which is right next to my exact copy of the Sphinx and down the hall from my faux Taj Mahal – it’s incredible what you can fit in a 900 ft.² apartment with a little ingenuity) summer is over and autumn is now upon us. Time for packing away the seersucker, preparing for the harvest, and getting ready for the ceremonial sacrificing of virgins. Luckily, there are no virgins available in my apartment, so we’ll probably make do with sacrificing some gourmet chocolates.

Wish I could say I had an exciting summer, but this one was actually quite dull. A big shout out to Multiple Sclerosis for that one, as the beast has been heavy-handed with me these last few months. Even though I have progressive disease and the overall trajectory of my symptoms is always steadily downward, their severity does tend to inexplicably wax and wane a bit. The last few months they’ve definitely been waxing, and boy, I’m more than ready for a little wane – and I’m not talking about L’il Wayne, the notorious hip-hop artist (click here).

Alas, my replica of the Temple of the Oracle at Delphi tells me that it’s time for another edition of Bits and Pieces, my semi regular compendium of interesting MS related news and notions. Can’t argue with the Oracle at Delphi, lest mighty Zeus unleash a lightning bolt in my direction, and really, I have enough problems. So here goes…

♦ First up, some MS drug news. A study out of Italy has found that Tysabri is even more effective in real life clinical practice than it was during the trials that led to its approval for use in treating RRMS (click here). This study of 343 patients from 12 Italian MS centers found that, over time, treatment with Tysabri resulted in a 68% reduction in MS relapses, that 93% of treated patients saw no disease progression, and that 53% of Tysabri treated patients were free of any signs of disease activity. Very impressive numbers, to say the least, despite the fact that Tysabri is not without its concerns (chiefly the possibility of contracting opportunistic infections, primarily PML, a potentially fatal infection of the brain).

When Tysabri was first introduced I was highly dubious of the stuff, thinking that the drug’s dangers far outweighed its potential benefits, but I must admit that time has, it seems, proven me wrong. I personally know a quite a number of RRMS patients whose lives have been dramatically improved by Tysabri, some so much so that they refuse to come off the drug even after developing a higher risk of contracting PML. I’m still not entirely comfortable with the idea of screwing with the workings of the human immune system for years on end, and it pisses me off immensely that medical science (or at least the pharmaceutical companies) seems content at treating the disease rather than curing it, but if I was a newly diagnosed RRMS patient with a low risk of developing PML (in other words, negative for JC virus antibodies), given all of the available data starting Tysabri would certainly high on my list of treatment options. That's honestly something I thought I'd never say six or seven years ago. There are currently trials ongoing testing Tysabri on progressive disease, and it will be very interesting to see how those turn out.

♦ There’ve recently been a spate of headlines to the effect that “HIV May Help Prevent Multiple Sclerosis” (click here). The basis for these headlines is a study that looked at MS rates among people infected with the HIV virus (the virus that causes AIDS), which found that HIV-infected people were far less likely to develop Multiple Sclerosis then the general population (click here). What could be behind these shocking findings? Well, it’s certainly possible that the HIV virus itself has some kind of anti-MS properties. It’s also possible that HIV, which can do serious damage to the human immune system, suppresses the aberrant immune cells that are thought to lead to the development of Multiple Sclerosis. More intriguing, though, is the possibility that the anti-retroviral drugs given to treat HIV patients, which have become extremely effective over the last decade, may be doing something to curtail the development of MS in HIV infected people.

About a year and a half ago I wrote about an emerging theory that ancient retroviruses which have become part of human DNA over millions of years of evolution may be behind a variety of illnesses, including cancer, schizophrenia, and, yes, so-called autoimmune diseases like Multiple Sclerosis (click here). These ancient viruses are in the same class of virus as HIV, called retroviruses. Long thought to be simply “junk DNA” and merely innocuous remnants of the ancient past, it’s recently been found that some of these viral bits, which are part of every human beings’ genetic structure, might be activated by the presence of certain environmental factors (other viruses, bacteria, or toxins), and thus cause all kinds of trouble. This hypothesis provides an elegant explanation of autoimmunity, in that, if correct, it would mean that under certain conditions our own cells might act as attackers, thus initiating a response by our body's own immune system.

Could it be that the powerful antiretroviral drugs being given to HIV patients are shutting down these ancient retroviruses (called Human Endogenous Retroviruses, or HERVs), and so are preventing the HIV-infected people on these drugs from developing Multiple Sclerosis? An intriguing possibility, and one which is currently being investigated by a group in London who are using some off-the-shelf HIV drugs to treat MS patients in a trial that is now underway (click here). Additionally, another related trial being conducted by a research group in Switzerland is testing a drug specifically designed to target an ancient retrovirus that has been linked by some scientists directly to Multiple Sclerosis. This group recently released the results of a small preliminary trial which tested the drug on progressive MS patients and showed it to be safely tolerated. Furthermore, the trial demonstrated some early indications that the drug may be effective in treating the disease (click here).

