Looking Forward: Dr. Peterson on ME/CFS Research, Treatment Options and Hope for the Future

Posted by Cort Johnson

(Looking Forward: Dr. Peterson on ME/CFS was derived from notes I took after a talk with Dr. Peterson; the views enclosed hopefully reflect the essence of the talk but any mistakes, of course, are mine. Materials were added from the IACFS/ME Ottawa conference to supplement the article). Thanks to Corinne for arranging a meeting with Dr. Peterson. 

Dr. Dan Peterson and Dr. Cheney were the doctors on the scene as the most famous outbreak in chronic fatigue syndrome history took place in little Incline Village on the shores of Lake Tahoe high in the Sierra Nevada mountains in the early 1980’s. Both caught ‘the bug’ and both have made CFS the focus of their careers.

The media firestorm that followed left them ostracized by some in the community. Dr. Cheney left in the midst of the outcry but Dr. Peterson stayed and has been treating the original cohort, and of course, many new patients over the next 25 years.

A key figure, he’s always been something of an iconoclast; his office has no website and is in the same building it was 25 years ago (but is finally moving) and he puts out no newsletters or pronouncements. From the beginning Dr. Peterson has basically kept his head down and worked. The Reno IACFS/ME conference, however, revealed him to be an engaging public speaker.

In contrast to other ME/CFS specialists Dr. Peterson has always been focused on one type of CFS patient; the acute onset, fluey, pathogen ridden patients that filled the corridors of his office in the Incline Village outbreak over 25 years ago.

On a trip to help one of his patients, Corinne, navigate her way around Incline Village, Dr. Peterson sat down with us for a talk.

The Key Test 

Dr. Peterson distinguishes what he believes to be an archetypal ME/CFS patient from the others primarily by using one test – the natural killer (NK) cell functioning test. The International Consensus Criteria for ME considers post-exertional neuroimmune exhaustion or PENE to be the hallmark of ME and Dr. Hyde focuses on SPECT scans, but Peterson has found the NK cell functioning test to be the most definitive.

He talked about a typical case he had just seen, a triathlete with CFS. He told the referring doctor he would take him on if tests showed he had low NK cell functioning; he did and Dr. Peterson took him on – and then found that he was harboring a bug – but then noted that the patient was only a year in – suggesting that pathogen detection may get more difficult as the years go on.

NK cells, Pathogens and Different Types of ME/CFS – Trolling the blood for evidence of pathogens, NK cells form the first layer of our immune defense. Does someone with low NK cell functioning necessarily harbor a pathogen? No, Dr. Peterson explained, they don’t; the situation is a good deal more complicated than that. Low NK cell functioning means that you have a dysfunctional immune system, but it doesn’t mean that you have a (detectable) virus.

What subset do I belong in, I asked? My guess was that I don’t belong in Dr. Peterson’s subset. I’ve never had my natural killer cell functioning tested but tests performed 15 years ago didn’t indicate increased pathogens (except for an intestinal parasite). I had a fairly gradual onset which I did not associate with an infection; I had middling OI problems, pretty severe MCS and inability to engage in much exercise without problems. I would guess I was in the hyper-sensitization subset – not the immune-probably-pathogen-infected subset.

On the other hand, there was Corinne with her super (super) low NK cell readings, her super high herpesvirus readings, her severe PEM, orthostatic intolerance, migraines, and her 5 pm bedtimes. We had some core similarities (OI, PEM, vertigo…) and some big differences.

Was I a version of Corinne without herpesvirus infections or was I something entirely different? He asked how I knew I was herpesvirus free if I hadn’t been tested using Lipkin’s arrays…. and this was really the nub of it. It’s simply hard to tell who belongs where until the technology improves, and it is improving. The improvement in the pathogen arrays (aka Lipkin) is just part of it.

The Science Moves Forward – Dr. Klimas and Fletcher appear to have got a handle on cytokine tests and Broderick appears to be differentiating subsets using his complex data mining techniques. It looks as if Baraniuk is uncovering subsets in his new, highly complex spinal fluid studies and, of course, the Lights’ gene expression studies have found their own subsets. CAA-funded researchers are using novel techniques to characterize the gut microbiome……ME/CFS researchers are pitifully underfunded but a lot of cutting edge work is being done on ME/CFS and our views of what ME/CFS is could change rapidly over the next couple of years.

