Saturday, November 22, 2014

A Tale of Two Meetings: CFSAC and P2P

Two important meetings are scheduled for early December: CFSAC (CFS Advisory Committee) and P2P (Pathways to Prevention). The CFSAC meeting will be held on December 3-4. The P2P panel will meet on December 9-10. Both will be in Washington, DC and both are available via webcast.

CFSAC was formed in 2003 in order to provide advice and recommendations to the Secretary of Health and Human Services (HHS) through the Assistant Secretary for Health on issues related to ME/CFS. It is currently under the auspices of Office on Women's Health, a division of the Office of Public Health and Science.

In 2010 the committee advised HHS that the name chronic fatigue syndrome should be changed to CFS/ME because the name wasn't being taken seriously. The idea was that the inclusion of ME might encourage more research into the illness. The CFSAC panel also recommended that a national CFS/ME network of treatment centers be created by HHS, "in order to expand access to care, to develop educational initiatives, and to allow researchers to share data."

Although the recommendations made by CFSAC over the years have been important, they have been ignored, or, even worse, "hijacked." The Federally Designated Officer, Nancy Lee, was considered a large part of the problem, and though she has been replaced is still a major obstacle in making progress. 

Of the two meetings, P2P will have the greater impact on the future of ME/CFS, for while CFSAC recommendations have been largely ignored, the P2P's conclusions will have an immediate effect on funding, and on subsequent treatment.

CFSAC is open to public comment. (Please see Jerrold Spinhirne's excellent comment below.)

If you would like to submit a public comment by phone to CFSAC, you must register by Monday, November 24th at 5pm. If you want to submit written comments, these are also due November 24th at 5pm. Registration and instructions for scheduling public comments and submitting public testimony are available at www.blsmeetings.net/cfsac. You can read the full agenda HERE.

If you would like to register to attend the P2P Workshop in person click HERE,

To register for the webcast click HERE


Advocates to NIH - "Pull the P2P!"

____________________

My Public Comment for the December 3-4, 2014 CFSAC Meeting

Comment for the December 2014 CFSAC Meeting by Jerrold Spinhirne, S.E.

Some important quotes regarding the neurological disease myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS):

1. Name: Myalgic encephalomyelitis, a name that originated in the 1950s, is the most accurate and appropriate name because it reflects the underlying multi-system pathophysiology of the disease. Our panel strongly recommends that only the name ‘myalgic encephalomyelitis’ be used to identify patients meeting the ICC because distinctive disease entity should have one name. Patients diagnosed using broader or other criteria for CFS or its hybrids (Oxford, Reeves, London, Fukuda, CCC, etc.) should be reassessed with the ICC. Those who fulfill the criteria have ME; those who do not would remain in the more encompassing CFS classification.

2. Remove patients who satisfy the ICC from the broader category of CFS. The purpose of diagnosis is to provide clarity.  The criterial symptoms, such as the distinctive abnormal responses to exertion can differentiate ME patients from those who are depressed or have other fatiguing conditions. Not only is it common sense to extricate ME patients from the assortment of conditions assembled under the CFS umbrella, it is compliant with the WHO classification rule that a disease cannot be classified under more than one rubric....

3. Research on ME: The logical way to advance science is to select a relatively homogeneous patient set that can be studied to identify biopathological mechanisms, biomarkers and disease process specific to that patient set, as well as comparing it to other patient sets.... Research on other fatiguing illnesses, such as cancer and multiple sclerosis (MS), is done on patients who have those diseases. There is a current, urgent need for ME research using patients who actually have ME. [Emphasis added]

– Myalgic Encephalomyelitis – Adult & Paediatric: International Consensus Primer for Medical Practitioners (Carruthers, 2012)

I felt for some time, Keiji, that those who have CFS are at a certain point along a continuum of illness in which fatigue is either the most dominant symptom or the most clearly articulated by virtue of impressions on the part of the patient or physician that such a complaint is important. I predict that fatigue itself will remain the subject of considerable interest, but the notion of a discrete form of fatiguing illness will evaporate. We would, then, be left with Chronic Fatigue that can be distinguished as Idiopathic or Secondary to an identifiable medical or psychiatric disorder. I consider this a desirable outcome. [Emphasis added]

– NIH official Stephen Straus in an undated letter to CDC epidemiologist Keiji Fukuda before the 1994 Fukuda et al. redefinition of chronic fatigue syndrome (Straus, undated)

We propose a conceptual framework to guide the development of studies relevant to the chronic fatigue syndrome. In this framework, in which the chronic fatigue syndrome is considered a subset of prolonged fatigue (>1 month), epidemiologic studies of populations defined by prolonged or chronic fatigue can be used to search for illness patterns consistent with the chronic fatigue syndrome.

Prolonged fatigue is defined as self-reported, persistent fatigue lasting 1 month or longer. Chronic fatigue is defined as self-reported persistent or relapsing fatigue lasting 6 or more consecutive months.

Diagnosis of the chronic fatigue syndrome can be made only after alternative medical and psychiatric causes of chronic fatiguing illness have been excluded. No pathognomonic signs or diagnostic tests for this condition have been validated in scientific studies; moreover, no definitive treatments for it exist.

[N]one of the provisions in these guidelines, especially the definition of idiopathic chronic fatigue and subgroups of the chronic fatigue syndrome, establish new clinical entities. Rather, these definitions were designed to facilitate comparative studies.[Emphasis added]

– Fukuda K, Straus SE, Hickie I et al. Chronic fatigue syndrome: a comprehensive approach to its definition and study. (Fukuda, 1994)

Fatigue is a totally undefinable concept. Fatigue is impossible to measure or quantify. Fatigue is so non-specific that it can be a common element in any acute or chronic disease and many psychiatric diseases. Worse, it redirects the medical and public attention to the totally undefinable fatigue and away from the obvious Central Nervous System changes in these patients. Much worse, it makes fun of a serious illness since most people and most physicians tend to equate fatigue with laziness, work avoidance, something that a bit of effort will chase away. It has turned out to be a damning indictment to all M.E. patients.

– Dr. Byron Hyde in a 2006 speech delivered in London

The recent Stanford brain imaging study (Zeineh, 2014), which found profound brain abnormalities in CFS-labelled subjects, is consistent with the neurological disease myalgic encephalomyelitis (ME) and shows the problem with the continued use the 1994 Fukuda "International" CFS case definition (Fukuda, 1994) to select research subjects for biomedical research. The results can only be applied to an undetermined subset of CFS patients which is never delineated.

The ME IC Primer (Carruthers, 2012), on the other hand, already lists brain abnormalities similar to those found in the Stanford study – white matter abnormalities and reduced regional gray and white matter volume – as associated with the neurological disease ME. ME is a well-described disease entity based on the documented, clinical observation by highly qualified medical doctors of thousands of actual patients with the disease. CFS, as it is currently case defined, is based on a political negotiation made between US Department of Health and Human Services (HHS) bureaucrats and medically unqualified UK psychiatrists in 1994. CFS corresponds to no single clinical entity ever observed in actual patients. In addition to chronic fatigue, the 1988 Holmes definition of CFS required 8 of 11 listed symptoms. The 1991 Oxford definition of CFS required no symptoms other than chronic fatigue. The CDC-assembled 1994 CFS definitional committee diplomatically split the difference and arbitrarily required any 4 of 8 listed self-reported and sketchily described symptoms for a case of CFS.