This is exciting stuff which could potentially change the way we view and treat many dread diseases in some very profound ways. My gut tells me that there is really something to this research, and I only wish more time, money, and effort was being devoted towards fully exploring this hypothesis and its many implications.

♦ Yet more research on viruses and MS: a recently released study using new testing methods found that the spinal fluid of Multiple Sclerosis patients is rich in antibodies targeted at Epstein-Barr Virus (EBV) and Human Herpes Virus-6 (HHV-6), rather than against human myelin and nervous system tissues, as might be expected if MS were truly an “autoimmune” disease (click here). Epstein-Barr Virus, and to a somewhat lesser extent HHV-6, have long been suspected in playing some role in the MS disease process. Fascinatingly, both of these viruses have been implicated in activating HERVs , the ancient retroviruses that I discussed in the previous item. Could it perhaps be that in genetically susceptible people, common infections such as EBV (which is carried by more than 90% of the population) can turn on DNA switches that lead the immune system to attack tissues of the central nervous system? In the decades before the autoimmune theory took hold, much of MS research was directed at finding the presumed infectious cause of the disease. Perhaps these now discounted theories were in fact on the right track, and strict adherence to autoimmune dogma over the last 20 years has led MS research astray. Again, clues like those divulged by this study demand that more attention be paid to this area of research.

♦ Here’s one that belongs in the MS version of Ripley’s Believe It or Not. The gold standard of medical research is the double-blind trial, in which one group of patients is given whatever treatment is under study and another is given a placebo (such as a sugar pill or saline solution), so that the responses between the two groups can be compared. In MS research, one of the most common measures by which an experimental drug’s efficacy is judged are annual relapse rates, the number of MS attacks experienced by relapsing remitting test subjects over the course of a year. Strangely, over the last two decades the annual relapse rates of patients in the placebo arms of late stage drug trials has dropped by half (click here). That’s right, since the 1990s the rate of relapses experienced by patients being given “fake” drugs has declined by 50%, while the rates of people getting MS worldwide have gone up (click here). And no one knows why. Isn’t that reassuring?

♦ Some more reassuring news: I came across a list of the 15 most misdiagnosed diseases (click here), and wouldn’t you know it, our good friend and close confidant Multiple Sclerosis is right up there. Given the many mysteries surrounding MS and the fact that there is no diagnostic test that definitively determines whether or not a patient does indeed have MS, this really shouldn’t come as much of a surprise. Truth is, most experts peg the misdiagnosis rate of MS at somewhere between 5%-15%, meaning that perhaps 1 out of 10 of the MS patients reading this don’t actually have the disease. There are literally dozens if not hundreds of diseases and conditions which can mimic MS. Here’s an academic paper on the subject, which lists at its end 100 illnesses that can be mistaken for MS (click here). It’s easy to drive yourself crazy with such information, so be careful, but if you suspect you may have been misdiagnosed, there’s a reasonable chance that you could be right.

♦ The relationship between diet and MS has become a very hot topic of late. Through the years, many different diets have been said to be “anti-MS”, most often low-fat or low-carb diets rich in anti-inflammatory and antioxidant foods. In fact, I’m currently trying the Paleo diet, a way of eating that is supposed to resemble the dietary habits of our ancient ancestors. The theory is that the function of our digestive systems evolved over the millions of years that our forebears were hunter gatherers, and that much of what we’ve taken to eating since the discovery of agriculture some 10,000 years ago is actually bad for our health. The Paleo diet cuts out all sugar, dairy, wheat, and some of the most common cultivated crops. This means that people on the diet can’t eat bread, milk, cheese, rice, potatoes, corn, or many of the other staples of the modern menu.

Given the fact that I’m giving Paleo a try, my interest was quite peaked by this article (click here), which details the results of a study that followed dietary habits of 185,000 women over 20 years and found that diet seems to have absolutely no impact whatsoever on whether or not they developed Multiple Sclerosis. In fact, the numbers appeared to show that those eating what is considered to be an unhealthy Western diet developed MS in lesser numbers, although this trend did not reach statistical significance.

