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Interview with Ian Lipkin

Andrew

Senior Member
Messages
2,513
Location
Los Angeles, USA
This interview is not specific to ME/CFS. But it is very interesting, if I take some of his general statements and speculate on how they might apply to CFS. For one, he offers a mechanism for how pathogens enter the brain after an auto accident. Also, a model for how immune response can throw the nervous system out of whack. And how different pathogens can lead to the same neurological problem. And how infection can cause psychiatric problems via brain damage. Which is actually not a new idea. For example, advanced stage syphilis used to be seen as a psychiatric disorder. But it's interesting to see how he applies the idea.

http://discovermagazine.com/2012/apr/15-most-celebrated-virus-hunter-ian-lipkin/
 

SOC

Senior Member
Messages
7,849
Interesting insights into Dr Lipkin. :) Clearly the man thinks for himself, which is hallmark of all our best ME/CFS researchers and clinicians. We're lucky to have him involved in biomedical research into our illness.

Did we know about the Japanese research that is mentioned on the 3rd page of the interview showing correlation between Borna virus and ME/CFS ? I know he says he couldn't confirm it, so the jury is definitely still out. It's just I don't remember hearing about it. Not that me not remembering something should be any great surprise. :rolleyes:
 

oceanblue

Guest
Messages
1,383
Location
UK
What a guy. I suspect he's as good at PR as he is at science, but that's still a pretty interesting and impressive career to date, including:
  • Starting off studying anthropology, the switching to medical anthropology with an interest in bringing back traditional medicines
  • But once qualified as a medic he wound up in London in 1977 studying the neuromuscular disorder Myasthenia Gravis
  • Then as a neuroscience medic at University of Califronia in the early eighties was one of the first doctors treating AIDS patients, then labelled 'Gay-Related immunodeficieny', or GRID
  • After being convinced by a neuroimmunologist that AIDS was a flash in the pan that would soon be controlled by a vaccine, he started studying another virus (wonder if he regretted that).
  • Moved on to study 'Borna disease': several years spent developing innovative genetic techniques led to his discovery of Borna Virus and:
    [Interviewer]. But when you were done, you had reinvented the field of pathogen discovery with your molecular techniques.

    [Lipkin]Of all the things I’ve ever done, I am most proud of that.
  • Got famous discovering the West Nile Virus after a big outbreak in New York in 1999
  • The Chinese persuaded him to run their SARS eradication programme in Beijing during the serious outbreak there. It worked.
  • Now looking at the links between viral infections in the womb or early life, and neurological and psychiatric disorders
From a ME/CFS perspective his work on Borna virus is particularly interesting. It was implicated in a number of diseases including CFS and even autism (sound familiar?). But a recent paper in Nature by Lipkin found no evidence of this in a blinded study. Lipkin commented about his Borna virus discovery that "if it had been proved to cause a significant human disease it would have been an even bigger deal". I wonder if that helped Judy Mikovits to trust him and his process ? Here was someone who'd made a name for himself discovering a new virus that was potentially responsible for many different human diseases putting his pet virus to the test in a blinded study. Pure speculation on my part, but I did find that intriguing.
 

Purple

Bundle of purpliness
Messages
489
I found this bit on page 4 interesting as it may be relevant to how ME/CFS may develop (even though he was talking about PANDAS) and it is in line with some things which are known about ME/CFS:

Antibodies don’t typically traffic much in the central nervous system. But if you have any one of a number of other infections or an insult like head trauma, the blood-brain barrier [which normally protects the brain from pathogens] opens transiently. Depending on how long and where the opening is, the antibodies get access to part of the central nervous system or brain.

Agree with oceanblue. What a guy!
 

Glynis Steele

Senior Member
Messages
404
Location
Newcastle upon Tyne UK
Here is an abstract regarding research into autism. For me personally this hits the nail on the head. My daughter Jasmine was tube fed due to fat malabsorption, and when we began feeding her orally, carbs caused her to develop autistic traits. When the oral carbs were stopped, so did these traits, although it took 3 days of no carbs for this improvement to be seen. No investigation by her GI or paed, in fact they did not believe me. Absolutely disgraceful. I believe Jasmine has some kind of small bowel bacterial overgrowth which perhaps ferment carbohydrates and causes these behavioural changes.
Impaired Carbohydrate Digestion and Transport and Mucosal Dysbiosis in the Intestines of Children with Autism and Gastrointestinal Disturbances


Brent L. Williams1, Mady Hornig1, Timothy Buie2, Margaret L. Bauman3, Myunghee Cho Paik4, Ivan Wick1, Ashlee Bennett1, Omar Jabado1, David L. Hirschberg1, W. Ian Lipkin1*

1 Center for Infection and Immunity, Columbia University, New York, New York, United States of America, 2 Division of Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital, Boston, Massachusetts, United States of America, 3 Department of Neurology, Harvard Medical School and Departments of Neurology and Pediatrics and Learning and Developmental Disabilities Evaluation and Rehabilitation Services (LADDERS), Massachusetts General Hospital, Boston, Massachusetts, United States of America, 4 Department of Biostatistics, Columbia University, Mailman School of Public Health, New York, New York, United States of America