The Fukuda case definition of CFS is a research concept that is an abstraction. No extensive clinical observation of actual patients was considered. The definition was allegedly only intended as a theoretical framework to assemble research subjects who MIGHT have an identifiable disease. Inexplicably, this abstract research concept was turned verbatim into CFS diagnostic criteria that can still be found in the CDC's "CFS Toolkit" of diagnostic and treatment guidelines today, 20 years later. In other words, doctors are presently diagnosing and treating a research abstraction called CFS, rather than any actual disease – or even any related group of diseases – found in nature. 

The "encephalomyelitis" part of the term ME means inflammation of the brain and spinal chord. Brain inflammation was recently confirmed in ME patients selected using the International Consensus Criteria for ME. (Nakatomi, 2014; Carruthers, 2011) This is completely consistent with the Stanford brain study findings. Dr. E. Donald Acheson in 1959 reviewing 14 outbreaks of infectious disease, by then named myalgic encephalomyelitis, involving thousands of patients stated:

"All the outbreaks shared the following characteristics: (1) headache; (2) myalgia; (3) paresis [muscle weakness, partial paralysis]; (4) symptoms or signs other than paresis suggestive ofdamage to the brain, spinal cord or peripheral nerves; (5) mental symptoms; (6) low or absent fever in most cases; (7) no mortality." [Emphasis added] (Acheson, 1959)

The common symptom of fatigue is not even mentioned in classic descriptions of ME – not because ME patients did not experience and report fatigue, but because fatigue is such a commonly reported symptom that it is not useful for making differential medical diagnoses. The ME International Consensus Criteria (Carruthers, 2011) and IC Primer do not even list self-reported chronic fatigue, or any type of fatigue, as a symptom of ME. Responses to standard fatigue questionnaires are, therefore, of no use for diagnosing ME, or for measuring its severity or improvement. Nevertheless, the concepts of CFS, ME/CFS, and CFS/ME are all based on self-reported fatigue which is only "measurable" by questionnaires – the "instruments" of social science.

Many patients and media reports viewed the Stanford brain study as vindication that CFS is "real." However, by the currently used Fukuda definition, CFS can never be "real." The fatigue must be "unexplained" and "self-reported." The findings of the Stanford brain study are likely to be found as "exclusionary" for CFS by the dogmatic US Centers for Disease Control (CDC) – as they have found all similar physical findings in CFS-labelled research subjects for the past 26 years.

How could brain-scan abnormalities ever be a "biomarker" for the diverse group of patients assembled under the umbrella term CFS? None of the poorly described symptoms that might indicate some neurological involvement – "impaired memory or concentration," "headache of a new type or severity" and "unrefreshing sleep" – in the current "CFS Toolkit" is required for a CFS diagnosis. Abnormal brain scans could never be a biomarker for CFS because an unknown portion of CFS-diagnosed  patients is likely to have no physical brain abnormalities, whatsoever. If the Stanford subjects had been evaluated for ME using the ICC, which requires at least three symptoms indicating neurological impairment, the results could be applied to a specific patient group – the group with the neurological disease ME. Instead, biomedical research using nonspecific CFS-labelled subjects will keep going around in circles as it always has done and always will do.

The fatigue experienced by ME patients is no more "unexplained" than the fatigue experienced by cancer and MS patients. Because the fatigue experienced by ME patients is a bioalarm indicating an underlying disease process and not "unexplained," no patient with ME, strictly speaking, can meet the Fukuda case definition of CFS. The impossibility of a single patient simultaneously meeting both the ICC-ME and Fukuda-CFS case definitions makes the CFS-hybrid terms "ME/CFS" and "CFS/ME" ambiguous and nonsensical.

The CDC has consistently denied any neurological involvement in their conception of CFS. After a quarter century of CFS research, there is still no symptom suggesting any neurological disease or, indeed, the presence of any specific disease, required for a CFS diagnosis or for use as a CFS research subject. The problem is bad faith at the CDC and the rest of the Department of Health and Human Services – not the lack of scientific evidence.

If the CDC, NIH, psychologists, and psychiatrists wish to continue their research of the subjective symptom of chronic fatigue or their search for a distinct chronic fatigue syndrome and its elusive subgroups, they should not do so at the expense of patients with the distinct neurological disease myalgic encephalomyelitis. It is unethical and hypocritical of the CDC and the rest of HHS to keep ME hidden within a hypothetical chronic fatigue syndrome. There is an urgent need for ME, as defined by the ICC, to be officially listed as exclusionary for a CFS diagnosis or for use as a CFS research subject. Just as the presence of CFS subjects without ME confounds ME research, the presence of ME subjects without CFS confounds CFS research. If the CDC is sincere in wishing to research CFS, they should immediately announce that subjects with ME – just as subjects with other fatiguing diseases such as cancer and MS – should be excluded from use as CFS-labelled research subjects.

Copies of the ME IC Primer must be distributed to doctors so they can recognize and rule out ME before making a CFS diagnosis. Doctors must also be educated that in the new US ICD-10-CM, official October 2015, ME is coded for billing and reporting purposes as G93.3 as a neurological disease. CFS and unspecified chronic fatigue are codedtogether as R53.82 as general symptoms.

HHS could actually make itself useful by distributing the ME IC Primer to doctors and medical personnel and informing them how to use the new ICD-10-CM codes. Instead, HHS has chosen to engage in expensive boondoggles such as the unneeded, million-dollar HHS/IOM redefinition of "ME/CFS" or the useless, farcical NIH P2P "ME/CFS" Workshop. Both of these HHS initiatives are set up and stage managed so that they can only cause more confusion, more harm to patient care, and more confounding of research.

References:

Acheson, ED. The clinical syndrome variously called benign myalgic encephalomyelitis,
Iceland disease and epidemic neuromyasthenia. Am J Med 1959; 26(4):569–595.http://www.name-us.org/DefintionsPages/DefinitionsArticles/Acheson1959.pdf

Carruthers BM, van de Sande MI et al. Myalgic encephalomyelitis: International Consensus Criteria. J Intern Med 2011; 270:327–38.

Carruthers BM, van de Sande MI et al. Myalgic Encephalomyelitis – Adult & Paediatric: International Consensus Primer for Medical Practitioners. Published online October 2012.http://www.name-us.org/DefintionsPages/DefinitionsArticles/2012_ICC%20primer.pdf

Fukuda K, Straus SE, Hickie I et al. Chronic fatigue syndrome: a comprehensive approach to its definition and study. Ann Intern Med 1994; 12:953–9.

Nakatomi Y, Mizuno K et al. Neuroinflammation in patients with chronic fatigue syndrome/myalgic encephalomyelitis: An 11C-(R)-PK11195 PET study. J Nucl Med 2014; 55:1–6.

Straus, Stephen. Undated letter on NIH letterhead to Keiji Fukuda quoted and posted online by Craig Maupin in The CFS Report, March 2014 post, CDC AND NIH Officials Discussed "Desirable Outcome" of Seeing A Distinct Illness "Evaporate. ”http://cfidsreport.com/News/14_Chronic_Fatigue_Syndrome_Definition_IOM_Straus.html

Zeineh MM, Kang J, Atlas SW et al. Right arcuate fasciculus abnormality in chronic fatigue syndrome. Radiology 2014; 273(2S). Published online October 29, 2014. 