Now, I know there are many patients who swear that a radical change in diet has noticeably lessened the impact of their disease and some have gone as far as to claim that diet can even cure MS, and I’m certain that most of these claims are made in all earnestness. I'm not saying that this study is the last word on the subject, but it should provide food for thought (pun intended). At the very least a healthy diet is, well, healthy, and that can only be a good thing especially for people suffering from chronic illness. And for those who are wondering how I’m doing after more than two months on the Paleo diet, I’m sorry to report that I’m feeling pretty crappy, worse, I think, than before starting the diet. I have dropped a few pounds, which is definitely good since I was beginning to resemble a walrus (sitting in a wheelchair does nothing for the physique), but given my lack of results otherwise I believe my time eating like a caveman may be drawing to a close. I’m thinking that the next diet I try might be one of my own invention, which I dub the “Nothing But Philly Cheesesteaks Diet”. Probably not very healthy but… Yum.

♦ Okay, time for yet another edition of ASININE RESEARCH! Once again, I present another in apparently endless stream of studies that that delve into the ever enigmatic conundrum that is the relationship between multiple sclerosis, difficulty walking, and falling down. This topic really seems to float the boats of top-notch medical researchers who apparently can’t get enough of publishing papers probing the seemingly unfathomable relationship between a crippling disease and its patently obvious effects on ambulation.

Today’s asinine research paper is tantalizingly titled “Concern about Falling Is Associated with Step Length in Persons with Multiple Sclerosis” (click here). The abstract starts out with this sentence: “Fear of falling is one of the major concerns of people with multiple sclerosis.” Yes, yes, a dazzling observation! And fear of ruining ones undergarments is one of the major concerns of people suffering from explosive diarrhea. From this auspicious start, the paper goes on to detail research looking at how concern about falling alters the way MS patients walk. While investigators suffering from severe oxygen deprivation might assume that MS patients stride like Rockettes and strut about with all of the bravura of a young Mike Tyson, after much mumbo-jumbo about “spatio-temporal parameters of gait” and “gait asymmetry patterns” this study instead shockingly finds that multiple sclerosis patients tend to walk slower and take smaller steps than their healthy counterparts, and that this astounding effect is greater in those with a higher fear of falling. The study concludes by postulating that measuring step length might be a good tool for assessing the level of fear of falling in people with MS. I suppose assessing the level of terror on their faces is just too bothersome.

Did it ever occur to the researchers that MS patients walked slower and took smaller steps as a result of the disease, and that this might in fact be the reason behind their fear of falling and not the other way around? I certainly don’t remember having a healthy fear of falling before, you know, the disease took a hammer to the connection between my brain and my legs and left me no choice other than to walk slower and take smaller steps. In fact, these days if my steps get any smaller or my walking gets any slower my attempts at ambulation might better be termed "standing still". Yes, this all makes for a frightening experience, but it's not the fear that keeps my legs from moving, it's some little-known phenomena called "weakness" and "paralysis". Sheesh.

♦ It’s become my custom over the past several Bits and Pieces posts to end with some music from the “Neo-Soul/Retro-Soul” movement. Words can’t express how smitten I am with much of this music, which never fails to put some funk in my junk, some glide in my stride, some pep in my step, and some growl in my prowl. Hey, wait a minute, as mentioned above these days I can barely manage a stride, step, or prowl, so I’ll have to amend that – this funky stuff puts some chimp in my limp, some jumble in my stumble, and some gall in my fall. Can I get an Amen? Hallelujah!

The following ditty is by St. Paul and the Broken Bones, a band I was lucky enough to see at a free concert outside of Lincoln Center a few months ago. I went to the show primarily to see Charles Bradley, who I featured in a previous Bits and Pieces, but I was unexpectedly blown away by these guys, who I’d never heard of before they took the stage. As I mentioned earlier, this summer wasn’t a particularly terrific one in my book, but this show was definitely a highlight…

Bits and Pieces: Arctic Vortex Edition

Okay, I know it’s considered terribly mundane and just downright boring to talk about the weather, but the winter here in NYC and in much of the Midwest and Eastern US has really been something else these last few months. Since weather reports here in The States only occasionally and very briefly touch on conditions outside of our borders, I’m only parenthetically aware that much of the rest of the world has also experienced extreme conditions this winter as well, but I do know that plenty of WK readers all around the world have been hit with some downright nasty tricks from mother nature this season.

Here in NYC, we’ve been subjected twice (so far) to a meteorological horror called the Polar Vortex, a huge mass of frigid air that descends from the North Pole, bringing with it plunging temperatures and loads of snow. In my previous 49 winters I don’t recall ever hearing anything about a Polar Vortex, though I do remember plenty of times freezing my ass off, so perhaps this is just a new name for an old song. Whatever the case, getting around in a wheelchair in temperatures fit for the Arctic can be brutal. Not that walking around when the wind chill hits instant frostbite territory is any great shakes, but at least the very act of walking generates body heat. Sitting in a wheelchair does no such thing, and the breeze added by zipping around at 7 or 8 mph only adds to the freeze.

