Why the International Consensus Criteria for ME needs to be immediately adopted.

Why There Is an Urgent Need to Widely Distribute the Myalgic Encephalomyelitis International Consensus Primer to Doctors

by Jerrold Spinhirne, December 17, 2014

A guest post today. With the radiation catastophes of Fukushima, WIPP, Honeywell, etc., and the enterovirus epidemics getting underway, proper diagnostic criteria is vital, and there is an immediate need to obtain biomarkers so that effective treatments can be found. The ICC is the only document I have found that describes this disease adequately.

The confusion and delay resulting from the recent December 9-10, 2014 National Institutes of Health (NIH) Pathways to Prevention (P2P) Workshop on “ME/CFS” and the issuance of the Agency for Healthcare Research and Quality (AHRQ) Evidence Report No. 219 “Diagnosis and Treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome” [Smith, 2014] emphasize the urgent need for the 2011 Myalgic Encephalomyelitis: International Consensus Criteria (ICC) [Carruthers, 2011] and particularly the 2012 International Consensus Primer for Medical Practitioners (IC Primer or ICP) [Carruthers. 2012], to be widely distributed to doctors, medical personnel, medical professional organizations, medical schools, and hospitals in the US. The reasons why this is necessary are as follows:

Myalgic Encephalomyelitis Is Not a Fatigue Syndrome

Myalgic encephalomyelitis (ME) is a distinct neurological disease described in the medical literature since the 1930s [Gilliam, 1938] and recognized by the World Health Organization (WHO) since 1969. Classic descriptions of the disease, based on thousands of cases, [Acheson, 1959; Ramsay, 1986] and the 2011 ME ICC [Carruthers, 2011] do NOT list unexplained fatigue, or any type of perceived, self-reported fatigue, as a diagnostically useful symptom of ME. Table 2 on page 14 of the AHRQ report [Smith, 2014] clearly shows that of the eight case definitions considered by the report, only the ME International Consensus Criteria case definition does not use fatigue as a criterion for diagnosis.

Indeed, people with ME do experience profound fatigue, but so do people with other serious neurological diseases such as multiple sclerosis (MS) and other forms of damage to the brain such as traumatic brain injury (TBI). Self-reported fatigue is a common feature of many medical diseases and psychiatric disorders, and, therefore, is not useful for making a differential diagnosis. Self-reported fatigue is a subjective and often retrospectively recalled experience that cannot be objectively measured. Self-reported fatigue can only be assessed using unreliable paper-and-pencil or computer-assisted questionnaires that produce highly variable and unstable results.

There is no research that indicates there is a correlation between changes in scores on fatigue questionnaires and changes in the underlying disease process of ME. Fatigue questionnaires, therefore, are of little or no use for measuring the effectiveness of various treatments for ME. CFS, on the other hand, is based on the subjective symptom of unexplained fatigue so an argument can be made that changes in fatigue scores indicate improvement or worsening of the condition in CFS-labeled patients or CFS-labeled research subjects.

Eliminating subjective fatigue as the defining characteristic and requiring a positive diagnosis based on objectively measurable features, as opposed to the CFS diagnosis of exclusion, further refutes the spurious claims that ME is based on medically unexplained symptoms (MUS) and can be considered a functional disorder or a “bodily distress syndrome.” The authors of the ICC make a strong case, supported by published research, that ME symptoms are not medically unexplained and that ME cannot be considered a functional disorder without observable and measurable physical abnormalities.

According to the US Centers for Disease Control and Prevention (CDC), chronic fatigue syndrome (CFS) is a diagnosis of exclusion – that is, CFS cannot be diagnosed until all other diagnoses that may account for a patient’s reported fatigue are ruled out. [Fukuda, 1994] No single patient, therefore, can simultaneously qualify for both a CFS and an ME diagnosis. In other words, ME and CFS are mutually exclusive diagnoses. If a patient meets diagnostic criteria for ME, he or she cannot rationally be diagnosed also with CFS because the ME diagnosis accounts for any fatigue reported by the patient – just as a cancer, rheumatoid arthritis, or multiple sclerosis diagnosis would do. However, how can doctors rule out ME, in keeping with the CDC’s CFS diagnosis of exclusion concept, if doctors do not have reliable, peer-reviewed, up-to-date diagnostic guidelines exclusively for ME?

Doctors in the US, therefore, need to have the IC Primer so they can make the differential diagnosis of ME rather than assign patients with ME to the broad, unexplained-fatigue-based diagnostic category of chronic fatigue syndrome.

The Term ‘ME/CFS’ Is Impossible to Interpret and Causes Confusion

The mutual exclusivity of the ME and CFS diagnoses renders the term “ME/CFS,” now favored by the US Department of Health and Human Services (HHS) and used throughout the AHRQ report, impossible to interpret. Does “ME/CFS” refer to only ME, only CFS, illogically both, or some other medical condition entirely? It is impossible to tell. No single patient can qualify for both diagnoses at the same time according to the separate case definitions for ME and CFS. [Carruthers, 2011; Fukuda, 1994] For this reason, the ICC and ICP call for ME patients to be removed from the overly inclusive CFS diagnostic category rather than to be placed in some logically incoherent, unclassifiable fatigue-based illness category called “ME/CFS” or “CFS/ME”. This means that doctors need to reassess their existing CFS patients for ME using the IC Primer and, going forward, rule out ME before making any new CFS diagnoses.

How could the hybrid diagnostic term “ME/CFS” ever be classified following WHO rules and the basic principles of scientific taxonomy going back to Linnaeus and Aristotle? WHO rules do not allow any diagnostic term to be listed under more than one classification because, by definition, individual categories and subcategories must remain mutually exclusive.

ME is an established neurological disease listed in the WHO International Classification of Diseases (ICD) as benign myalgic encephalomyelitis under “Diseases of the nervous system” as G93.3 since 1969. Holmes-defined chronic fatigue syndrome [Holmes, 1988] was placed in the alphabetical index of the WHO ICD-10 in 1992 referenced to G93.3 in the tabular index. However, the WHO is silent on the relationship of alphabetical index terms to their referent in the tabular index. There is no reason to assume the WHO ever regarded the two terms, ME and CFS, as synonymous or equivalent.

