No corium in Fukushima Unit 1 reactor vessel.

The muon scan of the Unit 1 reactor vessel at Fukushima has been completed. No nuclear fuel was fuel in it. No surprise.

According to this article at Simply Info,

TEPCO published the results of the muon scan done by IRID and their cooperating partners. No fuel was found in the reactor vessel of unit 1 Fukushima Daiichi… This was as expected by many (including us) who have been documenting the other evidence that indicated this was the likely case… Also noted on these images was the lack of detectable solid vessel in the bottom head area. The center lower section of the reactor vessel appears to be missing. The uniform dark outline of the reactor vessel is noticeably missing…

The corium has burned through the vessel and has melted through to the basemat and drywell floor. The question is whether it burned through that too, into the soil underneath. I would say this is very likely.

From this long Sandia pdf,

The drywell floor is subdivided into three regions (i.e., cavities) for the purposes of modeling molten-core/concrete interactions (see Figure 20). The first region, which receives core debris exiting the reactor vessel, corresponds to the reactor pedestal floor and sump areas (CAV 0).

Debris that accumulates in CAV 0 can flow out through a doorway in the pedestal wall to a second region representing a 90 degree sector of the drywell floor (CAV 1). If debris accumulates in this region to a sufficient depth, it can spread further around the annular drywell floor into the third region (CAV 2). This discrete representation of debris spreading is illustrated in Figure 20. (p. 64)

It was already assumed that the molten fuel had interacted with the concrete:

The three accidents (i.e., the accidents in Units 1, 2, and 3), while similar in many ways in terms of SBO accident progression, each proceeded to different degrees of core damage, with Unit 1 believed to be the most severely damaged of the three. It is believed that the Unit 1 core damage proceeded to the point of lower vessel head failure that released core materials to the containment cavity where core-concrete interactions likely initiated. Units 2 and 3 are believed to be less damaged. Collectively, the accidents likely reflect varying degrees of core/reactor damage and are therefore an invaluable source of information that can validate/confirm our current understanding of severe reactor accidents and provide new understanding not currently realized in our body of knowledge. (p. 18)

I was already talking about the corium-concrete reaction when I was still posting at the Japan Earthquake scribble. This must have been in early 2011. The corium-concrete reaction liberates all sorts of radionuclides that wouldn’t have been released otherwise, and the concrete particles help spread the radioactive particles into the wind.

Note high levels of Ba-140 and La-140 on March 15-16. Lanthanum-140 is the daughter product of Barium-140… If a TMI-style meltdown occurred, using Dr. Saji’s inventory figures (below), there would have been a 23:1 ratio of I-131 to Te-129m released. The Takasaki figures indicate a 1:2 ratio. The data do not support this scenario…

“This study describes the increase in iodine activity released to the atmosphere during a severe accident due to the radioactive decay of tellurium precursors… here it is seen that the iodine activity in the atmosphere is due disproportionately to I-132. Unlike the longer-lived isotopes, most I-132 (half-life of 2.30 hr.) existing early in the accident will decay before the significant atmospheric releases which follow reactor vessel failure. However, the supply is replenished by the decay of Te-132, which is released in large quantities from the drywell rubble.”

Takasaki is almost 100 miles from the Fukushima plant. Thus most of the I-132 which was released would be decayed. The large amounts of I-132 detected must have come from the decay of Te-132.

From p. 533, “Upon contact, the molten core material (the so-called “corium”) starts to react with the material of the basemat concrete… when the reaction zone is flooded with sump water… the highest temperatures might be reached… the molten-core – concrete interaction is the principal source of the release of the low-volatility fission products to the containment. The volatilization of these elements, such as barium, strontium, lanthanum, and cerium, is strongly supported by the gas bubbles which penetrate through the molten zone.”

Note again the high concentrations of barium and lanthanum, and that of tellurium.

Conclusion: The emissions observed at Takasaki were not due to a TMI-style accident, but one in which corium interacted with concrete and water. This released significant concentrations of barium, lanthanum, and strontium into the atmosphere.

Well, it’s about time they did this scan. It’s only been 4 years.

FUKU+4 HEALTH NOTE: Really nasty hand-foot-mouth rash on my hands and feet. This is from a disseminated enterovirus infection, from a virus I caught almost a year ago. I don’t know what strain or type of enterovirus it is. It has infected the neurons in the brain and spinal cord (thus it is myalgic encephalomyelitis). Minor improvement today… I did a technical thing, added a Mid-p feature to my Fisher’s exact test program for large samples. It is good to know that I can do math and scientific programming again. Things are still dire, though.

Fuku+4. Cancer rates start taking off.

The 4-year anniversary of the catastrophe at the Fukushima Daiichi is upon us. Radioactive emissions into the air and the Pacific Ocean continue, as they apparently will for centuries or millenia.