Fortunately, I’ve got some very good cold-weather gear. Never mind high-tech fleece and modern materials like Thinsulate, my warmest piece of kit is an exact replica of the shearling jackets worn by US airmen fighting high in the skies above Europe during World War II. Back then the interiors of military aircraft were unheated, and at 20,000 feet the temperatures were routinely well below 0°F. My B-6 flight jacket is so warm that I can’t wear it in temperatures much above 25°F, and even when the temperatures hit the single digits a T-shirt and a thin wool sweater worn under the jacket are more than enough to keep me toasty. I also have a replica of the shearling hat worn by World War II flight crews, so decked out in my vintage military gear I can zip around the frozen city making believe my wheelchair is a P-51 Mustang fighter plane engaged in fierce dogfights with the mighty Luftwaffe (represented by oblivious pedestrians staring at their cell phone screens despite the freezy conditions) on the streets of New York. I’m proud to say this winter I’ve achieved the lofty status of “ace”, having bagged far more than the requisite five kills. Mwah hah hah.

Unfortunately, donning the flight jacket requires wrestling with my arch nemesis, the zipper. The freaking things are almost impossible to use when you’re down to only one marginally good hand, so I have to allot myself an extra 10 or 15 minutes of prep time just to get my goddamned coat on. Have I ever mentioned that having MS sucks? (I’ll be presenting some exciting zipper related news later in this post, I hope you can bear the suspense.) Luckily, for temperatures just a bit below freezing I have a very special pea coat that my mother-in-law, who is quite the whiz with a sewing machine, made into a Velcro fastened wonder. She removed the buttons and then sewed them on top of the coat’s now sealed buttonholes, affixing Velcro fasteners to the garment where the buttons would normally hold the coat closed. The black Velcro patches exactly match the color of the coat, making them almost invisible, and when I put it on the coat practically “buttons” itself. The buttons sewed over the buttonholes give the illusion that the coat is fastened in the customary fashion, giving no hint of the Velcro customization within. I made sure to get a military issue pea coat, so the thing is quite warm and sharp looking to boot. I’m pretty sure I have the only Velcro fastened pea coat in existence, and I’m positively tickled with my piece of unique outerwear. It’s like haute couture for gimps.

So, between my World War II flight jacket and my MS friendly Navy pea coat, I’ve got the problem of winter wheelchair attire practically licked. I’m sure this comes as a great relief to all of you, so rest easy, the Wheelchair Kamikaze will not be found frozen stiff in his chair on the thoroughfares of New York anytime soon. And the Luftwaffe will not be menacing the sidewalks of NYC, at least not on my watch. After all, terrorizing the streets of New York is my job.

But enough about me, there’s been a lot of interesting MS and disability related news lately, so forthwith comes my semi regular compendium of noteworthy tidbits… Onward, doggies, mush mush…

♦ There’s no denying that in addition to being a horrible disease, multiple sclerosis is also a burgeoning multibillion-dollar a year industry, with many of the drugs developed to combat the disease attaining “blockbuster” status. Ever wonder just how much money MS drugs bring in? Well, wonder no more, because here’s a list of the top 10 selling MS drugs of 2013, along with the cash flow generated by each (in American dollars):

#1: Copaxone-$4.3 billion

#2: Avonex-$3.0 billion

#3: Gilenya-$1.9 billion

#4: Tysabri-$1.7 billion

#5: Betaseron-$1.1 billion

#6: Tecfidera-$876 million

#7: Rebif-$622 million

#8: Ampyra-$302 million

#9: Aubagio-$226 million

#10: Extavia-$159 million

Add up all of that mazuma, and the top 10 selling MS drugs generated sales of roughly $14,000,000,000 last year. Yup, that’s a lot of zeros. Keep in mind, the sales of Tecfidera only represent about one quarter of the year, since the drug was first approved midyear and didn’t reach patients in large quantity until the fall of 2013. Additionally, Tecfidera was only recently approved for use in Europe (click here), so expect sales of the drug in 2014 to approach at least four or five billion dollars. Factor in all of the money made by MS neurologists, MRI facilities, infusion suites, medical laboratories and other MS related services and facilities,  and it's easy to see that multiple sclerosis has become quite the cash cow. I don't know about you, but the idea of "disease as industry" makes me a little bit queasy. For more info on each of the above drugs (click here).