In any case, it is clear that CFS has never been case-defined as a neurological disease, but only as a variable grouping of self-reported symptoms. Chronic fatigue syndrome was first defined as a fatigue-based research “operational concept” in 1988 by a CDC-led committee. [Holmes, 1988] CFS was later redefined in 1994 for further research purposes as a grouping of self-reported symptoms with 70 different variations by another CDC committee. [Fukuda, 1994] The authors of the 1994 Fukuda definitional paper did not consider CFS a neurological disease or, indeed, even a clinical entity until verified by further research.

Consistent with its 1994 CDC case definition, CFS is presently classified in the US ICD-9-CM (CM stands for clinical modification) as 780.71 under “Symptoms, Signs, And Ill-Defined Conditions.” The US ICD-9-CM was written by the National Center for Health Statistics (NCHS), a part of the CDC, and on this basis must be considered authoritative for the classification of CDC-defined diagnostic terms. The current US ICD-9-CM does not list benign myalgic encephalomyelitis, deviating from the WHO ICD-9 on which it is based.

However, in the new US ICD-10-CM, official on October 1, 2015, benign myalgic encephalomyelitis is coded as G93.3 under “Diseases of the nervous system,” as ME is now coded in WHO ICD-10. Chronic fatigue syndrome is specifically excluded from G93.3 in ICD-10-CM and coded, along with the symptom of unspecified chronic fatigue, as R53.82 under “Symptoms, signs and abnormal clinical and laboratory findings, not elsewhere classified.”

How then will US doctors code the hybrid diagnostic term “ME/CFS” using the new US ICD-10-CM? The term consists of the neurological disease ME in the G-section blended, in some indeterminable fashion, with the symptom grouping CFS in the R-section. In practice, doctors will have to chose to code an “ME/CFS” diagnosis as either CFS R53.82 or ME G93.3 rendering the hybrid term “ME/CFS” ambiguous and useless for reporting and billing purposes. US doctors however, are unlikely to use the ME code because the neurological disease ME is unfamiliar to them or has been misrepresented to them as another name for CFS. “ME/CFS” in practice will become only the symptom grouping CFS and not the neurological disease ME unless doctors are informed, using the IC Primer, how to differentiate ME from CFS.

Doctors Need Basic Information on ME to Avoid Harming Their Patients

Very few doctors in the US now have the information, training, and experience needed to recognize and diagnose ME. Doctors currently give the inappropriate broad diagnosis of CFS to their patients who have the neurological disease ME. The result is that CFS presently includes patients both with and without ME. The common CFS misdiagnosis creates a medically dangerous situation for patients with ME and greatly increases their risk of serious, or even permanent, iatrogenic harm.

ME, according to the ICC, is characterized by an abnormal biological response to physical or mental exertion that the authors call post-exertional neuroimmune exhaustion (PENE). PENE is an objectively measurable, profound dysfunction of the body’s neurological, immunological, cardiovascular, and energy-production systems that can result in prolonged, or permanent, disability.

Iatrogenic harm to ME patients is especially likely now because the CDC and medical organizations informed by the CDC do not advise cautioning ME patients about the extreme risks posed by exercise. Instead, doctors are dangerously encouraging misdiagnosed ME patients to exercise or participate in so-called graded exercise therapy (GET) based on the CDC recommendations for CFS.

Without doubt, thousands of cases of extensive, or lifetime, disability in the US result every year from the inability of doctors to recognize, diagnose, and properly treat ME. It is essential for the nation’s health that US Department of Health and Human Services immediately begin informing doctors about ME and begin distributing the IC Primer to doctors before more people with ME are condemned to a lifetime of disability because of current unsafe medical advice and practices.

HHS has already had three years, since the ICC were published in the Journal of Internal Medicine, to inform doctors about ME and the grave risks to their patients caused by a missed ME diagnosis. HHS could easily and inexpensively begin almost immediately to advise doctors about ME by placing accurate information about ME on HHS websites with links to the ICC and IC Primer.

The CDC has distributed thousands of printed copies of their CFS Toolkit [CDC, undated] to doctors. Every one of these doctors urgently needs to have also a printed copy of the IC Primer so he or she can recognize and diagnose ME and avoid causing harm to their ME patients by misdiagnosing them with CFS.

The CDC CFS Toolkit Places ME Patients At Risk

The diagnostic guidelines in the CFS Toolkit are based almost word-for-word on a 20-year-old CDC theoretical research case definition. [Fukuda, 1994] This research framework was designed to search for illness patterns that might indicate the presence an identifiable disease. No such distinct illness pattern has ever been found by the CDC. However, the CDC is still using their broad 1994 research criteria in the current CFS Toolkit as diagnostic criteria to assign patients to a hypothetical symptom complex called chronic fatigue syndrome that has come mistakenly to be regarded as a specific diagnosis. As a consequence, the umbrella CFS diagnostic category contains many missed differentiable and treatable diagnoses that were not sufficiently investigated before a patient was assigned to the general symptom CFS category. These missed diagnoses are then left medically untreated. Foremost of these missed diagnoses is myalgic encephalomyelitis.

Placing ME within the broad CFS category puts ME patients at risk because of the objectively measurable, abnormal biological response to exercise or exertion characteristic of the disease. Exercise that may benefit CFS-labeled patients solely with clinical depression or the single symptom of chronic fatigue may cause irreparable harm to patients with ME. The CFS Toolkit fails to list ME in the section “Illnesses that may resemble CFS” despite myalgic encephalomyelitis having been well-described in the medical literature for many decades and having been listed by the WHO ICD as a neurological disease for 45 years. Presumably, with ME now readily diagnosable by US doctors using the 2012 IC Primer, updates to the CFS Toolkit will list myalgic encephalomyelitis as an exclusionary disease for a CFS diagnosis.

The “Treatment and Management” portion of the CFS Toolkit, along with general platitudes on “coping skills, “emotional issues,” sleep issues” and the treatment benefits of cognitive behavioral therapy (CBT) for “some patients with CFS,” has a section on graded exercise therapy (GET). Graded exercise therapy is defined in the Toolkit as starting at a low basic level of exercise and gradually increasing “to a level where people can go about their daily life.”