Radioactive contamination of air, water, and food is causing and will continue to cause cancer, heart disease, and all immune-related disease, including neurological disease, indefinitely.

But there is a latency period, or time lag, between initial radiation exposure and the development of these diseases. This document, issued by the World Trade Center Health Program, officially determines the minimum latency of types of cancers subsequent to the 9/11 disaster in 2001. This determination was stipulated by Congress after the passage of the James Zadroga 9/11 Health and Compensation Act of 2010.

The assessment of minimum latency periods for various types or categories of cancer is straightforward when exposures occur at a single point in time or regularly. However, most human exposures to carcinogens vary significantly over time, making a precise determination of minimum latency periods difficult… Therefore, the Administrator derived minimum latency estimates using several methods based on the best available scientific evidence for each type or category of cancer considered…

4B: Estimates of cancer latency obtained from statistical models used to estimate the lifetime risk of low-level ionizing radiation-related cancers.

The use of a radiation-induced cancer latency estimate is supported by scientific literature indicating shared mechanisms of carcinogenesis that apply to most solid tumors. Furthermore, cancers that may develop as a result of radiation exposure are indistinguishable from those that occur as a result of exposure to other carcinogens.

If multiple estimates of minimum latency based on statistical modeling in epidemiologic studies were available in the scientific literature, the Administrator’s policy is to resolve any uncertainties inherent in this method [Latency Method 4] in favor of the WTC Health Program member by selecting the shortest latency period…

For solid cancers as a group, an estimate of minimum latency of 4 years is available from statistical modeling of risk between exposure to low-level ionizing radiation and solid cancers [Latency Method 4B].

So cancer latency associated with 9/11 dust is the same as cancer latency associated with Fukushima radiation.

The Administrator has selected minimum latencies for the following five types or categories of cancer:

(1) Mesothelioma — 11 years;
(2) All solid cancers (other than mesothelioma, lymphoproliferative, thyroid, and childhood cancers) — 4 years;
(3) Lymphoproliferative and hematopoietic cancers (including all types of leukemia and lymphoma) — 0.4 years (146 days);
(4) Thyroid cancer — 2.5 years; and
(5) Childhood cancers (other than lymphoproliferative and hematopoietic cancers) — 1 year.

So leukemia and lymphoma started developing in some people a few months after 3/11/11. I’m thinking here of Kevin Blanch, who developed AML leukemia in this time frame… though there are many others.

All other childhood cancers (20 years old or less) started developing in March 2012.

Thyroid cancer in adults started developing in September 2013.

All solid cancers in adults start developing NOW.

Solid cancers are all cancers involving solid tumors like breast cancer, colon cancer, lung cancer, liver cancer, etc.

There is nothing hard and fast about this. Some people have developed cancer already, before this minimum latency period. But this is an official number that was developed as a result of a trade-off. These minimum latencies are in stark contrast to latencies of 5, 10, 20 years that are used in medical literature, and skew results to the pro-nuclear side.

But the Fuku+4 point is significant, not just for minimum latencies, but for the point when certain cancer rates start accelerating. Thyroid cancer in Chernobyl children started taking off at the Chernobyl+4 point.

Sickness in general, among Chernobyl liquidators and their children, also significantly rose at the Chernobyl+4 point. This is very simple, the subject is either sick (from anything), or not. The rise in the sickness rates of the children show that this phenomenon was not due to aging.

My research on myalgic encephalomyelitis.

I wanted to get this out there now. Big changes are coming… I have gotten much sicker after the cold weather started, and getting another virus infection. I am moving out of my home soon, and I don’t know how this is possible without significant muscle exertion, which will makes the disease much worse. So massive uncertainty clouds my immediate future.

I still think I will get better after the weather warms up, but right now there is more snow and severe cold in the forecast, and I don’t know when this will happen.

Most of the links are from Facebook. I apologize to those who cannot access it. There is a way to synchronize Facebook posts to this blog, but I am too sick to do it now.

Type I interferons and interferon-gamma in ME. (FB link)

Immunosuppression causes persistence of enteroviral infections in ME, is the foundation of exertion intolerance, and can be reversed by Type I interferon blockers. (FB link)

Enterovirus infections of the central nervous system. (FB link)

Enterovirus infection of the gastrocnemius muscle, IDO, and peroxynitrite. (FB link)

Serotonin, IDO, and reduced tryptophan catabolism in ME. (FB link)

Picolinic acid deficiency in ME and the kynurenine pathway. (FB link)

TGF-beta is released from muscles 24 hours after exercise, and reduces levels of interferon-gamma. (FB link)

TGF-beta reduces NK cell cytolytic activity and MHC I and II expression. (FB link)

Kynurenine as a possible treatment for ME. (FB link)