Monday, November 17, 2014

Cochrane review finds CBT not effective for medically unexplained symptoms

When a physician fails to find a cause for physical symptoms (medically unexplained physical symptoms, or MUPS), the patient is usually given a diagnosis of 'somatoform disorder,' or "it's all in your head."

Somatoform disorder is a relic of Freudian psychology, whose disciples believed that underlying emotional distress could manifest itself in physical symptoms. While it is true that some forms of emotional trauma can produce a release of adrenal hormones, which will in turn raise blood pressure, increase heart rate, and cause other transient physiological symptoms, the idea that emotional distress can cause significant long-term physiological consequences (e.g. gallbladder disease, cancer, etc.) is completely unfounded.

Although there is no scientific basis for somatofom disorder, it has become widely accepted as a diagnosis because it is easier to relegate patients to the dustbin of "it's all in your head" than to devote the necessary time and effort to figure out what might actually be wrong with them. In a medical system in which physicians only have 10 minutes (at most) to spend with a patient, and in which doctors are discouraged from taking their patients' complaints seriously, but instead rely on the results of a few simple tests, the diagnosis of somatoform disorder is a convenient means of disposing of "difficult" patients.

The diagnosis also saves money. National health care systems and insurance companies are especially concerned with costly medical outlays for chronic illnesses, which are becoming increasingly common. They are likely to embrace the idea that MUPS can be treated with comparatively inexpensive therapy, rather than pursue a line of treatment that may involve extensive testing and expensive treatments.

ME/CFS falls into the category of MUPS, and as a consequence many patients with the disease are consigned to psychological therapy. While there has been a great deal of resistance on the part of patients and specialists to the idea that psychological interventions are a legitimate treatment for ME/CFS (treatment being defined as something that can affect the actual course of a disease, rather than provide solace), there has not yet been a careful, unbiased evaluation of therapy in MUPS.

This systematic review found that compared with usual care (which is in most cases minimal) patients with MUPS did slightly better with psychological interventions. However, when compared with enhanced, or specialized, care CBT was not more effective. This finding would seem to be obvious. For example, for patients with heart disease, seeing a cardiologist would clearly be more efficacious than receiving CBT. However, because the "it's all in your head" diagnosis has become so popular, the report could only conclude that CBT was not more effective than enhanced care. This is, in essence, a negative conclusion, but it is still valid as a critique of CBT employed instead of specialized care.

To their credit, the authors pointed out that the studies they evaluated did not include any patients who were unwilling to receive CBT, thereby skewing the results. (If studies only include patients who are positively disposed to receiving CBT, outcomes will be more favorable.) They also pointed out that while no harms were reported, the studies did not include harms as part of their outcome measures. (Absence of evidence does not mean evidence of absence.) They also noted a high drop-out rate, and the fact that the studies were unblinded. When combined, all of these factors can only lead to the conclusion that evidence in support of CBT and other psychological interventions for treating ME/CFS is weak by anybody's standards.

_____________________

Non-pharmacological interventions for somatoform disorders and medically unexplained physical symptoms (MUPS) in adults

By N. Van Dessel et al.


BACKGROUND: Medically unexplained physical symptoms (MUPS) are physical symptoms for which no adequate medical explanation can be found after proper examination. The presence of MUPS is the key feature of conditions known as 'somatoform disorders'. Various psychological and physical therapies have been developed to treat somatoform disorders and MUPS. Although there are several reviews on non-pharmacological interventions for somatoform disorders and MUPS, a complete overview of the whole spectrum is missing.

OBJECTIVES: To assess the effects of non-pharmacological interventions for somatoform disorders (specifically somatisation disorder, undifferentiated somatoform disorder, somatoform disorders unspecified, somatoform autonomic dysfunction, pain disorder, and alternative somatoform diagnoses proposed in the literature) and MUPS in adults, in comparison with treatment as usual, waiting list controls, attention placebo, psychological placebo, enhanced or structured care, and other psychological or physical therapies.

SEARCH METHODS: We searched the Cochrane Depression, Anxiety and Neurosis Review Group's Specialised Register (CCDANCTR) to November 2013. This register includes relevant randomised controlled trials (RCTs) from The Cochrane Library, EMBASE, MEDLINE, and PsycINFO. We ran an additional search on the Cochrane Central Register of Controlled Trials and a cited reference search on the Web of Science. We also searched grey literature, conference proceedings, international trial registers, and relevant systematic reviews.

SELECTION CRITERIA: We included RCTs and cluster randomised controlled trials which involved adults primarily diagnosed with a somatoform disorder or an alternative diagnostic concept of MUPS, who were assigned to a non-pharmacological intervention compared with usual care, waiting list controls, attention or psychological placebo, enhanced care, or another psychological or physical therapy intervention, alone or in combination.

DATA COLLECTION AND ANALYSIS: Four review authors, working in pairs, conducted data extraction and assessment of risk of bias. We resolved disagreements through discussion or consultation with another review author. We pooled data from studies addressing the same comparison using standardised mean differences (SMD) or risk ratios (RR) and a random-effects model. Primary outcomes were severity of somatic symptoms and acceptability of treatment.

MAIN RESULTS: We included 21 studies with 2658 randomised participants. All studies assessed the effectiveness of some form of psychological therapy. We found no studies that included physical therapy.Fourteen studies evaluated forms of cognitive behavioural therapy (CBT); the remainder evaluated behaviour therapies, third-wave CBT (mindfulness), psychodynamic therapies, and integrative therapy. Fifteen included studies compared the studied psychological therapy with usual care or a waiting list. Five studies compared the intervention to enhanced or structured care. Only one study compared cognitive behavioural therapy with behaviour therapy.Across the 21 studies, the mean number of sessions ranged from one to 13, over a period of one day to nine months. Duration of follow-up varied between two weeks and 24 months. Participants were recruited from various healthcare settings and the open population. Duration of symptoms, reported by nine studies, was at least several years, suggesting most participants had chronic symptoms at baseline.

Due to the nature of the intervention, lack of blinding of participants, therapists, and outcome assessors resulted in a high risk of bias on these items for most studies. Eleven studies (52% of studies) reported a loss to follow-up of more than 20%. For other items, most studies were at low risk of bias. Adverse events were seldom reported. For all studies comparing some form of psychological therapy with usual care or a waiting list that could be included in the meta-analysis, the psychological therapy resulted in less severe symptoms at end of treatment (SMD -0.34; 95% confidence interval (CI) -0.53 to -0.16; 10 studies, 1081 analysed participants). This effect was considered small to medium; heterogeneity was moderate and overall quality of the evidence was low. Compared with usual care, psychological therapies resulted in a 7% higher proportion of drop-outs during treatment (RR acceptability 0.93; 95% CI 0.88 to 0.99; 14 studies, 1644 participants; moderate-quality evidence). Removing one outlier study reduced the difference to 5%.

Results for the subgroup of studies comparing CBT with usual care were similar to those in the whole group. Five studies (624 analysed participants) assessed symptom severity comparing some psychological therapy with enhanced care, and found no clear evidence of a difference at end of treatment (pooled SMD -0.19; 95% CI -0.43 to 0.04; considerable heterogeneity; low-quality evidence). Five studies (679 participants) showed that psychological therapies were somewhat less acceptable in terms of drop-outs than enhanced care (RR 0.93; 95% CI 0.87 to 1.00; moderate-quality evidence).