The Toolkit also now states that, “The GET Guide 2008 by Chronic Fatigue Syndrome/ME Service at St. Bartholomew’s Hospital can be helpful in structuring your graded exercise plan.” This unscientific and outdated guide is as unsafe for ME patients as the Toolkit. The GET Guide is now only available online archived at a Danish “functional disorders” website. The St. Bartholomew’s Hospital GET Guide “aims to help you overcome limitations caused by the symptoms of chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis (ME)” by gradually increasing exercise tolerance – similar to expecting diabetics to improve their sugar metabolism by gradually increasing their daily sugar intake.

Although the Toolkit warns to avoid “the push-crash cycle,” no mention is made of the fundamentally altered biological response of people with ME to exercise and the possibility of increased disability and permanent relapse. In contrast, the IC Primer has a chart on pages 3 and 4 that lists 25 physiological functions in which the response of ME patients differs from the normal response.

Another grave risk posed for ME patients misdiagnosed using the CFS Toolkit rather the appropriate IC Primer is failure to recognize, monitor, and treat the serious known cardiovascular abnormalities associated with ME. The CFS Toolkit makes no mention of any cardiovascular problems whatsoever being associated with CFS. The IC Primer on page 6 lists with references these cardiovascular and autonomic impairments associated ME:

Insufficient increase in blood pressure (BP) on exertion, low blood pressure and exaggerated diurnal variation may be due to abnormal blood pressure regulation, inverse relationship with fatigue, reduced blood flow and vasculopathy, arterial elasticity dysfunction – hyper-elasticity/contractibility of arterial walls, elevated response to acetylcholine, increased arterial wave reflection, ‘small heart’ with small left ventricular chamber, cardiac and left ventricular dysfunction, reduced heart rate variability during sleep suggests a pervasive state of nocturnal sympathetic hyper-vigilance and may contribute to poor sleep quality, low circulating erythrocyte volume (~ 70% of normal). Vascular abnormalities suggest there is insufficient circulating blood volume in the brain when in an upright position, and blood may pool in the extremities.

Doctors need to be aware of these serious possible cardiovascular impairments when treating and monitoring their ME patients. If an ME patient is given a CFS diagnosis and the CFS Toolkit is a doctor’s only guidance, how would the doctor ever know to be alert for and treat these impairments?

Similarly, in each of the sections – Post-Exertional Neuroimmune Exhaustion, Neurological Abnormalities, Immune Impairments, and Energy Production and Ion Transport Impairments – the ICP has detailed information useful for doctors, in contrast to the vague general information of the CFS Toolkit. The ICP has a step-by-step procedure for the ME diagnostic and reassessment process with checklists and charts to assist and guide doctors in the initial evaluation of patients, what medical tests to order, the diagnostic criteria, and how to monitor and reassess ME patients.

The IC Primer also lists over 30 medical laboratory tests and imaging studies specifically useful for the diagnosis and monitoring of ME, in addition to standard laboratory screening tests. The CFS Toolkit only recommends the standard laboratory tests to screen for other possible diagnoses based on the CDC’s CFS as a diagnosis of exclusion concept. The IC Primer lists the 2-day cardiopulmonary exercise test (CPET) [VanNess, 2007] as an objective confirmation of the characteristic ME feature of an abnormal biological response to exertion. There is no objective test for the characteristic CFS feature of self-reported fatigue.

The IC Primer has extensive treatment recommendations for ME including specific pharmaceutical and non-pharmaceutical treatments. The Toolkit “Drug therapies” section only gives general medication advice with no specific drugs mentioned. The section is mostly about what to avoid. The “Non-drug therapies” section includes, yoga, light exercise before bed, puzzles, and word games.

Very importantly, the ICP has a sections on pediatric considerations and pediatric personalized ME treatment. ME presents differently in children and requires specialized treatment. Knowledge of ME in children by doctors can help prevent the abuse of children and their parents caused by psychiatric misdiagnosis and inappropriate psychiatric treatment of the neurological disease ME in children. Parents of children with ME are sometimes accused of encouraging illness symptoms in their children to gain attention and a sense of importance. The specific pediatric considerations and diagnostic procedures in the IC Primer can help counter this abuse of the parents of children with ME. The CFS Toolkit makes no mention of pediatric CFS.

The diagnostic guidelines of the ICP eliminates the arbitrary 6-month waiting period of the CDC criteria from when symptoms first appear and the condition can be diagnosed. It is critical that ME be diagnosed as soon as possible so patients can be advised they need total rest and to avoid exercise and overexertion. It may be too late for this medical advice after six months have passed. Early diagnosis and treatment result in the best prognosis and limits the risk of severe or permanent disability. Pioneer ME doctor A. Melvin Ramsay stated:

The clinical picture of myalgic encephalomyelitis has much in common with that of multiple sclerosis but, unlike the latter, the disease is not progressive and the prognosis should therefore be relatively good. However, this is largely dependent on the management of the patient in the early stages of the illness. Those who are given complete rest from the onset do well… [Emphasis added]

The IC Primer was written by 26 highly qualified expert authors, representing 12 countries, who have collectively diagnosed and treated over 50,000 patients with ME and have over 500 years of experience. The ICP is supported by published research with over 150 references.

In contrast, the CDC CFS Toolkit was written by anonymous authors who do not support their diagnostic and treatment guidelines with a single reference. Doctors and other medical providers are expected to take the recommendations of the CFS Toolkit on faith because it was written by employees of the CDC and has a photograph of a man in a white coat on the cover.

The Current HHS/IOM Redefinition of “ME/CFS”

Instead of protecting the nation’s health and economic viability by supporting and distributing the IC Primer, which is available for use free of charge, the US Department of Health and Human Services is unwisely creating more confusion, delay, and medical misinformation by hiring the unqualified Institute of Medicine (IOM) for $1,000,000 to oversee the creation of unneeded diagnostic guidelines for an unclassifiable new hybrid fatigue illness HHS is calling “ME/CFS.”