Dysregulation of the STAT-1 protein in ME. (FB link)

Activin in ME, generated from muscle activity. (FB link)

Caffeine inhibits tryptophan hydroxylase, which is upgraded after exercise. (FB link)

Swimming exercise increases serotonin levels, and decreases corticosterone, interferon-gamma, TNF-alpha, and IDO levels. (FB link)

The TGF-beta autocrine loop in ME. (FB link)

Psychedelics and the desensitization of the 5-HT2A receptor. (FB link)

Exercise-induced reduction of interferon-gamma levels is the cause of post-exertional immune exhaustion in ME. (FB link)

GABA-B positive allosteric modulators are an effective treatment for ME, but are not yet approved by the FDA. (FB link)

List of TGF-beta inhibitors. I have determined that only those medications that use the Smad pathway are effective for ME. (link)

Brief moderate stretching is effective for reducing post-exertional symptoms after exercise. (FB link)

Moderate acute exercise increases TGF-beta, alpha-amylase, and IgA 24 hours after exercise. (FB link)

Noise increases tryptophan hydroxylase levels, which is a factor in noise hypersensitivity in ME. (FB link)

Brown fat, a key player in ME. (FB link)

Follistatin increases muscle mass after exercise, reduces TGF-beta levels via the Smad pathway, and is a myostatin inhibitor. The muscle repair process recruits interferon-gamma from tissues, and is the cause of exertion intolerance. (FB link)

Interferon-gamma deficiency in “chronic fatigue syndrome” – 1990, after the name change from ME. (FB link)

Ionizing radiation exposure is part of the ME disease process, by its generation of peroxynitrite (ONOO-) via radiolysis. (FB link)

Destruction of groups 1 and 3 innate lymphoid cells and the resultant distortion of commensal bacteria is a fundamental aspect of the ME disease process. (FB link)

Psilocybin reduces the activity of the default mode network. The inability to deactivate the DMN is behind the overwhelming neurological and cognitive symptoms in severe ME. (FB link)

Actimmune (interferon-gamma) is an effective treatment for ME. It does not reduce Type I interferon levels, though, which is necessary for a cure. (FB link)

Psilocybin reduces DMN activity by activating the 5-HT2A receptors. The receptors are typically desensitized in ME due to excessive serotonin production. (FB link)

A high-fat diet restores interleukin-22, and also restores the balance of microbiota in the gut. (FB link)

Limbic kindling vs. central sensitization in ME. My response to Leonard Jason’s research. (link)

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

How ME and radiation sickness has altered my mechanism of thinking. (link)

Origin of M.E. disease process in the immune system. I have found since this, that an enteroviral infection of certain immunoprivileged areas of the brain does the same thing. Any viral, radiotoxic, or other toxic infestation of these brain areas will cause this. It is now known that the upgrade of Type I interferons is behind the dysregulation of the JAK/STAT pathway. (link)

Radiation as the cause of my persistent viral and neurological illness.

I wrote this post about how my way of thinking had changed on July 22, 2014. I try to log everything that happens to me… “where and when” is always essential. The exact timing yields important clues.

I was touted as a “boy genius” as a child… but I am only moderately intelligent. My talent has always been a phenomenal memory. My memory has enabled me to visualize what is going on in large computer programs, and mathematical algorithms that I have developed. I was able to collate large amounts of seemingly disparate information and unify it into a whole. I always saw the “big picture” in front of me. I tried to utilize this in this blog.

Now my big picture vision is a tiny pinhole. I can still do easy tasks like Step 1, Step 2, etc… as long as they have no physical involvement, and I have absolute peace and quiet, with no interruptions.

At the time I wrote the post, I didn’t know how much of this was due to enteroviral ME or radiation exposure. Fukushima radiation has been affecting my memory. I remember in June 2013, when the last major cloud of radioactive iodine started moving across the US, and my thyroid started to swell again, I had a hard time completing simple tasks. I tried to replace a headlight lamp in my car… but I kept reaching for the wrong bulb. I had a heck of a time with it. Online memory tests indicated that I may have had Alzheimer’s. I was convinced that radiation had finally caused me to come down with Alzheimer’s disease. But this was “brain fog”, which is common with fibromyalgia, ME/CFS, SEID, etc.

After the severe enteroviral illness which started on April 1, 2014, encephalomyelitis symptoms started around April 20. The vision in my left eye started getting dark and blurry. Then nystagmus commenced in my left eye. I developed optic neuritis in the left eye, and Bell’s palsy, which is facial paralysis, on the left side of my face. It is common to have these kind of symptoms on one side of the body only with encephalitis and encephalomyelitis, and MS, which is a kind of encephalomyelitis.

In late May, I suddenly went completely deaf. Shortly after this, my hearing started creeping back in, but it was accompanied by very loud tinnitus. Loud noises started to bother me… soon it was any noise, however small. This is called hyperacusis.