Dr. Lipkin and Dr. Aschiero’s collaboration with the Chronic Fatigue Initiative adds yet another layer of innovation. Dr. Peterson, who has always been up on the latest technological advances, and is collaborating with Dr. Lipkin, is clearly impressed by Lipkin’s technology, and why wouldn’t he? Lipkin, after all, has developed several new techniques to identify and characterize viruses and he leads one of the busiest viral labs in the world.

Dr. Peterson and Dr. Lipkin’s collaboration on pathogens moves ME/CFS pathogen research in ME/CFS into a new realm of expertise and visibility. Pathogen findings in ME/CFS have not always been taken seriously but if Ian Lipkin finds something – that finding will likely stand in a research world that takes reputation and past work very seriously and penalizes those with lesser stature and experience. If he finds nothing, that will say something as well, of course.

The point is that technology is improving all the time and Dr. Peterson believes it is changing in the right direction for ME/CFS (and other chronic diseases) and this is one reason why he thinks the future holds promise. Even now, he said, you can get the flu today, take a molecular profiling test – and it can tell you exactly what kind of strain of flu you have. That’s just the beginning. Ultimately he thinks researchers/doctors will be able to tie specific types of immune abnormalities to certain kinds of infection.

A Patients Story – Dr. Peterson’s emphasis on natural killer cell dysfunction was borne out when I asked him how to explain somebody I knew who’d had a dramatic and acute infectious onset but over time eventually became well enough to exercise vigorously without problems. When he tried to go back to school, though, he relapsed and kept on relapsing even after he left school. His case was dramatic but not necessarily unusual; there are a subset of patients who go through dramatic up and down swings of health.

What, I asked, could cause this person to experience such dramatic fluctuations in health? He felt they were probably related to his natural killer cell functioning; pathogens probably became activated when his NK cells bottomed putting further stress on his system, perhaps allowing other pathogens to take hold, depl-eting the system further….creating a negative spiral he barely crawled out of.

Dr. Peterson’s emphasis on natural killer cells was certainly borne out by an immune section at the IACFS/ME Conference in Ottawa that could almost have been renamed Natural Killer Cells and CFS, there was such a focus on them. The Ottawa conference say several studies validated the low NK cell findings and several began to look at what might be causing them.

TcellTumorCytotoxic T-Cell Problems as Well? – Both Dr Peterson and Dr. Klimas believe a similar type of dysfunction also occurs in the heavy hitters of the immune system – the closely related cytotoxic T-cells. If NK cells are the first line of immune defense, cytotoxic T-cells – which appear several days later to wipe out the pathogen – are the last line.

Natural killer cells are kind of Johnny-comelatelies to the medical world and at the Reno conference two years ago Dr. Peterson bemoaned the number of medical doctors who knew nothing at all about them. As the early or innate immune response gets more attention, NK cells have risen in importance but for many years cytotoxic T-cells have received top billing.

These more complex cells are the big guns of the immune response but both they and NK cells use the same methods to kill invaders. That killing process is impaired in NK cells in CFS patients and both Dr. Peterson and Dr. Klimas believe the same may be true in cytotoxic T-cells. If research indicates that’s true, then you have a truly eyebrow-raising problem.

Finding problems in those cells should raise some eyebrows. At the IACFS/ME conference Brenu presented a paper suggesting that cytotoxic T-cell functioning is also impaired in ME/CFS.

The Central Locus 

Dr. Peterson has a strong focus on pathogens but does not believe CFS is tied to a specific virus or even necessarily a pathogen. While the disorder is often clearly initiated by a bug (something, he said, clearly swept through Incline Village about 30 years ago, causing somewhere around 10% of the community to get ill), it’s clear that ME/CFS is not tied to any one bug….or even a bug.

He noted that noted that 6% of SARS patients in an unpublished study have CFS – which adds SARS to an ever increasing list of pathogens (EBV, parvovirus, Coxsackie B) which have been shown to induce CFS . But it’s not just pathogens…. accidents can trigger ME/CFS as well. (Chemotherapy/radiation treatment in cancer triggers a CFS-like condition as well as does time in an ICU unit.

The point is that ME/CFS can be triggered in many different ways, and it appears that there is some background dysfunction common to all of them. (Dr. Clauw believes an FM/CFS-like condition is probably present in 20-30% of people with chronic disorders making it the single most common and expensive medical condition the medical field faces).

fluThe key ingredient in this disorder, Dr. Peterson believes, is something called ‘sickness behavior’, which he agreed was a terrible name for a serious, biologically based problem. Sickness behavior refers to the cytokine storm in the brain that causes the fatigue, muscle aches and pains, etc. that occur when we get a cold.