The IOM is unqualified to create diagnostic guidelines for diseases because of its institutional conflict of interest and its unjustifiable policy of using panels composed mostly of inexperienced non-experts to develop diagnostic criteria. The HHS/IOM “ME/CFS” panel has eight non-experts and only seven members with significant knowledge and experience in the field. Of these seven experienced members on the panel, four have previously participated in CDC-organized continuing medical education courses recommending the use of the overly broad 1994 CDC CFS case definition and exercise as a treatment for CFS. The CDC online courses fail to acknowledge that ME is a separate neurological disease requiring its own case definition and diagnostic guidelines that caution against using exercise as a treatment.

How could the recommendations produced by an unqualified and inexperienced HHS/IOM panel possibly have more credibility, reliability, and utility than the recommendations of the existing ICC and IC Primer written by 26 expert authors with collectively over 500 years of experience in the field of ME? It would be utter folly and a tragic waste for HHS to place the recommendations of an unqualified and inexperienced IOM panel above the recommendations of the highly qualified expert ME ICC panel.

The diagnostic guidelines and treatment recommendation of the HHS/IOM “ME/CFS” panel, composed mostly of neophyte, non-expert members, cannot possibly reduce the urgent need for wide distribution of the IC Primer for ME. Almost all of the worldwide experts on ME and CFS have agreed, on the record, that the product of the HHS/IOM “ME/CFS” panel will create more confusion, harm patient care, and impede future research. It is, therefore, vitally important for the reasons given above that doctors have the IC Primer now so they can recognize and diagnose ME and give their patients with ME the best chance to limit the disability caused by the disease and to provide ME patients the best quality of life until more effective treatments and a cure are found.


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. http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02428.x/full

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

Centers for Disease Control and Prevention. Chronic Fatigue Syndrome: A Toolkit for Providers. Undated. Accessed December 14, 2014. http://www.cdc.gov/cfs/pdf/cfs-toolkit.pdf

Fukuda K, Straus SE, Hickie I et al. Chronic fatigue syndrome: a comprehensive approach to its definition and study. Ann Intern Med 1994; 121: 953–9.

Gilliam, A. G. Epidemiological study on an epidemic, diagnosed as poliomyelitis, occurring among the personnel of Los Angeles County General Hospital during the summer of 1934. United States Treasury Department Public Health Service Public Health Bulletin, US Treasury Dept. No. 240. Washington, DC: United States Government Printing Office.1938.

Holmes GP, Kaplan JE, Gantz NM et al. Chronic fatigue syndrome: a working case definition. Ann Intern Med. 1988; 108:387-389.

Ramsay AM. Myalgic Encephalomyelitis and Postviral Fatigue States: The saga of Royal Free disease. 1st ed. London: Gower Medical Publishing; 1986.

Smith MEB et al. Diagnosis and Treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Evidence Report/Technology Assessment No. 219. (Prepared by the Pacific Northwest Evidence-based Practice Center under Contract No. 290-2012-00014-I.) AHRQ Publication No. 15-E001-EF. Rockville, MD: Agency for Healthcare Research and Quality; December 2014. http://www.effectivehealthcare.ahrq.gov/ehc/products/586/2004/chronic-fatigue-report-141209.pdf

VanNess JM, Snell CR, Stevens SR. Diminished cardiopulmonary capacity during post-exertional malaise. J Chronic Fatigue Syndr 2007; 14: 77-85.

The IC Primer is also available here: http://optimalprediction.com/files/ICC_primer.pdf

The International Consensus Criteria original paper is also available here: http://optimalprediction.com/files/ICC_criteria.pdf

Limbic kindling vs. central sensitization in ME.

I don’t believe in the trem “ME/CFS” any more. I know I wrote a post about previously, but I was still a newbie. There is a disease called Myalgic Encephalomyelitis (ME), which is diagnosed by the International Consensus Criteria. It always involves the appearance of neurological symptoms (Post-Exertional Neuroimmune Exhaustion) shortly after exercise. These symptoms may or may not include fatigue.

Chronic Fatigue Syndrome (CFS) is characterized by severe fatigue, which may or may not be exacerbated by exercise. It is not a disease, it is a syndrome, a cluster of symptoms. I maintain that it is a result of any one of 200 undiagnosed autoimmune diseases.

ME and CFS should not be combined. They are opposite in important ways.

Would you believe I never saw this research by Leonard Jason (and Jason’s paper) before now. I don’t read ME/CFS research at all. I go by symptoms, what has happened to me, and how they relate to other diseases.

But I got the same general outline of ME as he does with ME/CFS. He has the idea of limbic kindling in the limbic cortex. I have central sensitization in the limbic cortex.

He has the movement towards Th2 dominance (T-helper cells that promote allergy, not autoimmunity), because Th1 is downregulated, like I do. But for me, this is due to the initial viral infection (enterovirus, EBV, HHV-6 etc. which downgrade Th1) and radioactive toxins promoting TGF-beta, which also downgrade Th1. He has overactivity in the pituitary doing it. My pituitary is trashed, and all it was doing was spitting out prolactin and TSH from a pituitary tumor. Everything else was underactive.

They mention leaky gut. This is caused by anti-inflammatory TGF-beta wiping out Th22 cells.

Jason talks about increased NMDA receptor activity. But this is because of an increase in the number of NMDA receptors, not an upgrade in the activity per cell. And glutamate and GABA have to be created for all these cells, and the body robs alpha-ketoglutarate from the Krebs cycle to power them, reducing ATP in the mitochondria. There’s not enough of anything to go around with all these neurons sprouting.

He doesn’t have an explanation for post-exertional neuroimmine exhaustion, which results from TGF-beta being released from muscles 24 hours after exercise, which reduces follistatin levels, weakens muscles, leads to fibrotic tissue replacing muscle fiber, and further reduces Th1. This is key.

And of course nothing about reduced IDO, which is a straight-up inference from depleted Th1, which reduces catabolism of tryptophan and leads to disturbances in the kynurenine pathway (a classic neurological effect), and too much serotonin. Insulin delivers tryptophan to cells, and is part of the disease process. He acknowledges high serotonin levels without giving the reason, or mentioning that this might lead to the central sensitization in the first place, where too many neurons are produced. Serotonin receptors also give off more TGF-beta.