AUTHORS' CONCLUSIONS: When all psychological therapies included this review were combined they were superior to usual care or waiting list in terms of reduction of symptom severity, but effect sizes were small. As a single treatment, only CBT has been adequately studied to allow tentative conclusions for practice to be drawn. Compared with usual care or waiting list conditions, CBT reduced somatic symptoms, with a small effect and substantial differences in effects between CBT studies. The effects were durable within and after one year of follow-up.

Compared with enhanced or structured care, psychological therapies generally were not more effective for most of the outcomes. Compared with enhanced care, CBT was not more effective. The overall quality of evidence contributing to this review was rated low to moderate.The intervention groups reported no major harms. However, as most studies did not describe adverse events as an explicit outcome measure, this result has to be interpreted with caution.An important issue was that all studies in this review included participants who were willing to receive psychological treatment. In daily practice, there is also a substantial proportion of participants not willing to accept psychological treatments for somatoform disorders or MUPS. It is unclear how large this group is and how this influences the relevance of CBT in clinical practice.The number of studies investigating various treatment modalities (other than CBT) needs to be increased; this is especially relevant for studies concerning physical therapies. Future studies should include participants from a variety of age groups; they should also make efforts to blind outcome assessors and to conduct follow-up assessments until at least one year after the end of treatment.


Source
: Van Dessel N, Den Boeft M, van der Wouden JC, Kleinstäuber M, Leone SS, Terluin B, Numans ME, van der Horst HE, van Marwijk H. Cochrane Database Syst Rev. 2014 Nov 1;11:CD011142. [Epub ahead of print]

Friday, November 14, 2014

"Government unreasonable": Judge Vince Chhabria orders HHS and NIH to pay fees in FOIA suit

On January 9, 2014, Attorney Jeannette Burmeister filed a federal lawsuit against HHS and NIH in the U.S. District Court for the Northern District of California for failure to comply with the requirements of the Freedom of Information Act (FOIA) regarding documents she requested relating to the Institute of Medicine (IOM) “study” of diagnostic criteria for myalgic encephalomyelitis/chronic fatigue syndrome. 

On September 2, the Court ordered the government to comply with Attorney Burmeister’s request. You can read the full complaint HERE.

Federal Court awards $139,147 in Attorneys’ Fees Against HHS and NIH in IOM FOIA Case

Reprinted with the kind permission of Jeannette Burmeister and Thoughts About ME.

By Jeannette Burmeister

The U.S. District for the Northern District of California awarded me today–having won my FOIA lawsuit–my entire attorneys’ fees in the amount of $139,147. Judge Vince Chhabria ordered the defendants, HHS and NIH, to pay me these fees. Please see below for a copy of the order.

In the Court’s order, the Judge noted:
Ms. Burmeister is clearly the prevailing party in the litigation. Moreover, as outlined in the order granting Ms. Burmeister’s motion for summary judgment, the government’s conduct throughout its dispute with Ms. Burmeister was unreasonable. Ms. Burmeister stood to gain nothing financially from her attempt to obtain documents at issue from the government, and she conferred a benefit on the public through her successful effort to obtain a ruling against the government. [emphasis added]
The defendants’ conduct in this matter has been absolutely deplorable. They have fought tooth and nail trying to avoid compliance with federal law and to delay production of relevant documents relating to the IOM project as long as possible. Throughout the entire proceedings, the defendants have acted unreasonably and shamefully, really, in their relentless attempts to circumvent their obligations under FOIA. Their inexcusable conduct has put me through the wringer, which has had a direct and dramatic impact on my health. I will share with the community, at a later time, details of the many instances of the defendants’ appalling actions in this matter. But here is a high-level list:

The defendants failed to make a determination in response to my FOIA request (from more than a year ago, seeking documents relating to the IOM contract with HHS) within the 20 business days required by FOIA. I waited several weeks and sent them one last communication notifying them that legal action was imminent. When they still did not respond, I brought my suit pro se, i.e. I was representing myself in an attempt to avoid attorneys’ fees. After I filed the lawsuit, defendants produced a mere 88 pages, only 22 relating specifically to the IOM (one of them blank), for a very high-priority and extraordinarily controversial $1 million project. It was clear that their search and production of documents was woefully inadequate (as the Court later agreed when it granted my motion for summary judgment). The defendant’s subsequent response to my complaint was, once again, late. It was then that I realized that they had no intention of complying with the law in response to my entirely reasonable and very straightforward FOIA request, even faced with a lawsuit.
Therefore, I hired the law firm of Baker & McKenzie LLP.

Every taxpayer dollar spent by HHS and NIH in this lawsuit–every single one–was caused by the government’s appalling tactics. Instead of remedying the inadequate search and production, they went into full-blown attack mode, filing a meritless and unwarranted motion, making frivolous legal arguments, making false statements under penalty of perjury, misrepresenting my statements and actions, misrepresenting legal authority, etc. They went so far as to accuse me of lying under penalty of perjury, which shows their mindset very clearly: Since they had no qualms about blatantly misrepresenting the facts, they thought accusing me of the same might work. It didn’t.

A few days ago, in response to the Judge’s order from September to produce all documents I sought, Counsel for defendants delivered about 4,300 pages of supposedly responsive documents demonstrating very clearly the laughable number of documents originally produced. A cursory review of those documents shows that their misrepresentations–again made under penalty of perjury and in opposing Counsel’s motions–were far worse than it initially appeared. It is also obvious that this new production is again inadequate and does not comply with FOIA in many respects.

The community will be extremely interested in seeing the documents that they produced recently. I will make every effort to publish those of interest (I will save myself the energy of publishing the NICE guidelines or the IOM Gulf War Report from earlier this year.) as quickly as possible, but my health has been very poor as a result of this litigation, so I ask for some patience.

I want to thank Patricia Carter, the owner of MECFS Forums, for providing a helpful declaration in support of my attorneys’ fees motion. I also want to especially thank Eileen Holderman, the former and most effective patient representative on CFSAC in its history, for her invaluable assistance, including providing a declaration in support of my motion. Finally, my sincere thanks go to my attorneys, Bruce Jackson, Edward Burmeister and Christina Wong, as well as paralegal, Nada Hitti, and assistant, Chris von Seeburg, for their unflagging efforts and excellent representation in this case.

Note: I owe the entire amount to Baker & McKenzie and I would have had to pay it regardless of whether the Court had awarded me the fees. What I am saying is that I don’t get to keep the money, just to avoid a misunderstanding on that front.







Tuesday, November 11, 2014

Successful Treatment of GWI with CoQ10: Implications for ME/CFS?

Beatrice A. Golomb has been researching Gulf War Illness for over two decades. In 1999 she published a paper, A Review of the Scientific Literature As It Pertains to Gulf War Illnesses; Pyridostigmine Bromide, implicating acetycholinesterase inhibitors as primary contributors to the development of GWI. (Fifteen years later, the Boston University School of Public Health confirmed her findings.) Golomb is the head of the UC San Diego Research Group, where she and other researchers study conditions related to oxidative stress and energy impairments.