It’s possible that an initial insult somehow resets the immune system in the brain – turning it on permanently. (The Dubbo studies suggest that high cytokines levels early in the infection could somehow trigger this.) It could even be that in some people the brain has become so sensitized that it over-reacts to near normal cytokine levels in the blood. Other patients could have raging herpesvirus infections that are triggering this cytokine storm…there are multiple options but the key fact is that the central locus of ME is probably in the brain.

Sickness behavior was a major focus of the State of the Knowledge Conference and a good deal of work is currently being done in other disorders to what effects may be a result of cytokine storms in the central nervous system. . .

Autoimmune issues

The success of Rituximab in some preliminary studies has sparked interest in autoimmune issues in ME/CFS and at the NIH SOK Dr. Freeman described a group of CFS-like patients whose immune systems targeted portions of their autonomic nervous system shortly after an infection. The picture was so strikingly similar to many cases of ME/CFS – an infectious event in formerly healthy people that caused them very quickly to fall apart – I asked Dr. Peterson if he thought there was an auto-immune component to ME/CFS…

Epstein-Barr Virus (EBV Mimicry) – Dr. Peterson said he bought into the no-autoimmunity-in-CFS argument early on and even remembers patients he didn’t treat early on because they had high auto-antibodies titers – which meant by definition they didn’t have ME/CFS – but now he thinks they probably had CFS.

He believes autoimmunity is a part of CFS and that some of the autoimmune manifestations found in the disorder could be due to something called EBV mimicry. He noted that many of his patients have autoimmune thyroiditis and recent research has indicated that some of the proteins that EBV produces look very much like thyroid proteins. If the immune system targets those EBV proteins for destruction it could end up targeting the thyroid as well: i.e. autoimmune thyroiditis.

This, he said, is another example of what the continuing advance of technology may bring. It wasn’t until big gene databases were developed that researchers realized that certain aspects of EBV looked very much like our thyroid gland. Dr. Peterson noted that more and more studies are tying different types of infections to autoimmune diseases. (In another arena, Mady Horning of the Chronic Fatigue Initiative is hot on the trail of a pathogen that could cause schizophrenia and other mood disorders. This is not to say that there is conclusive evidence that these disorders are caused by pathogens but researchers are now investigating this possibility.)


The ‘X’ Drug for ME/CFS? CMX001 Promises Help 

CMX001 – The big news on the treatment scene is CMX001 – a new drug developed by Chimerix to treat herpesviruses and other pathogens which may come on the scene in the next few years. Chimerix is a relatively new pharmaceutical company built around a unique drug delivery system they believe significantly increases these drugs’ effectiveness and reduces their side effects.

Chimerix came to Dr. Peterson because they knew he was treating herpesvirus infection in ME/CFS patients and he is engaged in a trial study of the drug using his present patients.

The ‘Hammer’ Gets Stronger and Safer – CMX001 appears to be a safer and more effective version of cidofovir, otherwise known as Vistide. Vistide (cidofovir) is a powerful drug little used by ME/CFS physicians because it requires intravenous injections and can cause acute kidney damage.

Chimerix’s great innovation is to modify Vistide so that that it looks like a naturally occurring by-product of fat cells – causing the body to easily take it up into its tissues. Chimerix’s new ‘packaging’ process is innovative enough that the resulting drug is considered a ‘new chemical entity’ and thus is protected by patent laws. (Chimerix’s Phospholipid Intramembrane Microfluidization (PIM) Conjugate method is protected by 21 patents.)

CMX001’s two big plusses are ‘increased efficacy’ and ‘reduced toxicity’. CMX001 appears not to affect the kidneys at all and its only toxicity worries appear to involve the gastrointestinal system which, Chimerix reports, are ‘easily monitored and rapidly reversible’. Nor is intravenous administration a problem…Chimerix comes in the form of a pill….

Chimerix believes its new packaging process will ‘dramatically change the way certain viral diseases are treated. Its website states CMX001 is not just a little bit more, or even moderately more, but ‘much more potent’ than the original drug (Vistide) in in vitro studies against a wide variety of viruses. Vistide, referred in a tongue in cheek manner on the PR Forums as ‘the Hammer’, was already one of the more effective drugs against herpesviruses. Physicians were reluctant to administer it, however, because it required IVs and because of its potential side effects. Having this drug available in a safer, more effective form could be a big boon for physicians treating herpesvirus infections.