Since the neurons connect to a place in the hippocampus that involves the default mode network (DMN), and there is not enough GABA, the brain cannot switch out of the resting state to perform tasks, or multitask. This leads to paralysis is severe ME.

Since the publication of the ICC in 2011, Jason has published studies using the ICC, to his credit. And his research (along with Maes) is better than the run-of-the-mill ME/CFS quackery. But we need experts in internal medicine, neurology, and immunology involved in ME research. Most of all, we need to abolish the ME/CFS label, which contaminates studies with heterogeneity, and causes harm to ME patients.

New criticality in Japan. Not necessarily from Fuku.

Fukushima Diary is reporting that Manganese-54 was detected in groundwater in Reactor 1 seaside at Fukushima. It appears that the sample was taken on November 21, not the 24th as Tepco said.

Activation products are generated by neutron bombardment of materials. Manganese-54 results from neutrons interacting with iron or steel. This means fission has occurred. Mn-54 mimics iron in the body, like cesium mimics potassium, and strontium mimics calcium.

It sounds like a criticality has occurred recently. My thyroid agrees. On Wednesday night, Nov. 26, my thyroid swelled up, and it prevented me from sleeping. I took Lugol’s iodine and selenium, and it cleared up. Thyroid symptoms are not generated from ME, so this was not caused by this disease. As a matter of fact, the wildly overactive cellular immunity I previously had has gone away, and has been replaced with an immune deficiency. So I am much less sensitive to I-131 than I used to be.

November 26 was my birthday, so I suppose this thyroid issue was a birthday present from the nuclear industry.

However, there may be another player involved. On Nov. 22, a strong earthquake hit Nagano, Japan. Somebody saw steam or smoke coming out of the nearby Kashiwazaki-Kariwa nuclear plant. This is one of the largest nuclear plants on earth. An alarm went off at a spent fuel pool, purportedly due to sloshing in a pool due to the earthquake.

It is possible that an issue has occurred at this plant also. The draconian state secrets law in Japan, which has imposed nuclear slavery on the people of Japan, ensures that no information would be published on such an event, without the expressed approval of the Japanese government.

I have seen a lot of anecdotal reports of thyroid issues, aches and pains, and flu symptoms in the last few days.

Uranium hexafluoride release tonight at Honeywell Works, Metropolis, IL.

There was a confirmed uranium hexafluoride release at Honeywell Works in Metropolis, IL at 8pm tonight. Sirens have sounded and Honeywell guards have told people to shelter in place, close windows, and turn off A/C.



The Honeywell Works converts raw uranium into uranium hexafluoride. It is then pumped across the Ohio River to the Paducah plant, for the manufacture of nuclear fuel for nuke power plants.

There were two major releases of UF6 (uranium hexafluoride) from this plant in May 2012, they were covered here at:

Uranium hexafluoride releases at Honeywell Metropolis Works, May 2012. Part 1.

Uranium hexafluoride releases at Honeywell Metropolis Works, May 2012. Part 2.

UF6 is very dangerous. For one thing, it is a neutron emitter like plutonium. The hydrofluoric acid that is created on contact with water vapor is corrosive and deadly. You don’t want to breathe this stuff.

It was noted to be moving west from Metropolis. Wind maps indicate that the wind is from the southeast, so the plume would be moving northwest. Cape Girardeau MO and St Louis MO, or points in between, would seem to be where it is headed. And it won’t stop there.

UPDATE 10/29: From Radchick. NRC: Status of Honeywell Accident 10.29.14

NRC: Status of Honeywell Accident 10.29.14

*NRC is on-site, has been since Monday (one guy).
*Area in plant is still being decontaminated.
*Plant is SHUT DOWN until investigation is complete.
*Investigator interviews show sabotage was unlikely.
*Preliminary indications is there was a weakness in joint at bottom of one container, metallurgic forensic testing may be needed. Leak was stopped sometime Sunday evening, but he wasn’t sure exactly when.
*SO FAR it doesn’t look like contamination made it over the fence, but they are still looking at data. Sketchy answer.
*Aware of reports of people smelling and tasting something possibly toxic.
*Runoff “probably” went into drains and wells will show it, but he was unsure if drains even exist on property!
*No indication Ohio River was contaminated, EPA (and possibly Illinois FEMA?) is there testing too.
*Not aware of anyone from surrounding community that went to ER for treatment, but he was a bit sketchy about this. Community hospitals seem to have NO PLAN in the event of an emergency. I find it very surprising in light of the numerous leaks that have occurred there. That’s bad, and needs to be addressed by the local hospitals and community leaders at once imo.
30 days til final report is released, prelim report in as early as several days.

WIPP plutonium release next Monday, Oct. 20. Restart of contaminated fan.

This is from Myla Reson on Facebook. There was a town hall meeting in Carlsbad yesterday.

During the October16, 2014 WIPP townhall meeting, Nuclear Waste Partnership President, Bob McQuinn gave a presentation on the planned Monday October 20th restart of WIPP surface fan 860A.

Slide number 12 used during McQuinn’s presentation indicates that fan 860A was in use at the time of the mid-February 2014 release of Plutonium and Americium to the environment, and that when the fan is restarted this coming Monday “residual contamination may be released”.

see slide “12”:

I’d like to know who authorized the possible release of plutonium and americium that may occur when fan 860A is restarted?

According to the DOE document, “Precautions are being taken to ensure protection of workers and the 
environment”. Why don’t they simply replace the fan?

Time to get your Geiger counters out, and make sure your air filtration units are operating next week. Wish I could do a HYSPLIT prediction of the wind currents, but I can’t now.

Fukushima radioactive contamination is rapidly warming North Pacific seawater.

A recent post on Enenews brought attention to the extremely warm water in the North Pacific.

Sea surface temperatures in North Pacific relative to average

There is a massive pool of warm water in the Gulf of Alaska, NOAA scientist Nate Mantua said in an email. It is unprecedented in the historical record, he added… the past year is way out of the historical range — “so who knows what will happen?”…

Scientists across NOAA Fisheries are watching a persistent expanse of exceptionally warm water spanning the Gulf of Alaska that could send reverberations through the marine food web. The warm expanse appeared about a year ago and the longer it lingers, the greater potential it has to affect ocean life… “Right now it’s super warm all the way across the Pacific to Japan,” said Bill Peterson, an oceanographer with NOAA.