♦ Speaking of blockbuster MS drugs, the Israeli pharmaceutical company Teva has received FDA approval for a higher dose Copaxone regimen requiring injections only three times a week (click here), as opposed to the daily injections patients currently on Copaxone must undergo. Copaxone was among the first of the disease modifying therapies to be marketed for MS, and was first approved in 1996. Since then, the drug has been shown in several studies to effectively reduce relapse rates and enhancing lesions for those RRMS patients on whom it is effective by about 35%. Recent open label studies looking at the long-term effects of the drug indicate that Copaxone may also positively impact the rate of disease progression (click here).

One may wonder why it took Teva 18 years to seek approval for a thrice a week version of the drug, since the new dosing schedule is obviously much more appealing than the old daily injection regimen. Maybe I’m a jaded cynic, but the fact that several companies are preparing to introduce generic Copaxone on the market might just have a little something to do with it. All of the generic versions of Copaxone are undergoing trials as once daily injections, so by getting approval of the three injections a week dosing regimen, Teva has made good old-fashioned brand-name Copaxone a much more appealing option from the patient perspective. Additionally, the success of Tecfidera, an oral medication, may also have played a role in Teva seeking a way to make the administration of Copaxone a less painful proposition. As was illustrated in the above list of top grossing MS drugs, Teva has about four billion reasons to try to protect their Copaxone franchise. In any event, this is good news for patients who have had success with Copaxone, who will now be required to give themselves 60% fewer injections. Of course, if there are any Copaxone patients out there who are masochists, this could be bad news, but hey, you can't please everybody…

♦ As I reported in my last Bits and Pieces post (click here), the powerful experimental MS drug Lemtrada was recently denied approval in the US by the FDA. The drug has been approved in most of the rest of the world, including, most recently, Mexico (click here). This action by the FDA has raised the ire of US MS patients, researchers, and clinicians alike (click here and here).

The FDA claims that it did not approve Lemtrada because the trials undertaken to prove the drug’s efficacy were poorly designed, but the FDA had previously approved the design of those very same trials. Lemtrada is a very controversial drug, as it carries a very high risk/reward profile. In trials undertaken by the drug’s manufacturer, Genzyme, as many as 50% of patients with highly active RRMS given Lemtrada were shown to have no evidence of disease activity (no relapses or new lesions) five years after they received their last dose of the drug. This is a startling success rate, but it comes at a price, as up to 30% of Lemtrada treated patients develop autoimmune thyroid diseases, and some develop a potentially fatal autoimmune blood disorder. It’s important to note that autoimmune thyroid disease is easily treated using hormone supplements, and the risk of the autoimmune blood disorder can be at least in part alleviated through careful monitoring.

Lemtrada is a powerful immunosuppressive agent which works by essentially rebooting a patient’s immune system. For patients with highly aggressive relapsing remitting disease, suffering some of the worst ravages of MS, the potential benefits of the drug could very well outweigh the known risks. I personally spoke to an MS neurologist who has my utmost respect about the FDA’s decision, and he was extremely dismayed by the agency’s actions, telling me of one patient who was being laid to waste by one of the most aggressive forms of relapsing MS. Not only did the drug stop the disease in its tracks, but the formerly MS ravaged patient recovered enough to actually be able to go back to work. Given this level of potential benefit, shouldn’t the decision as to whether or not to use Lemtrada be left in the hands of neurologists and the patients they treat? Seems the rest of the world thinks so, but not the FDA. Nope.

♦ In a disconcerting piece of MS news, a recent study has found that MS does indeed negatively affect life expectancy in the patients it strikes (click here). Researchers used insurance claims to identify a group of over 30,000 MS patients, and compared them to about 90,000 non-MS patients, finding that the MS patient population lived on an average six years less than their non-MS counterparts. The results of this study mirrored those done in some other parts of the world, but this was the first time such data was examined for MS patients in the United States. It’s important to note that this study looked at patient data from 1996-2009, and thus doesn’t include patients taking some of the newer, more powerful MS drugs. One can only hope that these drugs will positively affect MS patient longevity, and that future treatments will have an even greater significant positive impact. One can also hope that researchers concentrating on areas other than immunosuppression will come up with drastically more effective treatments that – gasp – actually address the root cause of the disease. Fingers crossed.