A benign tumor had developed on my pituitary gland in 2011. This greatly increased symptoms of my autoimmune disease, and I suffered widespread inflammation. My thyroid in particular, was affected. In January 2012, the tumor had grown so large that affected the fluid transport in my right eye, and it started to bulge out. I lost vision in the eye, except for a small circular ring, and suffered severe migraines. Ololiuqui seeds, which providentially arrived in the mail at this very time, caused the tumor to shrink. I later found that these seeds contain hydergine (discovered by the great chemist Dr. Albert Hoffmann), and I started taking this medication in tablet form, which worked very well to shrink the tumor. Unfortunately, not all the pituitary functions had come back to normal.

So the first thing I thought when I developed tinnitus and hyperacusis, was that the tumor had come back. So I doubled my usual dose of hydergine. Within a half-hour, the tinnitus and hyperacusis had increased tremendously, and the elevated level of this lasted a week. I had researched this medication throroughly, and knew it had been banned in France, due to suspected effects on the heart. What happens is that hydergine binds with the 5-HT2B serotonin receptor, which then releases a large amount of the anti-inflammatory cytokine TGF-beta. This cytokine is implicated in heart injury. It also opposes interferon-gamma, and destroys immune cells which release this pro-inflammatory cytokine. IFN-gamma is the main cytokine responsible for the creation of the IDO enzyme. IDO dysfunction is implicated in many neurological diseases.

Well, this was coming on so fast, that by mid-June I had reached the point where more than one sound happening at once would make me freeze up. My brain could no longer process two things at once. My memory was completely gone, to where I could not remember one second ago. It was like my consciousness was completely erased. These bouts lasted for just a few minutes. But I became frantic. It was around this time that post-exertional malaise (PEM) started occurring. That means these bouts would occur 24-48 hours after any kind of exercise, going to the store, etc.

I had already come across the ICC, the International Consensus Criteria, and I knew I had myalgic encepahlomyelitis. I tried with great difficulty to find forums and FB groups, in order to talk to people who had this disease. But all I could find were people who lacked energy to do anything, who were housebound and bedbound in some cases, and who had “brain fog”. On a scale of 1 to 10, brain fog was 1, and what I had was a million.

It turns out that the disease these people have is not encephalomyelitis at all. It is now called SEID (Systemic Exertional Intolerance Disease). I have exertional intolerance too. A lot of diseases have this as a symptom. The problem was that the CDC changed the name of ME to “chronic fatigue syndrome” (even though it does not include chronic fatigue) in 1988. It also included the disease now called SEID. The name was changed again to ME/CFS in order that it would be “taken more seriously”. So the people with enteroviral encephalomyelitis, which ME traditionally referred to, were left out in the cold completely.

My research has now led me to understand that the exertion intolerance in true ME is due to immunosuppression. This is the shutdown of Th1 cellular immunity, and the lack of Th1 cells in the body. These produce interferon-gamma. This happens because, in certain important areas of the brain, cellular immunity causes destruction of neurons, and the body removes the inflammation completely, allowing the enterovirus to spread.

So there are two things going on. Severe IFN-gamma deficiency causes IDO dysfunction, and a greatly increased amount of serotonin and glutamate activity in the brain. This is metabolic, and in itself causes neurological symptoms. Also, these neurotransmitters bind to receptors, which are neurons infected with the virus. This is where encephalomyelitis in involved, and makes things unpredictably worse.

Muscles release TGF-beta 24 hours after exercise, which drives IFN-gamma and IDO down further. Muscle activity also causes enteroviruses to replicate. This is the cause of PEM.

So what does this have to do with radiation? Dr. Martin Pall has said that the main risk factors for getting ME are:

1. High levels of inflammation.
2. PPAR dysfunction (high blood pressure).
3. Abnormal cortisol levels.

I already had autoimmune disease before Fukushima. The pituitary tumor, as I noted, greatly increased the amount of inflammation. It also disturbed ACTH function by the pituitary, which produces cortisol.

Pituitary tumors occurred at elevated levels after Chernobyl in the affected areas. Iodine-131, cesium-137, strontium-90, and plutonium are implicated. My thyroid problems increased in late 2011 with the radioactive iodine cloud, which I believe were caused by the action of I-131 on the pituitary, not so much the thyroid itself.

The enterovirus caused a case of the “flu” which would have gone away in a week, without the pituitary dysfunction, and accumulation of radioactive toxins in my body. But instead the enterovirus was not cleared out, spread to the brain, and caused a lifelong neurological disease.

Yablokov has a section in his book (pp. 104-112) “Chernobyl: Consequences of the Catastrophe for People and the Environment” which is devoted to neurological illnesses of those contaminated by Chernobyl radiation.