Abstract Top
Gastrointestinal disturbances are commonly reported in children with autism, complicate clinical management, and may contribute to behavioral impairment. Reports of deficiencies in disaccharidase enzymatic activity and of beneficial responses to probiotic and dietary therapies led us to survey gene expression and the mucoepithelial microbiota in intestinal biopsies from children with autism and gastrointestinal disease and children with gastrointestinal disease alone. Ileal transcripts encoding disaccharidases and hexose transporters were deficient in children with autism, indicating impairment of the primary pathway for carbohydrate digestion and transport in enterocytes. Deficient expression of these enzymes and transporters was associated with expression of the intestinal transcription factor, CDX2. Metagenomic analysis of intestinal bacteria revealed compositional dysbiosis manifest as decreases in Bacteroidetes, increases in the ratio of Firmicutes to Bacteroidetes, and increases in Betaproteobacteria. Expression levels of disaccharidases and transporters were associated with the abundance of affected bacterial phylotypes. These results indicate a relationship between human intestinal gene expression and bacterial community structure and may provide insights into the pathophysiology of gastrointestinal disturbances in children with autism
 

ukxmrv

Senior Member
Messages
4,413
Location
London
I really could have done with someone like him when I had a head injury after a RTA. That theory of antibodies crossing the blood/brain barrier wasn't accepted by any of the "experts" hired by the insurance company that fought against my claim (funnily enough!). No NHS or private neurologist or immunologist I saw was willing to put this in a report to the court.
 

oceanblue

Guest
Messages
1,383
Location
UK
Picking up on Purple's comments, I too think Lipkin discusses some models (though not the specific diseases) that might be relveant to CFS:
Have we reached the point where we can link specific infections to specific psychiatric disorders?

No, the connection is much more complex. When I worked with LCMV, it became clear that any sort of perturbation could damage the nervous system... It may not make a difference what the infectious agent is—bacterial, viral, or parasitic.
...

Could autism be another version of a PANDAS-like disease?

It’s possible, in some people. There is probably a group of people who have a genetic component to autism, and for them, there may not be much of a trigger or any trigger at all required. Another group is genetically predisposed, and if they encounter some factor or factors, individually or in combination, it could result in either the onset or the aggravation of the neurodevelopmental disorder; by factors, I include everything from heavy metals to infection.

And lastly, there is a group that may be relatively or entirely normal but is exposed prenatally to some factor or factors that have an effect on their nervous system and that manifests as autism. This is the hypothesis, at least.

And this to me sounded like a very good idea:
How would you describe your overall approach to pathogen discovery?

In microbe hunting we start with the result, the disease, and work backward, examining the paths and pathogens that might have led there. Finding footprints of a microbe—whether you’re seeing antibodies or the virus itself—is just the beginning of solving the crime. Initially the evidence is circumstantial. Like in criminology: Seeing a suspect on the street corner where somebody was killed is not enough. We still need motive and opportunity. Motive is tropism [seeking nutrients or energy] and virulence [ability to multiply and cause disease]. Some microbes are known to infect the lungs or the intestines or the brain. Finding them in a typical location gives us confidence we are on the right track. Opportunity—could it have done the damage? Some infectious diseases are seasonal. Mosquito-borne diseases, for example, are common in the summer but rare in the winter. Noroviruses are common on cruises. That’s where biological plausibility comes in.

You sound a lot like an old Hollywood detective.

If you can find a smoking gun, if you can show that this preceded that and somebody’s been shot in the past, then you can get a conviction. That’s exactly what it’s like.
By contrast, in CFS research it often seems like the biopsychosocial researchers started with the theory and examined the paths that might lead to the disease...
 

redo

Senior Member
Messages
874
It was really fascinating to see how he's observed others deteriorate from just testing - which I guess several ME patients also experience when going about with stressful and demanding tests or tasks (my bolds).

HIV was turning the patients’ bodies against themselves, the hallmark of an autoimmune disease. But you found that their immune systems were attacking not just their blood but their nervous systems as well. How did that finding come about?

I discovered this because we then had the only MRI scanner in the world at UCSF. As a result, a colleague asked me to see a patient of his, a ski instructor from Vail, Colorado. The man was thought to have MS, multiple sclerosis. So this fellow arrived at my clinic early one morning, and I did a very detailed neurological exam. As I left him and came back to him over the course of an hour, his symptoms changed. He was becoming quite fatigued, because the testing is arduous. So I gave him a break of 15 minutes. And he came back in to see me and now both sides of his face were so weak he couldn’t smile. He had numbness and tingling and then, right there in my office, his face became so weak he couldn’t close one eye. Then he couldn’t close the other eye.
It was clear this wasn’t MS, and I thought of a couple of causes for what I saw. One was exposure to some kind of toxin. So I checked the man’s spinal fluid for the presence of protein indicating inflammation. His protein was orders of magnitude higher than anything I’d ever seen, and the spinal fluid came out like glue. My colleagues asked what I wanted to do, and I said, I want to do plasmapheresis.