♦ In some better news, researchers in Australia have had initial success treating a patient with secondary progressive MS by increasing his immune response to Epstein-Barr virus (click here). EBV has long been suspected to play a role in the MS disease process, and this is the first research to directly target the virus in an attempt to alleviate multiple sclerosis. The research involved isolating a specific type of immune system cells, called “killer T cells”, from the patient’s blood, adding an experimental anti-EBV vaccine to them, and then growing more of them in the laboratory. The cells were then injected back into the patient over the course of eight weeks. The patient reported less fatigue, fewer leg spasms, better cognition, and improved use of his limbs. Of course, this was only one patient, and this research is in its very earliest stages. But hey, hope springs eternal…

♦ More news on the “infectious” front. Researchers following up on the discovery of a rare foodborne bacteria in an MS patient (click here) have infected rodents with that same bacteria, and found that the little varmints developed a disease very much like MS (click here). It’s long been suspected that infectious agents play some role in the MS disease process, a belief based on a convincing body of evidence. In fact, before attention shifted to the “autoimmune hypothesis” and pharmaceutical companies started making billions of dollars by producing drugs that tinker with the MS immune system, much if not most MS research was directed at finding the presumed infectious cause of MS. This area of research has been widely neglected for the past couple of decades, though, but interest in it seems to be picking up. From a patient perspective, this is a very good thing, for if one or more infectious cause or causes of MS can be positively identified we would finally be making great strides towards curing the disease. So, let’s pick up our MS research cheerleader pom-poms and shout in unison: “Frika Fraka, Firecracker, Shish Boom Bah, Infectious Agents, Infectious Agents, Rah Rah Rah!” Unfortunately, because of my debilitated physical state, I’m only able to pick up one of my MS research cheerleader pom-poms, but I expect the rest of you who are more able-bodied to do some vigorous two-fisted cheering.

♦ Although the above rhyme is about as poetic as I get, another member of the MS blogger community, Judith Mercado, is a far more accomplished poet, and has now published a book of her inspired work. Author of the blog “Peace Be with You” (click here), Judith writes her poetry in the ancient Japanese form of haiku, and I’ve long been a fan of her work. I was greatly honored when Judy asked me to provide a blurb for the back cover of her upcoming book, Peace on the Journey, and was of course happy to do so. If I may take the liberty of quoting myself, Judy’s “words resonate with wisdom and truth, and grace the reader with intimacy, honesty, and understanding.” While Judith’s blog often references her MS, the poems in Peace on the Journey are meant for a more general audience, anybody who travels on the sometimes gentle but all too often tumultuous path of life. Peace on the Journey is available in paperback and electronic Kindle version on Amazon (click here). Highly recommended.

♦ As promised, here is the earth shattering zipper news I promised the opening paragraphs of this post. An inventor seeking to help his physically challenged uncle has come up with “Possibly the Most Radical Innovation to Zippers in over a Century” (click here). Eventually joined by his mom and a mechanical engineer neighbor, inventor Scott Peters spent six years and went through over 100 prototypes before coming up with the Quickzip, a magnetically assisted zipper that only requires one hand to fasten. Be still my heart! The team of the inventors struck a deal with athletic clothing manufacturer Under Armour, which plans to start marketing Quickzip (now renamed Magzip) equipped clothing in the fall of 2014. I’m not one to encourage patent infringement, but I call on clothing manufacturers worldwide to meet this challenge and come up with their own easy fastening zipper innovations. Must I pick up my cheerleader pom-pom once again?

Here’s a rather, um, dramatic video produced by Under Armour highlighting the new technology…


RIP Heidi Sherman

Can Anti-HIV Drugs Stop MS?

Animation of the structure of a section of DNA. The bases lie horizontally between the two spiraling strands. (Photo credit: Wikipedia)

(Readers who receive these posts via email are advised that this essay contains a video, which cannot be viewed in the email version. Please go to the Wheelchair Kamikaze website (click here) to view the video…)

I imagine the above headline might have furrowed a few eyebrows and crinkled some foreheads when first viewed by readers. HIV (the virus that causes AIDS) has nothing to do with MS, does it? Has Marc finally lost his last marble? Don’t MS patients have enough to worry about without having to contemplate AIDS?

Yes, MS patients certainly do have enough to worry about, and no, the virus that causes AIDS has nothing to do with multiple sclerosis. HIV, though, is a retrovirus, and, strange as it might sound, there is increasing evidence that ancient retroviruses that have become incorporated into the human genome through millions of years of evolution may play a key role in the MS disease process. This might seem like something out of a science fiction novel, but this discovery of prehistoric viral material in human DNA has the potential to completely change the way we understand and treat MS and other diseases (including cancer), and could potentially lead to – dare I say it – a cure.