Golomb recently finished a clinical trial using CoQ10 as a treatment for GWI. The results were impressive: 80% of treated veterans showed improved physical function after taking PharmaNord (Denmark) CoQ10 100 mg/day for 14 weeks. (You can read the abstract HERE.)

Oxidative stress and mitochondrial impairment are major players in ME/CFS, which is why there is so much overlap between the symptoms of GWI and ME/CFS. This is also why CoQ10 has been a staple in ME/CFS treatment arsenal since the late 1980s, when the Behans noted damage to the mitochondria in muscle tissues of ME patients in the UK.

_______________________________________


Coenzyme Q10 Helps Veterans Battle Gulf War Illness Symptoms

Press Release: UC San Diego, November 3, 2014. Roughly one-third of the 700,000 United States troops who fought in the 1990-1991 Persian Gulf War have subsequently developed a distinct set of chronic health problems, dubbed Gulf War illness. Their symptoms, from fatigue, muscle pain and weakness to decreased cognitive function and gastrointestinal and skin problems, persist decades after the conflict.

In a study published in the Nov. 1 issue of Neural Computation,  researchers at the University of California, San Diego School of Medicine report  that a high quality brand of coenzyme Q10 (CoQ10) – a compound commonly sold as a dietary supplement – provides  health benefits to persons suffering from Gulf War illness symptoms.

Forty-six United States Gulf War veterans participated in the randomized, double-blind, placebo-controlled study. Each veteran had been diagnosed with Gulf War illness.

“Gulf War illness is not the same as post-traumatic stress disorder or traumatic brain injury, signature illnesses of later deployments, which are caused by psychological and mechanical injury, respectively,” said Beatrice Golomb, MD, PhD, professor of medicine at UC San Diego School of Medicine and principal investigator on the study. “Evidence instead links Gulf War illness to chemical exposures, such as pesticides or pills given to soldiers to protect them from possible nerve agents. These chemicals can damage mitochondria, which generate the energy our cells need to do their jobs. When these powerhouses of the cells are disrupted, it can produce symptoms compatible with those seen in Gulf War illness.”

The connection to chemical and toxin exposures is fortified by evidence of mitochondrial problems in affected veterans, said Golomb, as well as evidence showing those veterans who became ill are significantly more likely than others to harbor genetic variants that render their enzymes less effective at detoxifying these chemicals.

CoQ10 is a fat-soluble antioxidant made by the body to support basic cell functions, including directly assisting mitochondrial energy production. Over a course of three and a half months, the veterans in the study received a pill form of either CoQ10 or a placebo. Researchers found 80 percent of those who received 100mg of CoQ10 had improvement in physical function. The degree of improvement correlated to the degree in which CoQ10 levels in the blood increased.

The researchers reported that Gulf War illness symptoms like headaches, fatigue with exertion, irritability, recall problems and muscle pain also improved.

“The statistical significance of these benefits, despite the small sample size, underscores the large magnitude of the effects,” Golomb said. “Mounting evidence suggests findings in Gulf War illness are relevant to toxin-induced health problems in the civilian sector, so what we learn by studying health challenges of these veterans, will likely benefit others.”

Golomb and colleagues are seeking additional funding to test a more complete “mitochondrial cocktail,” which combines CoQ10 with additional nutrients that support cell energy and reduce oxidative damage to cells.

Co-authors include:  Matthew Allison, Sabrina Koperski, Hayley J. Koslik and Janis B. Richie, all at UC San Diego; and Sridevi Devaraj, Baylor College of Medicine/ Texas Children’s Hospital and Health Center.

Funding support for this research came, in part, from the Department of Defense.

Journal Reference: Beatrice A. Golomb, Matthew Allison, Sabrina Koperski, Hayley J. Koslik, Sridevi Devaraj, Janis B. Ritchie. Coenzyme Q10 Benefits Symptoms in Gulf War Veterans: Results of a Randomized Double-Blind Study. Neural Computation, 2014; 26 (11): 2594 DOI: 10.1162/NECO_a_00659

Wednesday, November 5, 2014

The Elephant in the Room: Brain Studies, Politics, and ME/CFS

The recent national attention generated by Stanford's brain study of ME/CFS patients could not have come at a better time. 

The news that people with ME/CFS have a problem in their brains is not really news (although medical studies proving it are always welcome). After all, the name myalgic encephalomyelitis is a clear indication that brain involvement is key to the disease.

What makes the Stanford study special is not that it shows several anomalies, but that it was accompanied by huge amount of press. Coincidentally, the news that "CFS is real" (to quote USA Today) comes at a time when HHS seems hell-bent on proving that it isn't.

In one month, the P2P panel will meet to decide the financial fate of ME/CFS research. If the panel decides that ME/CFS can be cured with "a talk and a walk" (CBT and GET), it will be going head-to-head with the Stanford University School of Medicine, which is not only one of the most prestigious institutions in the country, but one that leaves any panel or committee assembled by HHS in the dust.

Up until now, the P2P and IOM efforts to redefine ME/CFS have been primarily opposed by ME/CFS patients, advocates and specialists. But with the publicity generated by the Stanford study, it now appears as if at least one major institution is also tacitly weighing in. 

And Stanford will be hard to ignore. 

For those who are interested in previous studies that have shown CNS and brain anomalies in ME/CFS, I have posted an excerpt from Chronic Fatigue Syndrome: A Treatment Guide, 2nd Edition below. To get a sense of the quantity of research that has been done, I invite you to look at the research section. (The 2014 study, Neuroinflammation in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis by Nakatomi et al. is not on the list.)

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CNS Involvement and Goldstein's Limbic Hypothesis

In the early 1990s, Dr. Jay Goldstein, a psychiatrist and psychopharmacologist (now deceased), developed a theory in which he proposed that CFS/ME was the result of an insult to the limbic system, which is composed of structures relating to the hypothalamus, such as the hippocampus, amygdala, cingulate gyrus, and dentate gyrus. The limbic system is an area located deep in the brain just above the brainstem, and is involved with memory, emotion, and regulation of the autonomic nervous system. This last function is of critical importance to maintaining homeostasis in the body, as the autonomic nervous system regulates appetite, body temperature, blood pressure, blood sugar, sleep, wakefulness, heart rate, digestion – in short, nearly every physiological function necessary for maintaining life.

Dr. Goldstein's theory, as laid out in his book, Betrayal by the Brain, was that CFS/ME is essentially a communication problem between the limbic system and the rest of the nervous system. His “limbic hypothesis” essentially states that no matter what the underlying cause of CFS/ME, the result is an injury (encephalopathy) to the limbic system, which subsequently causes widespread neuroimmune dysfunction. He identified CFS/ME as a “neurosomatic” illness, that is, a disorder of central nervous system processing. Dr. Goldstein based his theory on what he knew of the brain, which was substantial, as well as what he had observed of his patients' reactions to various psychotropic medications. In one sense, Dr. Goldstein was old-fashioned; he followed a time-honored scientific practice – observation. Recent studies, however, have shown that Dr. Goldstein was actually far ahead of his time, if not prescient.

Currently, there seems to be no doubt of central nervous system (CNS) involvement in CFS/ME, and a variety of approaches have been used to measure its extent. Typically, psychologists have employed cognitive tests to measure the overall performance of patients, while neurologists have used brain scans: MRIs to locate structural damage, functional MRIs to measure brain activation, SPECT scans to measure blood flow, PET scans to measure glucose uptake, and MR Spectroscopy to measure biochemicals associated with inflammation inside the brain.