Previous views claiming resistance of the nervous system to radiation damage are refuted by the mounting collective data that demonstrate nervous system illnesses among the populations of the contaminated territories, especially liquidators. Even rather small amounts of nuclear radiation, considered harmless by former measures of radiation protection, have resulted in marked organic damage. Clearly, the existing radiation levels in the contaminated territories have harmed the central nervous system of countless people.

For many inhabitants of the contaminated territories, especially persons that were radiated in utero and liquidators, nervous system functions, including perception, short-term memory, attention span, operative thinking, and dreaming, are deteriorating. These conditions are associated with deep cerebral hemispheric damage: diencephalic areas, deep frontal, and temporal lobes, and occipitoparietal parts of the cerebral hemisphere. Low-dose radiation damages the vegetative (autonomic) nervous system. The fact that intellectual retardation is found in 45% of children born to mothers who went through the Hiroshima and Nagasakai nuclear bombardment is a very troubling concern (Bulanova, 1996).

ME (myalgic encephalomyelitis) is not chronic fatigue syndrome or SEID.

This table indicates the rate of symptoms of 420 UK patients who were classified as having myalgic encephalomyelitis. This is from ‘Myalgic encephalomyelitis–a persistent enteroviral infection?’, a report published in 1990, shortly after Dr. Ramsay’s death. It was the last thing he did.

CFS and ME/CFS were introduced in 1988, after an outbreak of a fatiguing illness in the Lake Tahoe area. ME was already an established name for a particular disease. The new disease did not fit, so ME and the new disease were thrown together and conflated.

The Institute of Medicine has recently renamed ME/CFS to SEID, systemic exertion intolerance disease. The committee noted that ME/CFS did not feature myalgia (muscle pain), or symptoms of encephalomyelitis (inflammation of the brain and spinal cord).

Out of the 420 patients in the table, 383 had evidence of enteroviral infection. Only 3 had evidence of Epstein-Barr virus. ME is overwhelmingly an enteroviral disease.

Note that chronic fatigue is not even on the list. Muscle fatigue or weakness occurs in 100% of patients. Myalgia or muscle pain occurs in 80% of them. According to the IOM, all SEID patients have chronic fatigue, myalgia is not an important symptom, and muscle weakness is not mentioned.

Auditory phenomena occur in 69% of the patients. Tinnitus is very frequent, and deafness is mentioned. This is due to an infection of the central nervous system. Tinnitus is infrequent in SEID. Auditory phenomena occur at a rate three times that of orthostatic tachycardia in ME. POTS is much more infrequent than tinnitus.

Visual disturbances occur at a much higher rate than with SEID. Hyperaethesia, or sensory hypersensitivity, occurs at a very high rate.

It is clear that ME is an infection of the brain and spinal cord, which affects the muscles, and is an immune deficiency disease that allows the infection to persist. Enteroviruses spread by infecting neurons. High rates of neurotransmitter activity, primarily serotonin and glutamate, are brought on by the immune condition. The receptors that these neurotransmitters bind to are infected by the virus.

ME is a very serious disease. SEID was never ME, and the conflation of the two completely different diseases has brought harm to ME patients, and is continuing to do so.

The IOM’s renaming of ME/CFS to SEID is welcome for ME patients. And it is timely because there is currently an epidemic of enterovirus 68 that is infecting children in the US and Canada. Many of them may develop ME, not SEID.

I demand that all Facebook groups, ME associations, websites, blogs, and other entities that use the name ‘ME’ or ‘ME/CFS’ immediately change their names, unless they are devoted specifically and only to myalgic encephalomyelitis.

Cold weather and radiation.

With another bout of cold weather engulfing the US, it’s time to review a little meteorology and atmospheric chemistry. Enenews has posted an article that refers to how radiation increases in cold weather due to the air being compressed at the surface.

Our results illustrate that accidents… could have significant trans-boundary consequences. The risk estimate [shows] increased surface level concentrations of gaseous radionuclides in the Northern Hemisphere during winter and a larger geographical extent towards the north and the east… This is related to the relatively shallow boundary layer in winter that confines the emitted radioactivity to the lowest part of the atmosphere close to the surface…It is the view of the authors that it is imperative to assess the risks from the atmospheric dispersion of radioactivity from potential NPP accidents [for] emergency response planning on national and international levels.

Fukushima blew up in early March 2011, when there was an anomalously cold weather pattern in the US. Places like Florida, which are usually warm, instead were hit pretty hard, especially with iodine-131.

I started writing this paper in February 2011, before Fukushima started. It dealt with how cold weather concentrates toxins in the air, and this affects symptoms of fibromyalgia sufferers. I subsequently discovered some research, mostly by Japanese scientists, who observed that fallout from the ’60s bomb tests increase in cold weather.

