Article: Straight Talk From Dr. Montoya: the Stanford Hospital CFS Lecture

You can view the page at http://forums.aboutmecfs.org/content.php?381-Straight-Talk-From-Dr-Montoya-Stanford-Hospital-CFS-Herpesvirus-Lecture

 

Another stunning article Cort (still reading) sans blah, blah, blah - as it is !. Can you share him with the UK please. He has that unique capacity to assimilate all research findings and study/listen to patients. In case we need to remind anyone else - this is DISEASE.

 

This whole talk is worth watching if for no other reason than to hear a doctor speak so clearly and compassionately about people with CFS.

 

Another stunning article Cort (still reading) sans blah, blah, blah - as it is !. Can you share him with the UK please.

I wish we had a few more of him - passionate, articulate, smart and committed to ME/CFS - to pass around!

I imagine he is very convincing in person as well - which bodes good for the success of his program.

 

This whole talk is worth watching if for no other reason than to hear a doctor speak so clearly and compassionately about people with CFS.

Yes, he started off a little shakey and then picked up steam from then on. By the end he was in his element... I was very impressed by him.

 

Cort this is a disease process - millions in the States, millions world wide, collecting so much nastiness around it as to shake even those who are severely affected (if they could) . Montoya tells us what it is - and not in the imagined world of lesser people who resist what is in front of their eyes.

 

Great article and a great doctor. Like him I am convinced the immune system is causing most of our problems. I think these are the options:

a) the immune system is trying to fight off XMRV, but as a retrovirus it's very difficult to knock out, causing constant symptoms (resembling an autoimmune disorder).
b) XMRV has knocked out parts of our immune system, giving other infections the chance to spread. This requires continuous action from the immune system, causing constant symptoms.

It might even be a combination of both options, I guess.

So does anyone have any experience with immunosupressants, like Prednisone? Because of the immune connection, I am getting more and more interested in such drugs. There's a risk of course, because the immune system might barely be holding on... further supressing it might not be the best of ideas.

 

Great article and a great doctor. Like him I am convinced the immune system is causing most of our problems. I think these are the options:

a) the immune system is trying to fight off XMRV, but as a retrovirus it's very difficult to knock out, causing constant symptoms (resembling an autoimmune disorder).
b) XMRV has knocked out parts of our immune system, giving other infections the chance to spread. This requires continuous action from the immune system, causing constant symptoms.

It might even be a combination of both options, I guess.

So does anyone have any experience with immunosupressants, like Prednisone? Because of the immune connection, I am getting more and more interested in such drugs. There's a risk of course, because the immune system might barely be holding on... further supressing it might not be the best of ideas.

I think one problem is that one part of the immune system may be over-activated and another under-activated? Maybe this is why we really don't hear much about auto-immune (immune suppressant) drugs in CFS (?).

Right...if the bugs are being kept in check by the immune system then knocking it down could allow them to proliferate. Maybe that's why they are more focused on immune modulators - I think that's what Ampligen is.....(and Nexavir???? GCMaF???)

 

Yeah, I guess immune modulators might be a better direction to research. Still, if a virus like XMRV is the puppet master, we are mostly fighting symptoms and not the cause (unfortunately this seems to be the norm in our healthcare systems), as even a stimulated immune system will probably not knockout a retrovirus.

I want a breakthrough in research, so badly...

By the way, wasn't there some kind of gene that made sure that the immune response lessened during chronic infections it couldn't control (like HIV)? Why is that gene not kicking in, maybe because of all the different infections?

 

Ah yes, I found the article.

It was SOCS-3 that was putting the breaks on the immune system in cases of chronic infection and preventing the body from potentially attacking itself.

http://www.lifescientist.com.au/article/375419/immune_system_boosting_hormone_might_lead_hiv_cure/

That article even gives some hope that the immune system could be boosted enough to knockout a retrovirus like HIV.

 

I only watched the first two thirds, but I felt like he was rather over-hyping the improvements drug treatments brought to patients. They looked pretty trivial to me. That's not to say it won't lead on to something, but I'm not that interested in getting on them myself right now.

Cort mentioned it picking up as it went on, so maybe I should have stuck it out to the end, but considering the positive reception some patients were giving this talk, it didn't seem that great to me. Maybe my expecations were too high.

 

I only watched the first two thirds, but I felt like he was rather over-hyping the improvements drug treatments brought to patients. They looked pretty trivial to me. That's not to say it won't lead on to something, but I'm not that interested in getting on them myself right now.

Cort mentioned it picking up as it went on, so maybe I should have stuck it out to the end, but considering the positive reception some patients were giving this talk, it didn't seem that great to me. Maybe my expecations were too high.

It'll be interesting to read the study when it comes out. I agree that the improvements did not appear that signficant - my guess is in that group some people did very well - as in that one women he talked about - and others did not and they evened out.

I think this is a very complex field and I imagine that getting dosage right and accounting for other factor will be important and even after years on the job there is still much to learn.