From Chimerix’s website: 

Based on data obtained to date, CMX001’s profile may allow physicians to treat patients much earlier and more effectively in the disease course, as opposed to many current therapies where the risks of serious and harmful side effects delays treatment.

That makes CMX001 sound almost made to order for herpesvirus infected people with ME/CFS who often take large doses of antivirals for long periods of time. https://www.chimerix-inc.com/about-ch…ry/commitment/ . Its possible that some ME/CFS patients who can’t tolerate antivirals in the doses needed or don’t respond well to them might very well respond well to CMX001. CMX001’s increased efficacy might also make it more effective at getting at the ‘buried’ herpesviruses infections that often require such long treatment regimes in ME/CFS.….

An Effective Central Nervous System Antiviral? 
– Research into CMX001 is just beginning, but thus far two studies suggest it may be more effective in getting at hard to reach central nervous system infections. In one study CMX001 was fifty times more effective in vitro against herpes simplex viruses than acyclovir or cidofovir and was shown to reach deep into the central nervous system.https://pubmed.ncbi.nlm.nih.gov/20923374

CMX001 is also being touted as possibly the first effective drug able to treat progressive multifocal leukoencephalopathy (PML), a frequently fatal brain disease in immunodeficient patients, caused by the Polyomavirus JC .https://pubmed.ncbi.nlm.nih.gov/20923374

Not Just Herpesviruses – On their homepage, Chimerix emphasizes the ‘broad antiviral’ spectrum that the drug treats and they aren’t kidding. CMX001 was originally developed to combat smallpox, not herpesviruses; it was only later Chimerix realized it possibly has a broad spectrum antiviral on its hands. (Chimerix was recently awarded a $36 million NIH grant (10 years of ME/CFS research!) to investigate CMX001’s effectiveness against smallpox). Thus far, Chimerix has been shown to be ‘much more effective’ against multiple double-stranded DNA viruses (such as variola [smallpox], cytomegalovirus, BK virus, vaccinia, ectromelia, adenovirus and Epstein-Barr virus and cowpox viruses) in laboratory trials.

Chimerix, founded in 2002, is a young company and CMX001 is its first product. It will take time to determine how effective Chimerix is in patients but on the face of it it is the most promising drug since Ampligen to come before the FDA over 20 years ago.

Chimerix isn’t the only promising new drug that may come on the scene in the next couple of years. Dr. Chia stated that a drug he expects to come out in the next couple of years could be very helpful with enteroviruses and Dr. Dantini reported on another more powerful herpesvirus drug under development.
Other Treatments

Rituximab (Rituxian) is a chemotherapeutic drug that is also effective in some autoimmune disorders. Some small Norwegian studies have found excellent (if temporary) results in some ME/CFS patients and a Norwegian Journalist at the IACFS/ME conference reports new study results are expected soon.

With this paper on the way, I asked Dr. Peterson if he thought Rituximab could play a significant role in ME/CFS and he said he thought it could be a big player although he warned of the need to find the right type of patient. He said you need to be able to differentiate between patients who really do need their B cells and those that don’t. For the right patients he thinks Rituximab will probably be a big deal.

Immune Modulators/Suppressants 

There’s some good news on the immune modulation scene as well. Dr. Klimas talked about effectively using Etanercept in patients with high TNF-a activity. A wide variety of immune suppressing and immune altering drugs are coming available; I asked him if he saw a role for them in ME/CFS. . .

He said he well remembered telling a well known researcher early on that some of his patients’ TNF-a readings were as high as 50,000 and being told that was impossible because they would be dead. Not surprisingly, he thinks this type of drug will be very helpful and is using them in selected patients. A key issue, of course, is getting accurate immune readings – not always an easy thing to do – but he thinks Dr. Klimas has got her cytokine tests right and he is using her lab for some tests.

He said the cost of the most well known immune modulator in CFS, Ampligen, is coming down to around $6,000 a year.

Overall the news is improving on the treatment end. He believes that treatment possibilities for really ill people like Corinne are opening up and something significant will be ready for her and them in the next couple of years.