Cognitive deficits, because they among the most frequently reported causes of disability in CFS/ME patients, have received a considerable amount of attention from researchers. Dozens of studies have been performed in an effort to categorize the nature of these deficits, quantify them, and distinguish these cognitive deficits from those produced by other disorders (in most cases, depression). In general, the studies have revealed that patients with CFS/ME do, in fact, suffer from the very problems they report – slow processing of information, lack of concentration, and so forth. Researchers have found that people with CFS/ME have problems processing auditory information, experience mental fatigue quickly, and cannot multitask. These results are buttressed by studies such as those by Majer et al and Marcel et al, which show that cognitive impairment in people with CFS/ME is independent of depression, a disorder with which CFS/ME is often confused.

The most informative cognitive studies are those which have measured brain function during the performance of tasks requiring mental effort. Tanaka et al, in 2006, used functional magnetic resonance imaging (fMRI) to demonstrate distractibility in CFS/ME patients. In this study, subjects were given a visual task to perform while listening to intermittent noise. Over the course of the task, people with CFS/ME showed reduced responsiveness in the areas of the brain associated with task performance, demonstrating an inability to focus on a task while receiving simultaneous input from competing stimuli. A previous study by de Lange et al showed that given a visual and simultaneous motor task, patients with CFS/ME solved the motor imagery task by using additional cerebral regions supporting visual processes. The authors suggested that CFS/ME patients might rely on visual imagery to compensate for dysfunctional motor planning.

Tests of working memory also show impairments. Caseras et al conducted an fMRI study to objectively compare brain activity in 17 CFS/ME patients with 12 controls during a test of working memory. The study revealed significant differences in brain activation between the two groups. CFS/ME patients showed greater activation than control subjects in areas associated with working memory (prefrontal regions). Under more challenging conditions, patients, but not controls, showed a significantly activated large cluster in the right inferior/medial temporal cortex (an area associated with working memory and attention). These findings are consistent with earlier studies demonstrating that patients with CFS/ME could perform as well as controls, but that the effort involved greater brain activity.

A subsequent functional MRI study conducted by Cook et al confirmed that several areas of the brain are activated to a greater extent in CFS/ME patients compared to controls during challenging cognitive tasks. During a task that required no mental effort (finger tapping), neither patients nor controls showed significant differences in activation or fatigue. However, when presented with a complex mental task involving attention, working memory, and executive function, patient perceptions of fatigue correlated with brain activation: the greater the brain activity, the greater the fatigue.

Given that fatigue is the result of work of any kind, whether physical or mental, the conclusion that CFS/ME patients are more easily fatigued by mental effort than healthy people seems obvious. However, most cognitive studies are based on the assumption that people with CFS/ME merely “feel” fatigued. There is a lingering suspicion that the mental exhaustion experienced by people with CFS/ME may be form of neurosis unless physiological correlates can be identified.

In this regard, brain scans have been of enormous interest to the CFS/ME community because they provide concrete proof of neurological impairment. Dr. Ismael Mena and Dr. Jay Goldstein pioneered the use of SPECT (Single-photon Emission Computed Tomography) to document brain abnormalities in CFS/ME patients. SPECT scans measure blood flow in the brain, as opposed to MRIs, which show structure. Studies in the 1990s by Mena, Goldstein, Richardson, and Costa showed brainstem hypoperfusion (low blood flow) in a high percentage of CFS/ME patients.

In 1998 the late John Richardson conducted SPECT scans on some of his patients suffering from ME. The scans showed hypoperfusion in 90% of the patients in several areas. These included the brainstem (62%), the caudate nuclei in the basal ganglia (51%), temporal lobes (62%), parietal lobes (31%), and frontal lobes (23%).

A group of Australian researchers led by R. Casse also found a deficit in regional cerebral blood flow in similar areas: the brainstem, left medial temporal lobe, right medial temporal lobe, frontal lobe, and anterior cingulate gyrus. These are the areas of the brain responsible for auditory processing, attention, autonomic nervous system regulation, memory, sleep and pain.

The most recent studies to show brain hypoperfusion in CFS/ME have not used SPECT scans, but a xenon-CT. This type of scan measures the uptake of xenon gas by the brain. (When the gas is inhaled, it is distributed through the brain via the bloodstream.) Using this technique, Yoshiuchi et al found that patients with CFS/ME have reduced absolute cortical blood flow in broad areas when compared with healthy controls. Non-depressed patients with CFS/ME had reduced cortical blood flow in both right and left middle cerebral arteries. The authors concluded that their data supported earlier findings that CFS/ME patients without depression are the group most at risk for having symptoms due to brain dysfunction. In a 2011 study by Biswal et al, 9 of 11 patients with CFS/ME showed broad decreases in cerebral blood flow compared to healthy controls. While these are small studies, they are significant in that they used a different tool to confirm hypoperfusion.

Small lesions, called “unidentified bright objects” (UBOs), often appear on the MRIs of CFS/ME patients. UBOs are often ignored by radiologists unless they are profuse and accompanied by signs of MS or other neurological injury, such as stroke. However, CFS/ME researchers have repeatedly stressed the significance of UBOs, which have appeared on the MRIs of CFS/ME patients since the first scans were performed in the 1980s.

Coincidentally, the first MRI scanner in Reno, Nevada was being set up by Dr. Royce Biddle just as the Lake Tahoe outbreak occurred. From 1985 to 1988 Dr. Biddle performed hundreds of MRI scans on patients seen by Dr. Peterson and Dr. Cheney. In conjunction with Dr. Buchwald, and Drs. Komaroff and Jolesz of Harvard, scans of 142 patients were analyzed. UBOs were found in 79% of the scans. While Dr. Biddle could not definitively state that the UBOs were pathological, he theorized that the disease might involve edema in perivascular spaces.

As far as brain structure in CFS/ME is concerned, the most dramatic studies have been those showing loss of brain matter. In 2004 Okada et al found that patients with CFS/ME had reduced gray matter volume in the bilateral prefrontal cortex. Furthermore, the volume reduction in the right prefrontal cortex paralleled the severity of the fatigue of the subjects (the lower the volume, the more fatigued the subject). The researchers concluded that the fatigue experienced by people with CFS/ME was central, that is, the difficulty in the initiation of and the ability to sustain voluntary activities was generated in the brain.

In 2006 a group of researchers in Holland led by de Lange, mapped structural brain structure and volume in two cohorts of CFS patients (28 patients total) and 28 healthy controls with high-resolution structural magnetic resonance images using voxel-based morphometry, a form of statistical analysis that measures the shape, size and position of brain structures. The de Lange study found “substantial and consistent” reductions in gray matter volume in two groups of CFS/ME patients as compared with controls.

A subsequent study in 2011 by Barnden et al found reductions in both white and gray matter. In the midbrain, white matter volume was decreased, while vascular abnormalities were observed in the brainstem, midbrain gray matter, deep prefrontal white matter, caudal basal pons, and hypothalamus. According to the authors, their findings were consistent with an injury to the midbrain at the onset of the illness, which could affect many feedback control loops, resulting in suppressed CNS motor and cognitive activity and a disruption of homeostasis.