I wonder if the fact that they have to take these drugs for so long to have an effect really does mean that these drugs really are not that good. The drugs work apparently work quickly and well, from what I hear, in acute herpesvirus infections in other disorders but they take a long time and are not as effective in the type of infections he finds in CFS.

This trial is important, though, because it was very rigorously done and it had patients with high antibody titers. It'll be interesting to compare if doses or other factors are different i nthe Montoya study and the Lerner studies - which seemed to have more positive effects but which were not nearly as rigorous statistically.

 

Very nice talk, thanks for posting. We need about 500 more Dr. Montoya's looks at various aspects of CFS.

Since his focus is on viruses, I wonder if he thinks bacterial infections could play the same role for another subgroup. It sounds like he may, although I'm not sure he ever made it clear that he suspects bacteria can be the infection "ringleader" like the herpes virures. The problem is that antibiotics have typically met with fairly limited success even for patients that clearly have chronic infections such as lyme and mycoplasma.

I am also trying to understand his merging theories that CFS is "autoimmune" but also his focusing only on irradicating infections. I guess it is the interaction between the two (infection + autoimmune response = illness) and since we do not understand the immune system, we chase infections. I wonder how far that will get his research or if he will be able to work with immune specialists. My impression is that immunology doesn't have many answers for most chronic illnesses.

 

He undoubtedly turned heads as he said had a dream that the medical community will someday produce a formal apology to the patients for not believing them all these years that they were facing a real illness.

I loved that comment. I think I fell in love with Dr Montoya just a little bit for saying it. Maybe it could be filed under "ain't never gonna happen," but it's lovely to dream about anyway.

Dr Montoya is clearly compassionate. He didn't just reiterate the standard list of symptoms, but tried to convey what it's like. You get the impression he must really listen to the patients and trusts what they tell him.

I wish we could get him to give grand rounds on ME/CFS to doctors all over the country. I wish we could produce a CME training video for doctors with Dr Montoya and others like him teaching other doctors how to diagnose it.

 

Cort, Thanks for the write up of Montoya's talk. He is a very compassionate person who saw what he saw and it was not in his character to turn his back on the truth or patients in need.

He gets a lot of attention from CFS patients but this is not the only area in which he specializes. He's also Director, National Reference Laboratory for the Study and Diagnosis of Toxoplasmosis and he works closely with the Stanford Oncology Department on "Immunocompromised Host and Transplantation Medicine" (he has more CFS papers on the way but right now out of 54 publications, 19 are on toxo and one is on CFS).

As for the effect size, I think he made it clear that with "Infection-Associated Chronic Fatigue Syndrome" he sees subgroups. A significant percentage within these groups have a large response when on the right treatments (eg. HHV-6 / EBV patients on Valcyte - valganciclovir). Others patients don't respond or don't respond as dramatically. He's trying to figure out why the different responses. Even within just one subgroup there are a lot of variables; dose, schedule (once a day or four times a day?), do you pulse a medication?, how long does it take to see an effect. What about the effect of/approach to treating different combinations of co-infections. Which do you treat first? Do you pick one? Can a patient handle treating all co-infections simultaneously? All of these are still huge questions.

It has never been my impression that even when treatment is "successful" that Montoya sees "it" (anti-virals, antibiotics, immune support agents, etc.) as a cure. There is something going on that is allowing infectious agents that are widespread and typically controlled in the rest of the population to get out of control in CFS patients (or there is an abnormal immune response). It is my impression that patients testing negative for co-infections are very rare (if not non-existent) in his practice. That said, Montoya is looking very hard and in ways most physicians don't. My PCP said that he couldn't even begin to understand all of the tests that Montoya runs on a routine basis.

He undoubtedly turned heads as he said had a dream that the medical community will someday ‘produce a formal apology to the patients for not believing them all these years that they were facing a real illness’.

He's one of a very few that can hold his head high.

 

Very nice talk, thanks for posting. We need about 500 more Dr. Montoya's looks at various aspects of CFS.

Since his focus is on viruses, I wonder if he thinks bacterial infections could play the same role for another subgroup. It sounds like he may, although I'm not sure he ever made it clear that he suspects bacteria can be the infection "ringleader" like the herpes virures. The problem is that antibiotics have typically met with fairly limited success even for patients that clearly have chronic infections such as lyme and mycoplasma.

I am also trying to understand his merging theories that CFS is "autoimmune" but also his focusing only on irradicating infections. I guess it is the interaction between the two (infection + autoimmune response = illness) and since we do not understand the immune system, we chase infections. I wonder how far that will get his research or if he will be able to work with immune specialists. My impression is that immunology doesn't have many answers for most chronic illnesses.

I looked up EBV and auto-immune issues and there's actually quite a bit of research on that. The CAA last year tried to get two grants funded on auto-immune issues; what I thought was interesting about that was the number of new (to CFS) research groups which participated - which suggests that the subject is arousing interest.