These are certainly record high temperature levels. Bob Tisdale, a manmade climate change skeptic, has an excellent summary of this situation here.

This report here, by Howard Freeland and Frank Whitney, was linked to in the Enenews post.

In March 2014 there was something very unusual occurring in the Northeast (NE) Pacific that might have substantial consequences for biota in the Gulf of Alaska and southward into the subtropics… we see SST departures of 4.5 standard deviations… The anomaly field covers a large region of the N.E. Pacific… The authors of this article have never seen [such] deviations… Something as extraordinary as a 4.5-sigma deviation requires corroboration…

An increase of 4.5-sigma in sea surface temperatures is about one-fifth the probability of being dealt a straight flush in five-card poker, and twice the probability of being dealt a royal flush. In other words, it is wildly improbable that it is a result of a natural process.

The answer is that Fukushima Daiichi nuclear plant has releasing extremely radioactively contaminated water, starting in March 2011. The worst part was at the beginning. By early April 2011, humungous levels of iodine-131 and cesium-137 had been released.

Radioactive iodine at 7.5 MILLION times legal limit in water around Fukushima — Cesium-137 at 1.1 MILLION times limit

… Tokyo Electric Power Company says it detected 300,000 bequerels of iodine-131 per 1 cubic centimeter, or 7.5 million times higher than the legal limit in samples taken around the water intake of the No. 2 reactor at 11:50 AM on Saturday.

It also found 200,000 bequerels or 5 million times higher than the limit in samples taken at 9AM on Monday.

Monday’s sample also shows 1.1 million times higher than the national limit of cesium-137 whose half-life is 30 years. … (link)

300,000 becquerels per cubic centimeter detected in ocean water is 300 BILLION becquerels per square meter. Fukushima has been leaking ever since, but the worst of it occurred at the beginning of the catastrophe.

Models that predict the movement of particles in ocean water projected that it would move to the east, and be near North America by now:

Radionuclides give off heat by a process of radioactive decay. This is the reason that spent fuel rods have to be submerged in water, to keep them cool, so they don’t melt down. According to Arnie Gundersen of Fairewinds Associates:

Radioactive byproducts produce heat.

During the normal operation of a nuclear reactor, there is an accumulation of many man-made radioactive materials such as iodine-131, cesium-137, strontium-90, plutonium-239, and many others.

These radioactive byproducts continue to produce a lot of heat, even after the reactor is shut down, because radioactivity cannot be stopped. This unstoppable heat is called “decay heat.”

This decay heat occurs whether the radionuclides are in a reactor, in a spent fuel pool, or leaked into the sea. So it stands to reason that ocean temperatures would be extraordinarily high.

As you can see, the warm ocean plume is still moving to the east. The warm water itself creates a crisis for sea life, the salinity has dropped, and the winds that bring nutrients from the northern areas are blocked. From Freeland and Whitney,

Wind anomalies (Fig. 2a) show the cause of the warm anomalies in the ocean’s surface layer to be an unusual flow from the south as the North Pacific high pressure cell expanded northward. This pattern disrupted the path of the westerly winds that cross the subarctic Pacific, winds that normally transport nutrients from the subarctic North Pacific into the subtropics during winter… Without nutrients from the subarctic, the productivity of subtropical waters must decline.

An ecological crisis in the Pacific is launched, simply from the warm water, even not regarding the deadly radiation itself. It affects life in areas far away from the contaminated waters through changes in the wind patterns.

“As temperature rises, the zooplankton start to grow faster than the phytoplankton,” O’Connor explains. “The zooplankton are more abundant and faster-growing, and are able to eat all the phytoplankton in warmer water. This creates a bottleneck in the food chain that could have large implications for the ocean’s food web. (link)

Phytoplankton contribute up to 50% of the planet’s oxygen supply.

And this warm water is already profoundly affecting the climate of North America. The 500 mb geopotential height represents the temperature of the air at 18,000 feet. High values of this height (a ridge) correspond to warm temperatures, and low values (a trough) to cold.

Warm heights mean that the air is sinking, and little or no precipitation forms, and the surface air temperature is warm. Cold heights mean higher precipitation and cold surface temperatures. Air moves clockwise around the ridge, pushing north into the Arctic, where it pushes down cold air from these regions to the eastern US.

Last winter featured warm and dry conditions in the west, while the east had a cold and snowy winter. This is likely to happen again this coming winter.

And the ridge in the west has caused drought conditions in California:

The contaminated water will not move out for many years, but decay heat release will continue, so look for Pacific sea surface temperatures to keep increasing, and the drought to continue.

Ketogenic diet for M.E.: Can it really be this simple?

Can it really be this simple? A ketogenic diet…. or supplements like caprylic acid or medium-chain triglycerides… replace glucose metabolism with β-Hydroxybutyrate and acetoacetate, or ketosis.

In myalgic encephalomyelitis (and multiple sclerosis), the ability to break down amino acids like tryptophan is affected by reduced IDO level. IDO isn’t there because it needs interferons like IFN-beta and IFN-gamma, which are essential building blocks of the immune system, which these diseases reduce. The ketogenic (high-fat, low-carb) diet, or ketone bodies in general, bypass this problem.

Evidence points to an effect on brain handling of amino acids, especially glutamic acid, the major excitatory neurotransmitter of the central nervous system. The diet may limit the availability of oxaloacetate to the aspartate aminotransferase reaction, an important route of brain glutamate handling. As a result, more glutamate becomes accessible to the glutamate decarboxylase reaction to yield gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter and an important antiseizure agent. In addition, the ketogenic diet appears to favor the synthesis of glutamine, an essential precursor to GABA. This occurs both because ketone body carbon is metabolized to glutamine and because in ketosis there is increased consumption of acetate, which astrocytes in the brain quickly convert to glutamine.
The ketogenic diet and brain metabolism of amino acids: relationship to the anticonvulsant effect.

The extreme hypersensitivity to sound, and the whirlwind of discombobulated sensations that replaces ordinary thought in severe ME, and causes paralysis, is a type of seizure. GABA is a natural anti-seizure agent in the nervous system. This line of thought says that the neurological manifestations of M.E. are due to a metabolic disorder, which is triggered by imbalances in the immune system.