Significantly, this type of injury would include resetting some elements of the autonomic nervous system, which might account for why people with CFS/ME experience increased sympathetic nervous system arousal. In line with the findings of this study, Claypoole et al found that sudden onset was predictive of cognitive impairment, particularly reduced speed in processing information.

In the same year, Puri et al conducted a large voxel-based morphometry study comparing 26 CFS/ME patients with 26 healthy volunteers matched for age and gender. Reduced gray matter volume in the CFS/ME group was noted in the occipital lobes (right and left occipital poles; left lateral occipital cortex, superior division; and left supracalcrine cortex), the right angular gyrus and the posterior division of the left parahippocampal gyrus. Reduced white matter volume in the CFS/ME group was also noted in the left occipital lobe. The authors concluded that their data supported the hypothesis that “significant neuroanatomical changes occur in CFS, and are consistent with the complaint of impaired memory that is common in this illness.” Their data also indicated that “subtle abnormalities in visual processing, and discrepancies between intended actions and consequent movements, may occur in CFS/ME.”

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Biswala, Bharat, Pratap Kunwarb, Benjamin H. Natelson. “Cerebral blood flow is reduced in chronic fatigue syndrome as assessed by arterial spin labeling.” J Neurol Sci. 2011 Feb 15;301(1-2):9-11. http://www.sciencedirect.com/science/article/pii/S0022510X10005666

Capuron L, Welberg L, Heim C, Wagner D, Solomon L, Papanicolaou DA, Craddock RC, Miller AH, Reeves WC. “Cognitive dysfunction relates to subjective report of mental fatigue in patients with chronic fatigue syndrome.” Neuropsychopharmacology. 2006 Aug;31(8):1777-84. http://www.ncbi.nlm.nih.gov/pubmed/16395303 (Abstract)

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Monday, November 3, 2014

The P2P Posts Its Agenda: Are They Kidding?

The P2P will be holding its Workshop on ME/CFS on December 9 and 10 in Washington, DC. For two days the panel, which is composed entirely of non-experts, will be hearing "testimony" regarding the diagnosis, treatment, research and case definition of ME/CFS. 

While Jennie Spotila (see below) has correctly pointed out that psychologists dominate the treatment research portion of the workshop, it is also worth noting that out of the 21 participants (total), nine work either in the field of psychology or psychiatry. That's nearly half.

(David M. Murray holds a PhD in Psychology, as does Susan Maier. Leonard Jason is a psychologist, and Abigail Brown, with whom Dr. Jason has authored several papers, is also in the psychology department at DePaul University. Dedra Buchwald and Niloofar Afari are psychologists. Dr. Clauw is in the Department of Psychiatry at the University of Michigan. Fred Friedberg is in the Department of Psychiatry at Stony Brook. Renee Taylor is a clinical psychologist.)

Regardless of the worthy contributions of psychologists to the field of ME/CFS research (I am referring here to Dr. Jason and his colleagues), it is important to note that the predominance of psychology in this meeting means that other fields - notably neurology, endocrinology, and immunology, the areas in which the most significant ME/CFS clinical and research studies have been published - have been shortchanged. And in spite of Susan Maier's concern that "fatigue" is a public health problem, there was no attempt to include an expert in infectious diseases. (Considering the 60+ documented outbreaks of ME/CFS, the omission of a specialist in this area is unforgivable.)

Looking at the December agenda, it is clear that the P2P is intending to come up with nothing more than a reiteration of well-worn prejudices and outdated myths. What is not clear is how they will deal with the recent national attention garnered by the Stanford brain study.

In a game of chicken in which one car is the federal government with all its entrenched mediocrity, and the other is one of the nation's most prestigious medical schools, who will swerve first?

Related posts: Advocates to NIH - "Pull the P2P!"




How to Oppose the P2P (Without Chaining Yourself to the White House Fence)
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P2P Agenda: What the Huh?


Posted on October 31, 2014 on Occupy CFS

Reprinted with permission from Jennie Spotila.

By Jennie Spotila

Less than six weeks from the NIH P2P Workshop on ME/CFS, and we now have an agenda with speakers and talk titles.  So is it good or bad?

I reached out to the six ME/CFS members of the Working Groups for their thoughts on the agenda. Dr. Suzanne Vernon told me, “[T]he agenda uses a comparative effectiveness approach and format to address the key questions initially posed by the working group.  I think they’ve invited a relatively good mix of speakers with a range of expertise and experience to help inform the panel.” Three members did not respond and one responded but did not comment. The sixth member of the Working Group would only comment off the record, and said that some of the line up was solid but some of it was disappointing.

I agree that there are some bona fide experts on the agenda, speakers like Dr. Jason, Dr. Nacul, Dr. Klimas, and Dr. Snell. They are obvious choices for their expertise. But then there are some speakers that made me stop and think “What the what? Are you kidding me?”

The Problematic Cluster

The second main topic of the Workshop is titled: “Given the unique challenges of ME/CFS, how can we foster innovative research to enhance the development of treatments for patients?” This is a critical question, and brings to mind things like centralized data repositories, the case definition issue, drug repurposing, or systems networking and bioinformatics work like that of Dr. Gordon Broderick or Dr. Patrick McGowan.

Instead, this section focuses on studying diseases other than ME/CFS as a way to back into ME/CFS results. I’m fully in favor of out of the box thinking and learning from other scientific areas. Autoimmune and autoinflammatory diseases come to mind as one promising area. But that’s not what we’ll hear at the P2P Workshop.

The Speakers

The three speakers for this section are Dr. Dedra Buchwald, Dr. Dan Clauw, and Dr. Niloofar Afari. If anyone thought that psychosocial theories and functional somatic syndromes would not make an appearance at the Workshop, I’m afraid I must correct your false workshop belief.

Dr. Dedra Buchwald has been a CFS researcher for years, heading one of the ill-fated NIH CFS Research Centers more than a decade ago. She has built a large twin registry at the University of Washington, and has developed broad expertise in Native American health issues and studies. But her work on chronic fatigue syndrome is controversial.

Many of Dr. Buchwald’s publications focus on the predisposing role of trauma in CFS, the high rates of depression and anxiety in CFS, and an integrative view that blends it with FM and a broad view of the illness.

As just one example, Dr. Buchwald co-authored a topic summary on CFS with Dr. Craig Sawchuk (who did his postdoc work with Dr. Buchwald and was co-director of the Harborview Chronic Fatigue Clinic). This summary includes many elements from the integrative or psychosocial model of CFS. Under risk factors, the guide states, “Premorbid psychiatric illness can increase risk for CFS, including personality traits such as ‘action-proneness’ and emotional instability,” and “Historical patterns of persistent over- and underactivity levels may confer risk for CFS in adulthood.” For treatment, pharmacotherapies are not recommended, except for comorbid disorders. “CBT and graduated exercise therapy have the greatest cost effectiveness and probability of yielding symptom and functional improvements.” Exercise begins with 5-minute periods of aerobic exercise five times a week. CBT is “designed to modify thoughts, behaviors, and environmental contingencies that are maintaining or exacerbating symptoms and impairments.” Finally, “Treatment-resistant patients should be referred to a mental health professional.”