I thought it was interesting he found herpes simplex in a significant proportion of patients since I've never heard of that before.

 

The Montoya-Lipkin study is going to be fascinating! What is so exciting about that is that it's LIPKIN and if he puts his name on a paper and finds viruses my guess is that people are going to say "OK! They are there!" (Of course, if he says they are not there - then you have the OTHER problem ). Researchers might be able to ignore Lerner .....but not this guy...

Lipkin's group is pushing papers out like mad; he's already co-authored 7 papers this year. A good virus paper from Lipkin/Montoya could be the next best thing to XMRV....

As for the effect size, I think he made it clear that with "Infection-Associated Chronic Fatigue Syndrome" he sees subgroups. A significant percentage within these groups have a large response when on the right treatments (eg. HHV-6 / EBV patients on Valcyte - valganciclovir). Others patients don't respond or don't respond as dramatically. He's trying to figure out why the different responses. Even within just one subgroup there are a lot of variables; dose, schedule (once a day or four times a day?), do you pulse a medication?, how long does it take to see an effect. What about the effect of/approach to treating different combinations of co-infections. Which do you treat first? Do you pick one? Can a patient handle treating all co-infections simultaneously? All of these are still huge questions.

It has never been my impression that even when treatment is "successful" that Montoya sees "it" (anti-virals, antibiotics, immune support agents, etc.) as a cure. There is something going on that is allowing infectious agents that are widespread and typically controlled in the rest of the population to get out of control in CFS patients (or there is an abnormal immune response). It is my impression that patients testing negative for co-infections are very rare (if not non-existent) in his practice. That said, Montoya is looking very hard and in ways most physicians don't. My PCP said that he couldn't even begin to understand all of the tests that Montoya runs on a routine basis.

Montoya's paper doesn't seem overwhelmingly positive (we'll see when it comes out) but he clearly feels he's onto something - you can see it in his presentation - because he's had enough successes with some of these patients.

Montoya really needs a facility to just go after pathogens - it sounds like he has the whole thing planned out in his head already.

I'm so interested in that Lipkin study....where did they get their patients from? How many had gradual onset (like me), how many test positive to something? I pretty much tested negative to everything (altho the study never actually gave me the figures)..... This study sounds like its going to be the best pathogen study we've ever had.

Who knows if the study works out maybe Montoya will get his facility.

 

Thanks for all this, Cort.
It's very exciting to see it all coming together. And it will.

 

pine108kell

With regard to auto-immune diseases and infection, Multiple Sclerosis, which is very similar to ME/CFS, is an auto-immune disease (the immune system, of course, attacks the meylin - fatty sheaths - around the axons of the brain) with links to Epstein-Barr virus, among others. It's treated with anti-virals (amantadine) and interferon (betas), which is essential to fighting viral infections. While I haven't yet seen the video (I'm doing a naughty thing and skimming this article/comments while on the phone w/boyfriend at the moment! It's amazing I can even think/write coherently...or am I?), it sounds like Montoya views ME/CFS very much along the lines of MS.

My best friend has MS. We were diagnosed - with different diseases - at the same time. He was immediately placed on Avonex, a beta interferon, along with amantadine and nortriptyline (tricyclic antidepressant to help with sleep). While he has had a good chunk of damage to his cognitive skills (particularly unfortunate given that he is a PhD candidate), he's managed to adapt with the help of cognitive psychologists (they're only bad if they think they can cure you!) and occupational therapists and is slowly finishing his dissertation. Physically, you would never know he has MS. He works most of the day, 5 days a week. Goes to the gym each day. Went to the Middle East last year to do research. He drove down here to Portland from Seattle (a 3 hour drive) to help me move. While immune modulators and anti-virals have not cured him, he's "practically an Olympic athlete" in his words compared to me, who is mostly bedridden (I can use the bathroom on my own, make my own breakfast - not without going over my anaerobic threshold, however - but need help to take a bath, cannot drive, must limit use of my laptop in bed & can only read small portions at a time - despite being a PR member longer than almost anybody here, I've not reached the 100 post threshold because I can't post much - can only leave my apartment once a month to go to my dr's office to get my morphine script and my blood clotting time checked after developed blod clots in my lungs 5 years ago -- in other words, I'm seriously disabled).

If Montoya can give us the same options that MS patients have today, BRING IT ON!

 

one thing to remember about the difference between MS and ME is that in MS, they do not have PEM or the type of channelopathy where muscle weakness is progressive with use. In that regard, we are more like Myasthenia Gravis (which differs from other diseases, besides us which is like, in that the muscles become weaker with use).

However yes, with proper treatment and support, we should gain a lot of function and do a lot better. I suspect the SF-36 testing showing ME/CFS worse than most all other diseases is at least partly related to being totally (or almost totally, depending on the patient) untreated and generally without assitive devices or any other support.

and yes, Montoya is awesome!