There are currently two clinical trials underway attempting to shut down these ancient retroviruses in MS patients, and one of them uses a currently available anti-HIV drug. More on these trials a bit later, but first a little background, starting with a quick overview of virology. I know the mere prospect of “a quick overview of virology” is apt to make eyes glaze over throughout the Internet, but please bear with me, I’ll try to keep it as painless as possible.

We’re all familiar with viruses, the little buggers that cause influenza, the common cold, and a many other diseases. Of course, bacteria also cause diseases, but viruses and bacteria, though both infectious agents, are very different beasties. Bacteria are living organisms, and when someone suffers a bacterial infection they can usually be treated with antibiotics, drugs which kill the guilty bacteria and thereby cure the patient. Antibiotics have no effect on viruses, though, because viruses aren’t alive, and therefore can’t be killed. Viruses are kind of like the zombies of the pathogen world, undead infectious agents that exist only to infect living things. The fact that viruses are “undead” is what makes viral diseases so hard to treat, and why we still don’t have a cure for the common cold.

Unlike living bacteria, which can reproduce all on their own, undead viruses replicate by hijacking their victims’ cells and then using the resources within those cells to reproduce themselves. Most viruses kill the cells they invade by replicating to the point where the infected cells burst, releasing the reproduced viruses and thus spreading viral infection throughout the body. Another type of virus, though, called a retrovirus, actually inserts itself into the host cell’s DNA, and in effect become part of the organism they have infected, commandeering the host’s genetic material and cellular mechanisms to replicate themselves without destroying the cells they have invaded. This makes retroviral diseases (such as AIDS) extremely hard to treat, and coming up with ways to neutralize retroviruses has presented medical science with one of its most daunting challenges.

Now, here comes the really strange part. When the Human Genome Project (click here) completed the incredibly complex task of mapping all of the genes contained in human DNA, it was discovered that 8% of our genetic material is comprised of the remnants of ancient retroviruses, many of which inserted themselves into our genetic material tens of millions of years ago during the evolutionary process, before humans were even human. These retroviruses were at one time in the distant past infectious, but have long since been rendered dormant, and it was initially thought that they were nothing more than “junk DNA”, left over genetic material that plays no role whatsoever in the development or functioning of a human being. These ancient retroviruses that are now part of the human genome were named Human Endogenous Retroviruses, or HERVs. They are a part of all of us, genetic remnants of our evolutionary history.

Recent research into HERVs has provided tantalizing clues that rather than always remaining dormant, in certain circumstances these ancient viruses can be activated and may play a key role in many diseases, including multiple sclerosis, many autoimmune diseases, some cancers, and even schizophrenia (click here, here, here and here). The mechanism by which HERVs are activated are not fully understood, but the prevailing thought is that the presence of other viruses and environmental agents, such as Epstein-Barr virus (click here), the human herpesviruses (click here), and other environmental triggers, or a combination of these elements, may “wake” these bits of ancient viruses that are part of our DNA. Once activated, this ancient retroviral DNA can cause our own cells to secrete proteins and antigens that may identify the host cell as a hostile invader, or otherwise initiate critical disease processes.

Within the last five years or so, it’s been established that virtually every MS patient is infected with Epstein-Barr virus (click here), which is best known for causing mononucleosis/glandular fever. I know, many of you are saying, “but I never had mononucleosis or glandular fever, so I don’t have EBV!” The fact is that in the majority of cases infection with Epstein-Barr virus does not result in Mono, but rather can present as a bad cold or flu, or can even be completely asymptomatic. Over 90% of the general population is infected with EBV, but, remarkably, it appears that 100% of MS patients carry the bug. MS researchers have long puzzled over the role EBV might play in the MS disease process, since EBV infection alone certainly can’t be the sole cause of MS, otherwise far more people would have multiple sclerosis. The link between EBV and HERVs could finally clear up this mystery, for if a long-term EBV infection can turn on ancient retroviruses embedded in the DNA of genetically susceptible people, the connection between EBV and MS might finally be understood (click here).

Though the connection between HERVs and MS has yet to be proven, more and more evidence appears to be pointing in that direction (click here), and the hypothesis does pull together some of the “wildcard” factors that have confounded MS researchers for decades. Among these factors are indicators that there is an infectious component to MS, such as the existence of “MS clusters”, geographic locations where MS appears to run rampant among the local population (click here), and migratory studies which show that migration from areas of high MS to areas of low MS before the age of 15 decreases the risk of getting multiple sclerosis, with the reverse being true as well (click here). Through the years many possible infectious candidates have been proposed, to no avail, but if the HERVs theory is correct, it’s a combination of infectious agents, including some hiding in a patient’s own DNA, that may be responsible.