These kinds of recommendations are familiar to every patient with ME/CFS. It is a view of the disease based on disordered patient perception and secondary deconditioning. This view persists in the face of thousands of papers to the contrary. All the contrary data – and there is a lot of it – is ignored.

Dr. Dan Clauw is Director of the Chronic Pain and Fatigue Research Center at the University of Michigan. His focus has been fibromylagia and the “chronic multisymptom illnesses,” such as CFS and GWI, that accompany it.  Dr. Clauw treats FM with a balanced approach using both medication and exercise/CBT. He has extensive connections to pharmaceutical companies, including funding from Eli Lily to create FibroGuide, a CBT program for people with FM.

Dr. Clauw spoke at the P2P Workshop on Opioids and Chronic Pain at the end of September, and some of his comments were surprising, to say the least. Using the term “fibromyalgianess,” Dr. Clauw favors using a self-report questionnaire rather than “a stupid tender point count.” Acknowledging that he was being provocative, Dr. Clauw said, “I view opioids as the Kardashians in the chronic pain field. And the reason I say that is that I think they receive an undue amount of attention. We should really have just stopped the meeting after we went through all those slides showing that they’re not efficacious in chronic pain.” Then there was this gem:
I also think we can probably prevent the transition from chronic nociceptive pain to chronic centralized pain. I think that that’s something that we likely…. I can with a reasonable degree of accuracy, I can look at someone’s medical record at age 20 and tell you if they’re going to develop fibromyalgia at age 40. They would already have 2 or 3 regional pain syndromes by their early 20s and they’re marching down this course and we don’t do anything right now to try to do primary or secondary prevention and I think  most of us feel that fibromyalgia’s just sort of the end of a continuum.
I appreciate that Dr. Clauw is saying that early and adequate treatment of pain can prevent that pain from becoming chronic and refractory to treatment. But claiming he can look at the chart of a 20 year old and predict whether they will have FM? Really? Do you know what my chart looked like up until age 26? Perfectly clean, healthy, with a few short acute infections that fully resolved, and absolutely no other medical or psychological problems of any kind. Then I got sick with an apparent viral infection and here I am 20 years later, in my 40s, with ME/CFS and FM and POTS. The claim that this could be predicted from my chart at age 20 is ridiculous.

Dr. Niloofar Afari is a psychologist who was Associate Director of Dr. Buchwald’s center from 1998 to 2006, and is now at UC San Diego. Much of her work has focused on twin registry projects and treating a number of pain conditions. One of her more recent papers is an examination of the association between psychological trauma and functional somatic syndromes like CFS and FM. The study found that people with trauma were 2.7 times more likely to have a functional somatic syndrome, and CFS was included in that category.

Drs. Buchwald, Clauw and Afari overlap each other to a great degree. They have co-authored papers together, they’ve worked together. Their views on ME/CFS are at the opposite end of the spectrum from researchers like Dr. Klimas, Dr. Jason or Dr. Montoya. Having an opposite view does not automatically disqualify them from speaking at the Workshop, in my opinion. But their presence on the agenda, especially in the context of fostering innovative research, is a huge red flag.

We already have a systematic evidence review that combined eight ME and CFS case definitions, despite stated misgivings that it could include people without the disease. Layered on that, we have this attempt to create innovative research by looking at overlapping and co-morbid conditions – but only functional somatic syndromes. The Workshop is not going to look at the co-morbidities of orthostatic intolerance, Lyme disease, reactivated viral infections, cancers, or Ehlers-Danlos syndrome. Nor is it going to draw clean lines around ME/CFS for research purposes. If anything, this paves the way for broader cohorts. ME/CFS research and the care of ME/CFS patients will not be advanced through this dangerous sinkhole of examining trauma or lumping our already overly broad category into the shapeless mass of “fibromyalgianess.” Studying so-called functional somatic syndromes is not innovative research; this approach is outdated, and brings confusion instead of clarity to ME/CFS research.

The Overlap

There’s another layer of weird overlap, in addition to the research/publishing overlap of Buchwald, Clauw and Afari.

In 2012, NIH hosted a Workshop on Overlapping Chronic Pain Conditions. The meeting was co-chaired by Dr. Clauw and Dr. Beth Unger. Among the talks were:
  • Overview of the meeting and chronic overlapping pain conditions by Dr. Clauw
  • Understanding chronic overlapping pain conditions: Lessons learned from twin studies by Dr. Afari
  • What has the CDC’s ME/CFS program taught us about overlapping conditions? by Dr. Unger
  • Overlapping pain conditions: Disparities and special populations by Dr. Carmen Green (University of Michigan)
That last talk is important, because Dr. Carmen Green is the chairman of our P2P Panel. Dr. Green is on the faculty of the University of Michigan, as is Dr. Clauw. She is also a member of the Interagency Pain Research Coordinating Committee (IPRCC). Dr. Green and Dr. Unger serve together on the subcommittee on Public Health Disparities for the IPRCC.

Does this seem weird? One section of the P2P Workshop is being given to Buchwald, Clauw and Afari, who have published together and share a particular disease view of ME/CFS. Then we throw in this 2012 meeting, which Dr. Unger co-chaired with Dr. Clauw, and where she spoke about what CDC’s program on ME/CFS can teach us about overlapping conditions. Also presenting at that meeting was Dr. Green, who not only serves on the IPRCC, but also serves on a subcommittee of IPRCC with Dr. Unger.

ME/CFS is a small field, and there is going to be overlap among researchers, meetings, and programs. That overlap does not in and of itself disqualify anyone from participating in other activities like this Workshop. But recall that the P2P Panel is selected by NIH to be ME/CFS bias-free. The idea is to form an impartial “jury” that has not researched or treated people with ME/CFS. We already have a high obstacle given that 85% of doctors believe CFS is wholly or partially psychological, so finding a blank slate group of experts was always going to be a challenge.

We can’t know for sure what Dr. Green’s views are, especially as the Panel selection process has been completely hidden from the public. She may or may not share views with Unger, Clauw, Afari or Buchwald. Maybe she thinks they’re wrong, or maybe she is keeping an open mind and will listen to all the speakers. But the overlaps here are a cause for concern.

Now someone could very well say, Hey, you’re not complaining about the overlap between Klimas and Natelson on the IOM committee and this meeting. Or the connections between Dr. Jason, Dr. Taylor and Ms. Brown. But Dr. Green is the P2P Panel Chair, and so her connections with some speakers who view CFS as part of a broader morass of fatigue and pain conditions is a legitimate concern.

Old Guard

This looks like old guard NIH. That “innovative research” section represents the same disease view that filled the CFS Special Emphasis Panel with experts on TMJ and FM. It is the disease view that refuses to acknowledge the muddle of case definitions, including the disproportionate selection of people with primary depression. This is the disease view that, as stated on the draft agenda I received through FOIA, has Dr. Susan Maier speaking about “overwhelming fatigue or malaise as a public health problem.”

The first part of the equation is the fundamentally flawed evidence review that ignored all of the most promising biomarker and treatment research. Add that to this Workshop which has an entire section based on the innovative old view of CFS as a condition perpetuated by deconditioning and emotional problems. What can we expect the sum of those two factors to be? Speakers like Klimas, Snell, Jason and others have an uphill climb to present all the evidence that contradicts this old guard view, and succeed in convincing the unknown Panelists that it is time for NIH to move forward.