Dr. Peterson is well aware of the holes in our pathogen detection systems. He noted that flavivirus – a tick borne disease – is the most common form of encephalopathy in Europe but is not tested for in the US. Why? Because of an old study stating that flaviviruses are not found in the ticks in the US. He wanted to be clear that he was not saying that CFS patients have flavivirus – he was merely pointing out that there are holes in the system. When I asked him about enteroviruses, I learned that Dr. Peterson, like most doctors, does not test for enteroviruses because they don’t know how to treat them and he noted that the incidence of enteroviral infection could be wildly underestimated.

The Lipkin/Montoya pathogen study will be very illuminating. He described it as being extremely rigorous with long questionnaires and rigidly defined protocols. The study will be looking at the sickest of the sick. Even if it comes up with just 10% positives Dr. Peterson believes it will be a big boon to the field.

XMRV – Dr. Peterson, of course, ended up leaving the Whittemore-Peterson-Institute approximately 8 months after the XMRV Science paper was published. Dr. Peterson didn’t want to dwell on past issues but he did say that the retrovirus theory never completely fit for him for a couple of reasons. First he felt the epidemiological evidence never fit and that there’s little evidence of a contagious side to ME/CFS. Another problem was that XMRV’s primitive nature (it’s not nearly as complex as HIV) suggested from the beginning that it would have difficulty evading the immune system (and research suggests that it can’t).

The BIG Problem – Money – he stated if they had thrown the amount of money they’ve spent on CFS on HIV they never would have figured it out. Lack of money remains the key stumbling block to resolving CFS. The money that has been provided is too little to really do anything. I asked him about the cancer cluster study that showed up at the Reno IACFS/ME Conference. The news of a cancer cluster in CFS patients in Incline Village was startling, but the money ran out….and we have no published study at this time.

General Research 

Hydrogen Sulfide – Dr. Broderick’s complicated gene expression research recently and unexpectedly pulled up a hydrogen sulfide link. The link is enticing because high rates of H2S could lead to lethargy, fatigue, gut problems and other symptoms. Dr. Peterson has been having some of his patients test for H2S. What about hydrogen sulfide?

He noted that the really ill patients most often test positive for hydrogen sulfide and he believes it is a player but he was adamant that he believes the main problem is the brain, not one of the other organs of the body. He did note that he felt that leaky gut syndrome is getting a good bit of money and research now and findings there could help explain ME/CFS. He felt we could really use better tests for the gut.

Genetics Coming to the Fore – Genetics is another area of promise. Several genes keep showing up in both CFS and FM studies and Dr. Peterson noted that the kind of widespread vulnerability to infectious or other stressors he sees in ME/CFS suggests that a strong genetic susceptibility is present. (A paper recently suggested that a VERY strong genetic susceptibility is present in CFS. See the Clauw talk in the IACFS/ME Ottawa coming up soon for more on the stunning strongly genetic susceptibility that has emerged in fibromyalgia as well).

There was more news on the research front but this time it involves Dr. Peterson directly.

Simmarron Research Inc. – A New Research Institute Opens

“We envision a future where CFS/ME is a treatable disease”

Several years ago in a CFIDS Association publication Dr. Peterson was clearly torn between the need to care for a large underserved patient population and the need to further the science. Perhaps Dr. Peterson’s short time with the Whittemore-Peterson Institute scratched an itch that will not let him go…but, for whatever reason, it appears that Dr. Peterson’s appetite for research has been whetted.

After he left the WPI he began work on forming a non-profit Research Institute and this year the Simmarron (Sim -Sierra Internal Medicine -marron) Research Institute was born. Simarron is using the same model as the research arm of the CFIDS Association of America: compile enough strong data in small seed studies to make way for a major NIH grant.

Dr. Peterson and two of Simarron’s representatives were present throughout the IACFS/ME conference where Simarron also rented space. One of Simarron’s reps, Gunnar, described the complex (and tedious) process of transferring reams of data from the biobank (Dr. Peterson’s minus 80 degree freezer) in which he has been storing precious samples for over 20 years, into an electronic data base.

One of eight researchers associated with the Chronic Fatigue Initiative (add link), Dr. Peterson and Simarron Research have also begun the process of gathering data and ultimately samples from the patients they and other ME/CFS physicians (Drs. Klimas, Lapp and Montoya) will use to fill the CFI’s Bio and Databanks. Peterson and other investigators met with CFI director Scott Carlson during the conference.

The most interesting work Dr. Peterson and Simarron are engaged in currently, however, isn’t taking place in this country at all. Now a member of the faculty at Bond University in Robina, Australia, Dr. Peterson has formed a collaboration with the Staines group there that the IACFS/ME Ottawa conference materials indicated was quite fruitful.