Both EBV (which is itself a human herpesvirus) and retroviruses have proven to be extremely difficult to eradicate, as can be illustrated by the fight against HIV. HIV is a retrovirus, and although medical science has made great strides in developing drugs that keep HIV infection under control (deaths from AIDS have plummeted in the last decade), there is still no way to completely eradicate the virus from the body of an infected person. One anti-HIV drug, Raltegravir (brand name Isentress) (click here) has proven to be quite effective in combating HIV, though, and also shows promise as an anti-EBV weapon.

A clinical trial now underway at Queen Mary University in London, England, called be INSPIRE trial (click here), is attempting to use Raltegravir to treat MS patients. Researchers hope that the drug will deactivate any activated retroviral material in the DNA of MS patients, while perhaps also combating EBV, and thus stop multiple sclerosis in its tracks. Another group of researchers in Switzerland are trying to accomplish the same outcome using an experimental drug that targets a protein on a specific HERV that is thought to be directly connected with MS, which has been dubbed the Multiple Sclerosis Associated Retrovirus, or MSRV (click here). This is a small, 10 person Phase 2 trial whose primary goal is to establish the safety of the experimental drug being tested. Results from the INSPIRE trial, which is just getting underway, are not expected until August, 2014, and the results from the Swiss trial are expected in July of this year.

It’s impossible to overstate the potential that this research has to completely reshape the multiple sclerosis landscape, with vast implications impacting the quest to wipe out many other horrendous diseases as well. If indeed prehistoric viruses embedded within our own DNA are at work driving the MS disease process, shutting down these viruses could amount to a cure. Yes, a cure for multiple sclerosis! Though it may be hard to believe, there is precious little work being done elsewhere to uncover the roots of MS, as so much research time and money is devoted towards finding newer and more effective (and more profitable) ways to suppress the aberrant immune response that is seen in the disease, a response that is in fact a symptom of some as yet unknown underlying cause. All of the current crop of MS drugs, and the vast majority of those in the experimental pipeline, either modulate or suppress the immune system, a mechanism of action which can sometimes dramatically improve the quality of life of RRMS patients, but will never do anything to cure multiple sclerosis. The research going on in London and Switzerland at last holds out hope for a cure, and represent a radical rethinking of the cause of many of the diseases that plague mankind.

My intuition and instincts tell me that these research scientists are onto something, and it’s something potentially huge. It’s long been known that genetics play a role in MS, and it has also long been suspected that infectious agents are at work. The idea that Human Endogenous Retroviruses, bits of viruses that are in a very real way a part of us, encoded into our DNA, could play a key role in the MS disease process ties together both of these observations, as well as several others. The evidence to support this idea is mounting, and to me this hypothesis feels right in a way that no other MS related theory I’ve come across has before. Of course, you can (and probably should) take my “gut feelings” with a grain of salt, but I find myself brimming with enthusiasm that the science of treating MS is finally moving in the right direction. Of course, as I’ve often cautioned before, it’s vital not to let hope eclipse reason, and this research might well lead to nothing. But, somehow, I just don’t think that it will…

Here’s a terrific video presentation by one of the lead researchers involved in the INSPIRE trial, which does a great job of explaining the research and the ideas behind it in a very accessible, easy to understand manner. I urge all readers to watch this video, as the information it contains has tremendous potential…

More CCSVI Info

The momentum behind the Chronic Cerebrospinal Venous Insufficiency (CCSVI) theory of MS really seems to be picking up steam. Though not yet covered extensively in the American press, in Europe and Canada print and television journalists have eagerly picked up on the topic.

I'll continue to post intelligent links to CCSVI info as I come across them, and as more studies get started, I'm hopeful that the theory will move into the realm of fact. As of now, I will remain optimistic but skeptical. I've seen many other MS "miracles" turn into faerie dust, but my gut tells me that there really is something to CCSVI.

Here's a link to a news piece on CCSVI from CBC radio, in Canada. It's an interview with Dr. Samuel Ludwin, a professor of neuropathology at Queen's University who's been researching Multiple Sclerosis for over 30 years. Though cautious, he does express enthusiasm for the radical new idea that MS may in fact have a heavy vascular component.

One of the problems I've had in fully embracing CCSVI is the fact that it doesn't account for the almost certain association of the Epstein-Barr virus (EBV) with MS. Numerous studies have shown that people who are not infected with EBV do not get MS. Here's a letter to the editor of the Journal of Neurology, Neurosurgery and Psychiatry that postulates a convincing link between EBV and CCSVI.

We may be witnessing a shifting in the paradigm of the understanding of Multiple Sclerosis...