Actually it’s not just when it’s cold at the surface. It’s the average temperature between the surface and 18,000 feet. This is highly correlated with the 500 mb atmospheric height. When air cools down, it takes up less space. The 500 mb atmospheric height (HT500) is the point where the weight of the air from a certain altitude to the surface is constant.

When there is less space for the air, the concentration of toxins increases. This causes increased symptom ratings for fibromyalgia patients. This works for ME (myalgic encephalomyelitis) too. I got a horrible relapse just before New Year’s when it got really cold, and it shows no signs of departing.

But when the air is hot, toxins increase also. This is because the air is stagnant, and local sources of pollution like chemical plant emissions and auto exhaust tend to linger, and descend to the ground. There is also a health effect in hot weather. This works for ME too.

It turns out that toxins that originate from distant sources (like Japan) tend to increase in cold weather, while locally produced toxins increase in hot weather. Which one affects your health depends on the individual.

Miyake et al. (1962): “It was found that the specific radioactivity in rain water or the air activity was much higher when there was a trough at the 500-mb level [low HT500] or above and the core of a jet stream was located above or a little south of Tokyo.”

Miyake et al. (1960): “There is little correlation between the surface weather conditions and fallout while a considerably higher correlation was found among a trough at 500 mb, position of jet stream and air activity… These facts will account for the increase of the concentration of radioactive debris in the air and the rain with the passage of a trough line at 500 mb across an observation point.”

Chen et al. (1970): ”The dates of occurrence of peak concentrations of fallout particles generally coincided with (a) the arrival times of air masses at 500 mb and/or 300 mb after completing a cycle around the world, and (b) the passage of 500 mb troughs at Fayetteville… All these peaks have a direct correlation with the passage of the 500 mb trough. The dynamic explanation of this process is that to the immediate west of the upper-level trough, we usually find low-level divergence and upper-level convergence with the descending motion. It is this descending motion that brings down upper air and thus tends to increase the particle concentration. Miyake et al. (1960) also reported that similar meteorological conditions play an important role in the transport of radioisotopes from the stratosphere to the troposphere. They noted that the Sr-90 concentration in the ground-level air showed an increase after the passage of a 500 mb trough.”

Here is the forecast for HT500 at 1 PM on Friday:

This means that HT500 500 mb heights at that time will be low (cold) for Pennsylvania & Maryland, and also southern California. They are high for Montana and South Dakota. See if you can correlate it to your own health.

This is really cool. It’s a novel kind of cluster analysis technique I invented for the occasion:

This means that there are 3 groups of symptoms that move in tandem with respect to the weather conditions.

1. Pain and stiffness
2. Fatigue, concentration problems, memory problems, and sleep issues
3. Anxiety, depression, and gastrointestinal problems

All 3 might get worse when it’s cold. Or pain & stiffness will get worse, while fatigue, etc. get better. Or anxiety etc. might be worse when it’s hot. It depends on the individual and the particular toxin he or she is sensitive to.

I later associated it with beta radiation levels from the EPA data.

So those strange symptoms you are dealing with might be a result of nuclear fallout, as well as a host of other toxins.

WIPP kitty litter theory takes another hit.

A story published today in the Albuquerque Journal says nitrates are now believed to be a part of the cause of the WIPP leak of americium and plutonium last February.

Before there was a cat litter problem in the packaging of waste at Los Alamos National Laboratory, there were nitrates.

The public focus on why a LANL waste drum popped open, causing a radioactive leak that shut down the nation’s nuclear waste repository near Carlsbad in February, has been on organic cat litter that shouldn’t have been combined with oxidizing nitrates. That apparently created a combustible mix that somehow ignited and breached the drum.

But it turns out a red flag should have been raised about any processing of waste containing nitrates, even without organic materials added in, before waste drums were shipped from Los Alamos for storage at the Waste Isolation Pilot Plant.

About two years ago, a procedural change was made at Los Alamos, without the standard safety review, removing requirements to stop waste processing and inform management if “Class 1 oxidizers” like nitrates were encountered in the waste stream.

LANL self-reported the issue and it was disclosed last month in a brief public report by the Defense Nuclear Facilities Safety Board.

The Dec. 19 report says that personnel at LANL’s Waste Characterization, Reduction and Repackaging Facility recently indicated that “a procedural change” in waste processing was made without an adequate review called an “unresolved safety question determination.” “The procedural change,” says the safety board report, “was made over two years ago and removed the requirements to stop waste processing and inform management if, among other things, Class 1 oxidizers (such as nitrates), flammable metals or pyrophoric materials were encountered.”

The report goes on to add that the basis-for-operations plan for the Los Alamos waste facility “does not allow processing of these types of materials.”