It is well known by the ME community (not ME/CFS) that this disease features abnormalities in cellular energy utilization.

This review article explores the rationale for using the KD and related dietary treatments in neurological disorders outside of epilepsy, and summarizes the clinical experience to date. An underlying theme of such diet-based therapies is that nutrients and metabolic substrates can exert profound effects on neuronal plasticity, modifying neural circuits and cellular properties to enhance and normalize function. At a fundamental level, any disease in which the pathogenesis is influenced by abnormalities in cellular energy utilization – and this implies almost every known condition – would theoretically be amenable to the KD. It is important to acknowledge that much of the data discussed here are preliminary and anecdotal, and hence need to be validated by well-controlled prospective studies. Nevertheless, that diet and nutrition should influence brain function should not be altogether surprising, and there are already abundant clinical and laboratory data linking defects in energy metabolism to a wide variety of disease states (Waldbaum and Patel, 2010; Roth et al., 2011; Schiff et al., 2011). Thus, the potential for interesting and novel applications of the KD and related dietary therapies is almost limitless (Stafstrom, 2004).
The Ketogenic Diet as a Treatment Paradigm for Diverse Neurological Disorders

Oxidative stress is the first link in the ME chain, ahead of even STAT-1 inhibition. Oxidative stress in increased by exercise, which brings on post-exertional neuroimmune exhaustion. Radioactive contaminants in the body also lead to free radicals and oxidative stress, since radiation causes radiolysis, the splitting of water into hydrogen and oxygen:
Suppression of Oxidative Stress by β-Hydroxybutyrate, an Endogenous Histone Deacetylase Inhibitor

Ketosis reduces the amount of glutamate available for neurotransmitter usage, and is then available for GABA synthesis. Glutamate as a neurotransmitter causes neural excitability, and the hypersensitivity and paralysis in severe ME, and GABA causes the opposite, neural inhibition:
Availability of neurotransmitter glutamate is diminished when β-hydroxybutyrate replaces glucose in cultured neurons

An increasing number of data demonstrate the utility of ketogenic diets in a variety of metabolic diseases as obesity, metabolic syndrome, and diabetes. In regard to neurological disorders, ketogenic diet is recognized as an effective treatment for pharmacoresistant epilepsy but emerging data suggests that ketogenic diet could be also useful in amyotrophic lateral sclerosis, Alzheimer, Parkinson’s disease, and some mitochondriopathies. Although these diseases have different pathogenesis and features, there are some common mechanisms that could explain the effects of ketogenic diets. These mechanisms are to provide an efficient source of energy for the treatment of certain types of neurodegenerative diseases characterized by focal brain hypometabolism; to decrease the oxidative damage associated with various kinds of metabolic stress; to increase the mitochondrial biogenesis pathways; and to take advantage of the capacity of ketones to bypass the defect in complex I activity implicated in some neurological diseases.
Ketogenic Diet in Neuromuscular and Neurodegenerative Diseases

Here we hypothesize that CNS depressants may promote consciousness recovery by reversing a condition of GABA impairment in the injured brain, restoring the normal ratio between synaptic excitation and inhibition, which is the prerequisite for any transition from a resting state to goal-oriented activities (GABA impairment hypothesis). Alternative or complementary mechanisms underlying the improvement of consciousness may include the reversal of a neurodormant state within areas affected by diaschisis (diaschisis hypothesis) and the modulation of an informative overload to the cortex as a consequence of filter failure in the injured brain (informative overload hypothesis).
Silencing the brain may be better than stimulating it. The GABA effect.

Enterovirus 68 may cause polio-like paralysis in children.

A respiratory virus has sickened thousands of children across the US, and is rapidly spreading across the country. The CDC has analyzed samples, and found 40 incidences of enterovirus 68 (or D68) in Kansas City and Chicago. This infection may be life-threatening.

In addition to the states listed on the map, this illness has been reported in Michigan, New York, Virginia, South Carolina, and Alabama as of today.

Enterovirus 68 has aspects similar to rhinoviruses, which cause the common cold, and it spreads like the common cold, that is, from contaminated surfaces, person-to-person contact, and aerosols from sneezing.

Last February, it was reported that five cases of a polio-like illness had been observed in California children since late 2012. These patients also had severe respiratory symptoms.

Over the past 18 months, physicians in California have observed on rare occasions what may be a new disease, one in which patients, usually children, quickly and permanently lose muscle function in an arm or leg.

In some cases, patients have had infectious respiratory symptoms before the paralysis begins. The illness shares some features with polio, but it is not the same disease.

The cause of the disease is still unknown, but a strong possibility is that it is caused by a virus known as enterovirus-68, which was detected in two of five cases that Emmanuelle Waubant, MD, PhD, of UCSF Benioff Children’s Hospital, and Keith Van Haren, MD, of Stanford University’s Lucile Packard Children’s Hospital, will present in detail at the annual meeting of the American Academy of Neurology this spring.

An audio presentation by these neurologists can be found at this link. At 5:25 Dr. Van Haren states his belief that the polio-like paralysis was caused by enterovirus 68.

WIPP cover-up.

There was an interesting post on Enenews today about WIPP.

The Santa Fe New Mexican, Sept 6, 2014: Flynn accuses feds of blocking WIPP probe — New Mexico’s top environmental regulator lashed out at the U.S. Department of Energy this week, accusing it of impeding the state’s investigation into [the WIPP] radiation leak… Secretary Ryan Flynn warned [about] Energy Department roadblocks that have protracted the probe… Increasingly in recent weeks, the federal Energy Department has thwarted attempts by the state… Flynn accused the Energy Department of muzzling scientists with crucial information about the waste…. [They] asked for documentation supporting the scientists’ observations [but] the Energy Department has repeatedly refused… his frustration with the Energy Department grew as its denials… became more frequent… The Energy Department’s refusal to provide information raised suspicions among Flynn’s investigators…

Ryan Flynn is the cabinet secretary of the New Mexico Environment Department. This is a state agency which is independent of the Department of Energy, which is in charge of the Waste Isolation Pilot Plant. It’s a part of the state government, so it’s not an environmental watchdog group, but they have done things like block Hanford waste from being stored in the facility.