From the IACFS/ME conference
– Submitting four studies to the IACFS/ME Conference, the Peterson/ Bond U group was among the most prolific at the conference. These are preliminary studies but some appear to be attempts at developing comprehensive findings with researchers looking in several compartments (blood and spinal fluid) at once.

  • Immune Regulation and Pain Sensitization in the Central Nervous System : The studies presented preliminary findings that promise some fascinating results in the future. A blood and spinal fluid study suggested that neuropeptides involved with a central nervous signaling pathway called the purinergic system were abnormal in ME/CFS patients. The purinergic system showed up in neon lights in the Light gene expression studies and the Lights’ “a-dysfunction” there could play a key role to ME/CFS. Purinergic signaling primarily affects adenosine pathways which in turn regulate immune functioning.The purinergic receptors (P2X4/P2X5) the Lights found to be greatly increased in people with ME/CFS after exercise play a role in several areas of interest in CFS including the smooth muscles lining the blood vessels, pain sensitization in the immune cells in the spinal chord and brain, and in sympathetic nervous system functioning.
  • Pregnancy and Hormones – a Key to Female Predominance in ME? – This study was prompted by two observations: (1) that some women with CFS temporarily get better in the midst of their pregnancy and (2) that women with autoimmune disorders such as multiple sclerosis often experience the same pattern. A gene expression study suggested genes which get expressed during pregnancy may be abnormally expressed in people with ME/CFS.This is a fascinating much under-investigated area in ME/CFS area given the gender predominance in CFS and it goes nicely with a CDC story showing strikingly high rates of women with CFS with heavy rates of bleeding, premenstrual problems and other gynecologic abnormalities including disturbing high rates of hysterectomies.
  • Vaccinations – A Window into the Immune Problems in ME/CFS? – A third study is looking at, as Dr. Peterson noted, another long standing question in CFS, but one for which we have few answers – the possible effects of vaccinations on the disorder. The group assessed immune functioning before and after people with ME/CFS were vaccinated and found evidence that vaccinations may be significantly affecting immune functioning. Their conclusion of this still very preliminary study was that vaccination may be linked to pathophysiological problems in ME/CFS.A study indicating overt immune changes in a group following vaccinations should prick up a few ears, and would lend credence to the other studies indicating that abnormal immune networks and abnormal immune functioning are present in this disorder.
  • Natural Killer Cell Functioning – Researchers are (finally) starting to move past the fact that natural killer cell functioning is low in ME/CFS and getting to the question – why? This last study, which focused on patients with low natural killer (NK) cell and diminished VO2 max testing suggested that cytokines and lytic proteins such as granzymes and perforin could be responsible for the low NK function. Interestingly miRNA’s that regulate immune function were abnormal as well.

Impressed with the Schutzer/Natelson spinal fluid findings, Dr. Peterson hopes, in another project with Bond, to use cytokines to go beyond their findings. Ideally he would like to set up a three-legged study that would correlated spinal fluid findings with cytokine levels in the blood (presumably using Dr. Klimas techniques) and then correlate those with findings with the Lipkin study – setting up a kind of multisystemic validation study showing alterations in three distinct areas. If that works out you could get two immune and one pathogen signatures in one package.

Dig Deeper: Check out Simmaron Research


Objectivity – Dr. Peterson noted that his interest in ME/CFS is primarily driven by two things; intellectual curiosity and compassion for his patients which he thinks of as his extended family. He has always maintained a kind of ruthlessly objective viewpoint that has left him unattached to any theory; he is willing to go where the science leads him…

No Cheese Down The Conspiracy Theory Tunnel – He believes it would be a huge mistake for the ME/CFS community to go down the conspiracy theory tunnel. Dr. Peterson has been involved in ME/CFS since Incline Village since the 1980s and he’s very clear about all the problems ME/CFS has had getting recognition. Has an almost criminal lack of attention for ME/CFS been present? Yes. Do some researchers not believe the disease is real? For sure. Does bureaucratic inefficiency and inertia dog progress in ME/CFS? Absolutely. Has some cabal set out to undermine legitimate findings in the disorder? No way. He was emphatic that that was not true and that he felt there was no cheese down that tunnel for the ME/CFS community. The hyper-aggressive patients impugning researchers’ integrity are, from his stance, only hurting the community and their own chances for help.

On the other hand he believes effective, aggressive advocacy is critical.

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