So the organic litter, an idiotic choice of material of absorbent material, reacted to the nitates, which is a Class 1 oxidizer. But the nitrates shouldn’t have been there. Waste processing should have stopped and management should have been informed if nitrates were present in the nuclear waste. But a procedural change was made two years ago that relaxed this requirement.

But the procedural change did not only refer to nitrates. It also refers to flammable metals and pyrophoric materials. So these substances might have been in the drums too.

A pyrophoric substance (from Greek πυροφόρος, pyrophoros, “fire-bearing”) ignites spontaneously in air at or below 55°C (130°F).[1] Examples are iron sulfide and many reactive metals including uranium, when powdered or thinly sliced. Pyrophoric materials are often water-reactive as well and will ignite when they contact water or humid air. (Wikipedia)

Plutonium itself if pyrophoric. Why was the rule relaxed, and why were they putting known dangerous materials in the drums?

It was also revealed that WIPP will not be reopening until 2018.

While limited operations are expected to resume sometime in 2016, officials said a new ventilation system and an exhaust shaft would need to be installed before shipments of waste could be accepted again by the plant. That work could take until 2018 to complete…

Watchdog Don Hancock, who attended Wednesday’s meeting in Carlsbad, said officials confirmed that workers would have to wear protective clothing and use breathing equipment while sealing the bunker.

“The initial closure of Panel 6 was supposed to be one of the quick and easy things to be done. It’s not done. It’s not quick. It’s not easy. There are going to be risks to workers just to do that,” he said.

“This is in fact unprecedented and very hard and it’s taking longer and it’s going to cost more than what they’ve generally wanted to talk about,” Hancock said of the overall recovery effort.

Despite delays and added costs, Hancock said WIPP’s reopening shouldn’t be driven by any particular date. He said alternatives need to be considered and the public and technical experts should be part of that process.

A remote video camera is being installed. Supposedly, visual evidence as to how many and the extent of the damage to the waste drums will finally be obtained.

Crews are also using a video camera attached to a special mechanical arm to get a better look at the area where the drum from Los Alamos ruptured. That work is expected to be complete in about two weeks, clearing the way for investigators to finish their final accident report.

Health update: I developed a bad ME relapse just before New Year’s, around the time of the last post here. I have not been able to concentrate or remember anything longer than 10 seconds. That means, any thought or effort has to be formulated within 10 seconds before it goes away. I think the relapse had something to do with the very cold weather we have been having. It has gotten better today, and hopefully it will stay better.

‘Second Chernobyl’ may be underway in Ukraine.

Denis Pushilin, a pro-separatist leader in southeast Ukraine, has said the Ukraine faces a ‘second Chornobyl’ due to Ukraine’s decision to use nuclear fuel supplied by Westinghouse for its Soviet-built nuclear power plants.

He said radiation has increased to 14 times the acceptable norm at the Zaporizhia nuclear plant. This is the largest nuclear power plant in Europe, and the fifth largest in the world.

The Russian news agency Interfax reported that in a statement on December 28, Pushilin said Ukraine faces “a second Chornobyl” due to Kyiv’s decision to use nuclear fuel supplied by Westinghouse — a reference to the deadly 1986 nuclear power plant accident that spead radioactivity over parts of Europe.

Pushilin said that “currently the level of radiation is 14 times higher than the acceptable norm” in the area around the Zaporizhzhya plant and that the problem started November 28 “after an unsuccessful attempt to replace rods in the Russian-made third block (reactor) with the product of the American company Western house.”

According to authorities, Unit 3 of the Zaporizhia plant suffered a short circuit on Nov. 28, and theis reactor was shut down for a week. Pushilin alleges that the reason for the shutdown was the unsuccessful replacement of Russian-made fuel rods with Westinghouse fuel rods.

Today a story came out on a Russian website, documenting a report by Ukrainian emergency services that radiation had increased to 16.8 times the acceptable norm. This story was picked up at

Radiation levels were at 5.05 mSv/yr. The criterion for evacuation in Ukraine from Chernobyl was 5 mSv/yr.

This comes out to 0.58 μSv/hr. Presumably this does not include background radiation. According to the plant operator’s website, background radiation at the plant is 0.10 μSv/hr, which gives a 0.68 μSv/hr dose.

This is equivalent to the less contaminated parts of Fukushima prefecture. It might be around half the amount of Fukushima City. But it seems to be increasing.

But this is from one reactor out of the 6 at the plant. Today, it was announced that Ukraine had reached a deal for Westinghouse to supply nuclear fuel to all Ukrainian nuclear power plants.

Ukraine’s switch to the use of upgraded nuclear fuel from the United States at its nuclear power plants (NPP), built in the Soviet times, could threaten safety both at the domestic level and in Europe as well, the Russian Foreign Ministry said in a statement on Tuesday.