From the referenced article in the Santa Fe New Mexican,

On Friday, Flynn accused the Energy Department of muzzling scientists with crucial information about the waste stream.

He said at times during the state’s investigation into the leak, LANL personnel have provided “outstanding communication” about the possible cause of the radiation release. But when the Environment Department has asked for documentation supporting the scientists’ observations, the Energy Department has repeatedly refused to provide it.

“During those positive meetings, information will be referenced, and there’s a willingness [by LANL personnel] to provide information that’s referenced during those meetings or presentations,” Flynn said. “After those meetings, information gets communicated up the chain of command and someone back at [Energy] headquarters decides that no, they’re not going to provide that information to the state.”

Well, they want to know what the nature of the chemical reaction that burst open the drum(s), for one thing.

Another thing is why the isotope ratios in the alleged waste stream from Los Alamos do not match the ratios determined at Station B at WIPP.

Oh, and how much plutonium was released would be nice to know, too.

Greg Mello, executive director of the watchdog organization Los Alamos Study Group, echoed Flynn’s angst that the Energy Department hasn’t openly shared details with regulators about the radiation leak and the waste suspected of causing it.

“Anything else is a sign of a poor safety culture and could be a danger signal for workers and the public,” Mello said. “Mislabeling drums and withholding information can be criminal. That’s one way serious accidents can happen.”

Right, I guess one way for the isotope ratios to not match would be that the drums were mislabeled in the first place. So what is in the drums? Perhaps high-level waste? Did it even come from Los Alamos? Maybe from Hanford?

Yes, it’s criminal. Criminal actions done by criminals in the government or working for the government.

[Los Alamos National Laboratory’s] review of the incident has led to uncertainty over the volatility of hundreds of other drums… The lab notified state environment officials late last month that it was re-evaluating and relabeling as “ignitable” or “corrosive” the contents of 86 drums at LANL… The Department of Energy also is reviewing and relabeling more than 300… stored in WIPP’s underground… [This] raises questions about the scope of the problem that led to the leak at WIPP.

Nobody knows if the other 300 drums involved are going to blow up.

Chris Harris, former licensed Senior Reactor Operator & engineer, Aug 28, 2014 (at 22:15 in): “It sure seems like that there’s a combination of a cover-up, and a combination of slip-shot record keeping. Now there’s talk of whether they ditched those records after the fact or before the fact, but those records are nonexistent. One would expect really good records as to what is being stored, where it’s being stored, when it was put away, when it was stored, all that – every bit of information that one would expect to have in a nuclear storage facility and these are missing, there’s a lot of information.

A new company was put in charge of WIPP records in May, TFE, Inc. Now the records are nonexistent. Hmmm….

TFE contracts with all sorts of nuclear facilities like Oak Ridge. I wouldn’t think it takes a lot of technical knowledge to shred documents, but I am sure they have the experience.

This is a cover-up of a plutonium release that potentially covers half the land mass of the United States.

From the ECRR 2010 recommendations:

We’re talking about plutonium. We’re talking about something that is deadly in infinitesimal amounts.

Sick for the last 5 months.

It is now September 1. I have been sick for 5 months.

The worst neurological symptoms of M.E. (myalgic encephalomyelitis) have subsided in the past couple weeks (though this disease is unpredictable and they could come back at any time). I finally started to work again on the programming project which was interrupted by the sickness and the WIPP catastrophe, though I have to pace myself and I am much slower than I used to be. The cognitive aspects are getting better, but the physical aspects of the disease (pain & fatigue) are still there and are worse in some ways.

This has been the damndest thing, everything I have done to cope with this disease I have learned myself, through trial and error, but especially going to Pubmed and trying to figure out what the hell is going on based on the symptoms I was having. This is a distinct neurological disease, but the medical establishment insists on confounding it with an inflammatory syndrome called CFS, or chronic fatigue syndrome. They even call it ME/CFS. This intentional confusion on the part of insurance companies and psychiatrists has caused untold suffering for people with severe ME. I have had a taste, just a taste of these very bad symptoms, and it is torture. There are people who have been suffering this torture for decades with no treatment, nothing to relieve the misery whatsoever. This is in spite of medications avaliable that are already in use for other diseases which have potential to relieve this suffering.

I have no doubt that oxidative stress from internal radionuclides is the cause of this disease in my case, but it was triggered by the flu-like virus that hit me 5 months ago. Something funky happened to my fingers a couple days before I got sick, they got pruney like they had been submerged in water. I also got minor Raynaud’s-like changes on the cuticles and nails. This is not a normal thing for flu or ILI (influenza-like illness) viruses. Perhaps I ws infected with two viruses. Usually ME is associated with enteroviruses or herpes viruses, which have a Th2 profile, and suppress Th1 cellular immunity. This suppression is augmented by the oxidative stress from radiation. When cellular immunity is deficient, the body cannot clear the viruses out.

Or it could be that the violent illness brought out the HHV-6 virus that hides in the brain, and that everyone has. According to the HHV-6 Foundation,

Like the other herpesviruses—Epstein Barr virus, varicella zoster virus, etc—HHV-6 establishes life-long latency and can become reactivated later in life. This reactivation has been associated with many clinical manifestations that can be seen in the “Associated Conditions” section of this site. Reactivation can occur in locations throughout the body, including the brain, lungs, heart, kidney and gastrointestinal tract. In some cases, HHV-6 reactivation in the brain tissue can cause cognitive dysfunction, permanent disability and death.

A growing number of studies also suggest that HHV-6 may play a role in a subset of patients with chronic neurological conditions such as multiple sclerosis, mesial temporal lobe epilepsy, status epilepticus and chronic fatigue syndrome.

I had incredible skin and joint inflammation since WIPP. And I had a pituitary tumor for over two years that shut down cortisol production. Dr. Martin Pall has said that inflammation and low cortisol are major risk factors for ME.

I am taking it one day at a time. Just barely hanging on.

“My bone cleaveth to my skin and to my flesh, and I am escaped with the skin of my teeth.” – Job 19:20