“Moscow was somehow alarmed as Ukrainian Prime Minister Arseny Yatsenyuk announced on December 30 the signing of an agreement with US company Westinghouse concerning nuclear fuel supplies for Ukrainian nuclear power plants,” the ministry said in its statement…

“It seems that the Chernobyl tragedy did not teach Kiev authorities any lessons concerning a scientifically feasible approach to the [peaceful] use of nuclear energy,” the Russian ministry said in its statement. “In might be in fact, that the nuclear safety is sacrificed for the sake of political ambitions or, even more, other tangible interests.”…

“Consequences of possible accidents and meltdowns [at nuclear power plants] will be in the full responsibility of the Ukrainian authorities and US suppliers of [nuclear] fuel,” the statement added.

Safety concerns regarding Ukraine’s switch to the US supplied nuclear fuel were repeatedly voiced by Russian experts and some officials, including by Sergey Kiriyenko, the head of Russian state-run nuclear corporation Rosatom.

So it seems that all 6 reactors will have their fuel rods replaced with Westinghouse fuel at some point. Crimea is nearby Zaporizhia, and it is now part of Russia. Irradiation of Russian citizens, especially due to a switch in fuel supplier from Russia to Westinghouse, would add even more tension to the Ukraine crisis, which is already threatening to lead to global nuclear war.

The reason Ukraine is switching to Westinghouse fuel is political. Russia has already agreed to supply its fuel to Ukraine, and there are no sanctions involved. Ukraine has become a vassal state to the West after the coup earlier this year. It is being used as a pawn, and a place to deploy missiles near the Russian border, in an encirclement strategy by the US and NATO.

In 2012, during a routine inspection, Energoatom reported that Westinghouse’s assemblies had structural damage. It had to swap those for Russian-made fuel assemblies, which the utility estimated cost it $170 million.

After a suit threatened by Energoatom, Westinghouse tried to make good on its deal and produced modified fuel rods for the Russian built VVER-440 reactors. These, too, were found defective.

Indeed, Westinghouse has not fared well in other markets dominated by Soviet built reactors. In 2000, it began supplying nuclear fuel to CEZ, a Czech utility, for two reactors that it helped to modify at CEZ’s Temelin station. In 2009, Russian company TVEL took that business away.

This document enumerates the technical reasons for the defects in Westinghouse nuclear fuel in these plants:

During a core reload in 2012 on the unit №2 and №3 YUNPP the mechanical damages
of TVS-W FAs have been found. Damages have been found at visual inspection of FAs. The some of spacer grids has been damaged. Breakages of SG fragments, squeeze, deformation of petals and an attrition have been detected. Two FAs are recognised as an unsuitable to the further operation, some FAs can be use in a core only after repair, a part of FAs it is ready to operation one cycle and then obligatory inspection at the stand of repair and inspection. The reasons of problems at a core reload and of defects of FAs:
− Lacks of a design of the top nozzle of the FA. The FAs are placing «one on another».
− Insufficient mechanical strength of SGs to radial and axial efforts.
− Lacks of a design of the bottom nozzle of the FAs. Corners, sharp edges increase probability of FAs damage at a core reload.
− Bending of FAs.
− Loading in transitive cycles of FAs of type TVSA for which the bending above design values and at the same time high rigidity of a skeleton also is typical. (Maximum design value of a FA bend is 7 mm. Maximum measurements value of blend is 29 mm [ZNPP, 7])…


The rods don’t fit right, lack the features needed for the Soviet-era equipment, and the boric acid formulas don’t work.

“Only one aspect is important: that the nuclear industry has absolute security priority,” Kiriyenko said. “If the nuclear industry begins to make decisions for political reasons, this already poses a threat.,” Kiriyenko said in April and voiced the same opinion two days ago addressing the 58th General Conference of the International Atomic Energy Agency (IAEA) in Austria’s Vienna…

Sergei Kondratyev, a senior expert with the Russian Institute for Energy and Finance, voiced concern over the sharp switch from Russian-to US-produced nuclear fuel as it could pose a threat to the safety of Ukrainian nuclear power plants, which were built in the Soviet Union era.

In an interview with ITAR-TASS Kondratyev said that Ukraine’s decision to switch to the US-produced upgraded nuclear fuel did not take into account technical characteristics and peculiarities of the Soviet-built NPPs.

“The current management of Ukraine’s Energoatom sets the main task to significantly reduce fuel purchases from Russia and switch to the US fuel,” he said. “However, such sharp alternation of nuclear fuel use could result in safety drop at the exploited nuclear power plants and this is definitely unacceptable.” (link)

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.

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.

Centers for Disease Control and Prevention. Chronic Fatigue Syndrome: A Toolkit for Providers. Undated. Accessed December 14, 2014.

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.

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:

The International Consensus Criteria original paper is also available here: