Elevated TSH levels among California newborns after Fukushima.

Well, something is going on. Yesterday I went to two stores, and I actually went for a walk halfway around the shopping mall. I have not walked that much in two months. In fact, I hardly have been going out of the house at all more than once a week. I did pay for it today, with increased neurological symptoms.

But I decided the hell with it, I was going to do an analysis. I haven’t done any programming for four months, ever since the flu/M.E. nightmare started.

Let me tell you how important computer programming is to me. I started programming in 1971, when me and my friend Joel would sneak into the computer lab after hours in high school. They had a phone modem thingy. My first program was a computer baseball program written in BASIC. I picked up the language as I went along.

When I went to college, I learned FORTRAN by using punchcards. This ain’t easy. Punchcards are hardcore. They teach you to not make mistakes. This isn’t the touchy-feely BS they teach nowadays. I am a scientific programmer. I need speed and control.

I bought the original IBM PC in 1982. One of my first programs was an astrology program. I programmed the movement of the planets, any day for 1,000 years. I had to learn Bessel functions and that kind of stuff.

I have developed large database-driven systems for corporations. I have been invited to organize two major conference sessions in academic systems engineering. I have been wined and dined by corporate executives for a printing press scheduling program I wrote. (There is a story behind this. It goes into the inexplicable-things-that-have-happened-to-Bobby1 category. Not right now.)

So I have been always programming, for work, or for my own enjoyment or interests. Till I got sick.

Today, after four months, I was able to do an analysis. It just involved programming in VBA, nothing special. Though the data set was so large I had to expand MegaODA, so I had to find the program, expand its limits to 3 million observations, and recompile it in FORTRAN. I forgot if my computer had SSE4.1 on it, so I had to find and run CPU-Z to verify this.

This is like a marathon runner who suffers a devastating injury, and four months later, is able to take a few halting steps, while everyone applauds. Except nobody is applauding. I have a warm feeling in my heart, that’s all.


Oh, and by the way, this is the most significant result yet on American patients’ health in relation to Fukushima. It is more significant than my 2011 mortality study.

The data came from the Genetic Disease Screening Program at the California Department of Public Health. These are TSH (thyroid stimulating hormone) levels of California newborns for the period 2009-2012. Mangano, Sherman, and Busby used this same dataset for their paper on congenital hypothyroidism which was incomprehensibly botched. Dr. Yarnold and I made comments on this paper here.

While Mangano et al. created arbitrary classifications of hypothyroidism, which are not used in practice, these results reflect TSH levels before and after Fuku. TSH is implicated in many diseases, not just hypothyroidism. It affects the entire hypothalamus-pituitary-thyroid axis. For one thing, increased TSH levels cause the newborn to absorb more iodine-131 than average TSH newborns would.

This is also important because it involves the effect of all species of radioisotopes, I-131, Cs-137, Pu-239, etc. etc. We don’t know if only I-131 affects newborns, in fact Dr. Bandazhevsky has shown that Cs-137 affects thyroids too.

The data have been split up into three seasons:

1. January 1 – March 16
2. March 17 – June 30
3. July 1 – December 31

It involves virtually the entire population of California newborns for the years 2009-2012.

AFTERFUK is an indicator variable, which equals 1 if the birth was after Fukushima, and 0 otherwise. “IF 4.5 < TSH THEN AFTERFUK = 1" means than if TSH is greater than 4.5 (actually 4.99 in the original data), then the newborn is classified as being born after Fukushima. ODA uses maximum-accuracy classification - no model of this form achieves higher classification accuracy. No distributional assumptions are involved.

All three seasons, and the combined data also, show increased TSH levels after Fukushima, and all are statistically significant by two-tailed UniODA at the p<.01 level.

The ESS levels vary from 3.90% to 8.02%. The effect is weak, but I am not a thyroid doctor. Since over two million newborns are involved, even a small effect has consequences for many newborns. I would think that something that would affect even 100 newborns is a big huge deal.

Analysis for January 1 – March 16.

Analysis for March 17 – June 30.

Analysis for July 1 – December 31.

Analysis for the combined seasons.

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

Yablokov et al. in their Chernobyl book demonstrated how radiation exposure affected the brains of liquidators and others at Chernobyl. The brain and central nervous system are some of prominent organs affected by radiation.

Profound cognitive changes have occurred since I came down with ME (myalgic encephalomyelitis) in April. It has affected the way I think, it has affected this blog, it has destroyed my career.

The first image below is a lattice. It reflects the way I used to think, in my previous 59 years. In developing large scientific computer programs, I would sit in a state of concentration for 7 hours at a time. “347 is related to 13, which is related to 3, which is related to 1245″ etc. I was able to visualize the entire thing in my head at once, and move up and down, changing something at the bottom, then moving to the middle or the top, and conceptualize how the small changes affected the entire system. This is also the way I digested information by reading, and how I was able to present it in writing. This whole blog deals with unifying disparate pieces of information on Fukushima and other issues, and combining them into an argument. This is why there is a unique perspective here, as I discover new things by seeing patterns.

Nonlinear lattice thinking.

Linear thinking.

Lattice thinking has gone away. This is difficult to adjust to. It is impossible to multitask in the slightest.

The other image describes linear thinking. “A leads to B, B leads to C, C leads to D”, etc. It’s a chain, not a lattice. I have never been good at this kind of thinking.

But it seems that, while I am now incapable of lattice thinking, the alterations in neurotransmitter functions of serotonin, glutamate, and GABA have IMPROVED linear thinking.

The slightest distraction or exertion will cause me to forget what I was just thinking a second before. Or it will simply go away, POOF. With linear thinking, that means I forget what B is. What I do is simply go back to A and start over. It doesn’t affect this type of thinking like it does the lattice. The only thing I have to do is remember A.

In fact, since I no longer have to remember the entire lattice, this condition has streamlined things, making it easier.

I made a post on Facebook extolling the virtues of fat, for my own health, and ME patients in general.

FAT IS GOOD (for me at least)…

I should go back to the redneck diet I had years ago. I want to have grease dripping out of my mouth. I want pulled pork in my teeth.

Fat increases lymphotoxin, which increases IL-22, which provides immunity to bacteria, and repairs gut tissues, and alters the balance of gut microbiota.

This was without reading any testimonials whatever from ME (ME/CFS) sufferers. It is a product of the thought process behind this blog post I recently published.

1. I had read from UNSCEAR and the National CFIDS Foundation that radiation exposure impairs STAT-1 functions in the JAK/STAT pathway.

2. When I suddenly came down with ME, my plaque and guttate psoriasis suddenly disappeared. This NEVER happens like this to anyone. The inverse psoriasis remained, but that really isn’t psoriasis of the same kind, it’s due to skin damage from uranium and fluoride, some from Fuku, but mostly from Honeywell.

3. I knew from my previous research in psoriasis that there are two mechanisms for psoriasis, one based on IL-17, the other based on IFN-γ and IL-22. It was obvious that the inverse was based on IL-17, and the plaque and guttate were based on IFN-γ and IL-22.

4. Since STAT-1 contains the genes that produce IFN-γ, and this cytokine had suddenly dramatically decreased, I started a chain of reasoning, A -> B -> C etc.

The lack of IFN-γ causes a lack of SMAD7. The lack of SMAD7 causes an increase in TGF-β. The increase in TGF-β causes Th22 cells to not be differentiated. The lack of Th22 cells causes a lack of IL-22.

See, it explains why the psoriasis suddenly disappeared. It’s all about STAT-1 impairment.

Also, IFN-γ is expressed in group 1 innate lymphoid cells (ILC1). ILC’s are located in Peyer’s patches of the intestines, and other lymphoid nodules. ILC3, or group3 cells, express IL-22. The damage to ILC1 causes damage to ILC3. This causes tissue damage to the gut, and bacterial translocation from the gut to other parts of the body.

I was able to predict that eating fat would repair ILC3, and cause improvement in symptoms. I mentioned this is an ME group, and found that others already do this. In fact, ketogenic diets are popular in treatment of this condition. I had not known this.

So I was able to reason, starting from a particular kind of radiation damage, and presented a hypothesis, which was confirmed. This is what science is all about.

I know that I am on the right track, I know that ME is really radiation sickness, and I know that ME is not an autoimmune disease, but an immune deficiency disease, characterized by a loss of cellular immunity. But I’ll be damned if I can organize something which would demonstrate or prove this. That requires lattice thinking.

But maybe I am still good for something, maybe I can work again, but I don’t know just at what yet.

Latest Fukushima plume. Worst since Sept. 2013?

Lots of alarm bells ringing. Fukushima Diary has a story about a spike in radiation after a small earthquake. This is corroborated by many other monitors nearby Fukushima. Majia has been reporting on increased webcam activity. I saw on Facebook that radiation levels in Taiwan have risen, and there are high readings in the Midwest US. And there is this reading from a rain sample in Alberta, Canada:

Radioactive Rain – July 17 2014 – 11:20pm

4.98 μSv is pretty bad. Probably 25-40 times normal background. There were previous spikes this year in January and May, but this might be worse. The Aug-Sept 2013 release was really bad. It remains to be seen if this new one is worse. I haven’t looked at sludge data yet.

I can’t tell anymore from my own health. The ME swamps everything with its own signals. Autoimmune disease was so easy then.. relatively.

Origin of M.E. disease process in the immune system.

The sudden onset of M.E. (myalgic encephalomyelitis, ME/CFS) 3 months ago occurred when I when I was experiencing a flare of psoriatic arthritis, an autoimmune disease. The virus infection caused an huge amount of inflammation. Everything suddenly changed virtually overnight… so I have a personal insight into the ME disease process that doctors and other patients may not have.

Internal radiation exposure causes damage to the JAK/STAT pathway.

The JAK-STAT signaling pathway transmits information from chemical signals outside the cell, through the cell membrane, and into gene promoters on the DNA in the cell nucleus, which causes DNA transcription and activity in the cell. The JAK-STAT system is a major signaling alternative to the second messenger system.

The JAK-STAT system consists of three main components: (1) a receptor (2) Janus kinase (JAK) and (3) Signal Transducer and Activator of Transcription (STAT).[1]

Many JAK-STAT pathways are expressed in white blood cells, and are therefore involved in regulation of the immune system.

The receptor is activated by a signal from interferon, interleukin, growth factors, or other chemical messengers. This activates the kinase function of JAK, which autophosphorylates itself (phosphate groups act as “on” and “off” switches on proteins). The STAT protein then binds to the phosphorylated receptor, where STAT is phosphorylated by JAK.The phosphorylated STAT protein binds to another phosphorylated STAT protein (dimerizes) and translocates into the cell nucleus. In the nucleus, it binds to DNA and promotes transcription of genes responsive to STAT… (link)

The STAT protein (Signal Transducer and Activator of Transcription, or Signal Transduction And transcription) regulates many aspects of growth, survival and differentiation in cells. The transcription factors of this family are activated by Janus kinase (or ‘Just Another Kinase’, JAK) and dysregulation of this pathway is frequently observed in primary tumours and leads to increased angiogenesis, enhanced survival of tumours and immunosuppression. (link)

Specifically, radiation impairs the activity of STAT-1 protein, which is required for IFN-γ signalling. (link) IFN-γ is the hallmark Th1 cytokine, which is involved with cellular immunity.

We have recently characterized different mutations responsible for partial STAT1 functional deficiency. STAT1 is an essential protein for the signal transduction induced by IFNγ, under its homodimeric form (STAT1/STAT1, known as GAF) as well as its heterotrimeric form (STAT1/STAT2/p48, of ISGF3)… As a result, these observations prove that IFNγ-mediated anti-mycobacterial immunity depends on STAT1 and GAF. The characterization of patients with a STAT1 complete deficit and showing severe viral infections demonstrates that type I IFNs-mediated antiviral immunity is STAT1-dependent and ISGF3-dependent, at least for Herpes viruses. (link)

ME/CFS is usually linked to herpes viruses, Epstein-Barr viruses, or enteroviruses. Degradation of the STAT-1 pathway reduces immunity to these viruses. Herpes viruses hide in the immune system. They can become reactivated at any time. Everyone has these viruses latent in their systems since childhood. They are just waiting for a trigger to come back.

Smad7 is a protein, the expression of which is induced by STAT-1 and IFN-γ.

SMAD7 is a protein that, as its name describes, is a homolog of the Drosophila gene: “Mothers against decapentaplegic”. It belongs to the SMAD family of proteins, which belong to the TGFβ superfamily of ligands. Like many other TGFβ family members, SMAD7 is involved in cell signalling. It is a TGFβ type 1 receptor antagonist. It blocks TGFβ1 and activin associating with the receptor, blocking access to SMAD2. (link)

Here we present a basis for the integration of TGF-beta and IFN-gamma signals. IFN-gamma inhibits the TGF beta-induced phosphorylation of Smad3 and its attendant events, namely, the association of Smad3 with Smad4, the accumulation of Smad3 in the nucleus, and the activation of TGFbeta-responsive genes. Acting through Jak1 and Stat1, IFN-gamma induces the expression of Smad7, an antagonistic SMAD, which prevents the interaction of Smad3 with the TGF-beta receptor. (link)

So radiation damages the STAT-1 pathway, reducing IFN-γ, and reducing Smad7, which causes uncontrolled growth in TGF-β levels. This cytokine suppresses the immune system further, and causes the development of Treg cells, which regulate and suppress the immune system.

TGF-beta and CD4+CD25+ regulatory T cells (Treg) both play an important role in the control of immune responses and the maintenance of immune homeostasis. The mechanism of suppression induced by Treg and the factors which regulate Treg function and number, have only begun to be elucidated. TGF-beta seems to act as an effector cytokine involved in the immunosuppressive function of Treg in vitro and in vivo, although its origin and mechanism of action remains to be defined. In addition, TGF-beta signaling in peripheral Treg seems to be essential for the regulation of peripheral Treg numbers and for their immunosuppressive function in vivo. This review will focus on the role of TGF-beta for the generation and expansion of CD4+CD25+ Treg, as well as for their immunosuppressive function in vitro and in vivo. (link)

IL-22 (interleukin-22) is a cytokine that is produced by Th17 and Th22 cells. TGF-β counteracts IL-22 and reduces the differentiation of Th22 cells.

IL-22 a member of a group of cytokines called the IL-10 family or IL-10 superfamily (including IL-19, IL-20, IL-24, and IL-26),[4] a class of potent mediators of cellular inflammatory responses… IL-22 is produced by activated DC and T cells and initiates innate immune responses against bacterial pathogens especially in epithelial cells such as respiratory and gut epithelial cells. IL-22 along with IL-17 is rapidly produced by splenic LTi-like cells [6] and can be also produced by Th17 cells and likely plays a role in the coordinated response of both adaptive and innate immune systems. (link)

IL-22 is an important part of immune protection against enteropathogens. Depletion of Th22 cells depletes IL-22.

Th22 cells are an important source of IL-22 for host protection against enteropathogenic bacteria…

Interleukin-22 (IL-22) is central to host protection against bacterial infections at barrier sites. Both innate lymphoid cells (ILCs) and T cells produce IL-22. However, the specific contributions of CD4(+) T cells and their developmental origins are unclear. We found that the enteric pathogen Citrobacter rodentium induced sequential waves of IL-22-producing ILCs and CD4(+) T cells that were each critical to host defense during a primary infection. Whereas IL-22 production by ILCs was strictly IL-23 dependent, development of IL-22-producing CD4(+) T cells occurred via an IL-6-dependent mechanism that was augmented by, but not dependent on, IL-23 and was dependent on both transcription factors T-bet and AhR. Transfer of CD4(+) T cells differentiated with IL-6 in the absence of TGF-β (“Th22″ cells) conferred complete protection of infected IL-22-deficient mice whereas transferred Th17 cells did not. These findings establish Th22 cells as an important component of mucosal antimicrobial host defense. (link)

IL-22 suppresses bacterial translocation in the intestines, and promotes regeneration in the cells of the epithelial wall. It also activates STAT-3. IL-22 deficiency counteracts all this.

Intestinal mucus functions as a lubricant and a physiological barrier between luminal contents and mucosal surface (59). Mucin (Muc) 1, which is a heavily O-glycosylated membrane-bound mucin, represents one of the major components in the intestinal mucus (59)… Interestingly, a recent study proposes the ability of Muc1 to suppress the expansion of both Th17 cells and IL-17-producing ILCs presumably by blocking the translocation of bacterial products from intestinal lumen into intestinal lamina propria (62)… Interestingly, the ability of IL-22 to promote the production of functional Muc1 through activation of STAT3, but not STAT1, has been demonstrated using human colonic cancer cell lines (T84 and HT29) and primary colonic epithelial cells from mice (9,67)… IL-22 has been demonstrated to promote the epithelial cell regeneration with goblet cell restitution under intestinal inflammatory condition, but it may play no obvious role innormal colonic epithelial homeostasis in the healthy state (9,21). (link)

Cinnabarinic acid is a product of tryptophan metabolism, activates the aryl hydrocarbon receptor (AHR), and is an important source of IL-22.

The aryl hydrocarbon receptor (AHR) binds to environmental toxicants including synthetic halogenated aromatic hydrocarbons and is involved in a diverse array of biological processes. Recently, the AHR was shown to control host immunity by affecting the balance between inflammatory T cells that produce IL-17 (Th17) and IL-22 versus regulatory T cells (Treg) involved in tolerance. While environmental AHR ligands can mediate this effect, endogenous ligands are likely to be more relevant in host immune responses. We investigated downstream metabolites of tryptophan as potential AHR ligands because (1) tryptophan metabolites have been implicated in regulating the balance between Th17 and Treg cells and (2) many of the AHR ligands identified thus far are derivatives of tryptophan. We characterized the ability of tryptophan metabolites to bind and activate the AHR and to increase IL-22 production in human T cells. We report that the tryptophan metabolite, cinnabarinic acid (CA), is an AHR ligand that stimulates the differentiation of human and mouse T cells producing IL-22…

Although the AHR was initially proposed to affect Treg and Th17 development, a Th17-associated cytokine, IL-22, is even more specifically dependent upon AHR activation [13]. Ahr -/- mice retain the ability to generate some Th17 cells but are compromised in terms of IL-22 production [13,17]. Human T cell differentiation also exhibits distinct requirements for the AHR: activation of the AHR in stimulated human T cells was found to inhibit Th17 differentiation and to promote the differentiation of CD4+ T cells that produce IL-22 [18]…

Potential enzymatic modulators that can regulate the generation of CA from 3-HAA would predictably affect the resolution of inflammation. Such enzymes include ceruloplasmin [39], super-oxide dismutase [33], catalase [33], and the fungal virulence factor, laccase [39]…

We have shown previously that tryptophan catabolism can result in a loss of Th17 cells in the context of HIV disease through generation of 3-HAA [30]. We hypothesize that this loss, particularly within the gut mucosa, allows for ongoing inflammation due to continued microbial translocation. Conversion of 3-HAA into CA could reverse the effects of 3-HAA within immune cells, and thereby restore IL-22-producing cells in the context of increased IDO activity. This would allow for the resolution of the inflammatory signaling cascade by strengthening the mucosal barrier, thus stopping a vicious cycle that might otherwise drive disease progression [30]. Although IL-22 was initially linked to IL-17 as a pro-inflammatory cytokine, recent evidence suggests that it probably plays an independent immunoregulatory role in the context of non-hematopoietic cells, maintaining epithelial cell homeostasis in the mucosal tissues [50,57,58]. If so, the pathways that lead to the generation of CA may operate in tandem with the immunosuppressive mechanisms linked to tryptophan metabolism to generate a population of IL-22 producing cells that plays a specific role in tissue repair following inflammation [58]. (link)

So the initial insult of the disease that triggers ME causes massive inflammation, but the lack of IL-22 causes the damage from this inflammation to not be healed, which results in bacterial and viral translocation from the gut. Consequently, the patient is repeatedly re-infected with these pathogens. The lack of IFN-γ and IL-22 reduces innate and adaptive immunity to these pathogens. Tryptophan metabolism is also affected, and its normal function in healing of the gut is abrogated by excessive amounts of TGF-β.

This immune process begins a dysfunctional process that affects the entire body. But it begins with STAT-1 impairment. An effective treatment for M.E. would target the source. Everything else has to do with reducing symptoms.

The canary died.

Well, it has come. I am no longer a radiation canary. The ME (myalgic encephalomyelitis) I have developed after a very bad bout with influenza has its own ups and downs, and I can no disentangle the radiation ups and downs from it… and I am not sure that I even have radiation ups and downs anymore. I’m just screwed.

canary in a coal mine

An allusion to caged canaries (birds) that mining workers would carry down into the mine tunnels with them. If dangerous gases such as methane or carbon monoxide leaked into the mine, the gases would kill the canary before killing the miners, thus providing a warning to exit the tunnels immediately.

(idiomatic) Something whose sensitivity to adverse conditions makes it a useful early indicator of such conditions; something which warns of the coming of greater danger or trouble by a deterioration in its health or welfare. (link)

I have been researching, writing, keeping a diary of my symptoms, talking about radiation-induced fungus, plant damage, other Japanese, Chinese, and American nuclear power plant meltdowns, the Bravo bomb, Fukushima, Honeywell Works, WIPP. I’ve been yelling and screaming.

That’s all behind me now, the rubber has hit the road, the shit has hit the fan. I am FRANTICALLY trying to stay one step ahead of this stupid disease, which few seem to know anything about, and especially doctors. Basically I have figure out what it is, from my own symptoms, and infer the whole damned disease process on my own, with increasing physical and cognitive impairment going on the whole time. I have to prioritize getting a handle on the symptoms so I can keep thinking, and so be able to find a more lasting solution to it.

So everything is all biochemistry now. I’m sorry… this is a radiation blog, but ME and its cousin CFS (chronic fatigue syndrome) are really radiation sickness anyway. So it is somewhat on topic. Maybe I will be able to help the rapidly expanding number of people who will come down with this.

I’ve done all I can. I have to try to save my own ass now. Thanks everyone.

Fukushima AIDS, part 4: ME/CFS.

Fukushima AIDS, part 1 here, part 2 here, part 3 here.

I spent the day looking for a treatment for the encephalomyelitis I developed after a severe viral infection. It appears that TGF-beta (the immune system cytokine, transforming growth factor beta) levels suddenly shot up a couple weeks into the illness, back in April. TGF-beta antagonizes IL-22 (interleukin-22), which is one of the pathways for psoriasis. It also causes an autoimmune reaction to the optic nerve. This is what happened. I developed uveitis on the back of the eyeball, where it joins the optic nerve, and the psoriasis suddenly went away. IL-22 also protects the intestines against inflammation, and when it went away, bacteria and viruses suddenly started moving through the blood-brain barrier. I had a “Th2 shift” from autoimmunity to allergy, and an immune reaction to serotonin developed… I am showing demyelinating symptoms like nystagmus and Bell’s palsy. Antibodies to the 5HT receptor myelin are being created. The myelin acts as an insulator for nerve impulses in axons, and it is being degraded, so this is affecting electrical transmission in the nervous system. Multiple sclerosis is a demyelinating disease, and there are some similarities to this.

The immune reaction to serotonin basically means that I have become allergic to my own nervous system.

I was having an extraordinary psoriasis flare when I came down with the flu. Psoriasis sufferers say the one good thing about their disease is that they never get sick. Well I had psoriasis real bad and I got real sick. The result was an extreme amount of inflammation. Massive amounts of cells were killed. So there were dead cells all over the place, full of bacteria, viruses, and radionuclides like plutonium. My immune system suddenly shifted to clear these dead cells out (apoptotic cell clearance). (link) Macrophages came to eat up these dead cells. But the cell clearance facility was impaired. The dead cells started leaking out.

It has been known for 25 years that TGF-beta levels shoot way up with radiation exposure. TGF-beta also causes hair loss… when you hear that radiation causes hair to fall out, it is because TGF-beta levels are elevated in the hair follicles.

This is really ME/CFS, or actually myalgic encephalomyelitis. (link) Both the serotonin antibodies and the bacterial translocation from the intestines are symptoms of this disease. (link)

Myalgic encephalomyelitis was officially listed as a neurolgical disease by the WHO in 1969. In 1988, the FDA changed the name of it to “chronic fatigue syndrome”. This was in the wake of Chernobyl. CFS became a “wastebasket diagnosis” when a doctor that couldn’t find out the reason for the fatigue would diagnose it as CFS, even if it was really due to heart disease or for some other reason. The upshot was that when researchers attempted to find biomarkers for the disease, the ME people were mixed together with the CFS people, and no consistent results could be found. This was by design. The Russians knew from Mayak and Chernobyl that encephalomyelitis was a consequence of chronic radiation sickness. There is almost no money allocated by the government for ME/CFS research.

The pituitary tumor medicine which I was taking, which is an agonist for the serotonin receptors, caused a reaction, and I had to stop taking it. If the tumor gets huge again, and I have this disease, I am in uncharted territory. I have searched Pubmed and there are no case reports for such a thing. There is nothing for a doctor to base his opinion on. I know it can’t be good. Anyway ME/CFS has no cure or effective treatment by itself, either.

So the idea is to reduce TGF-beta… alpha lipoic acid is an antioxidant that seems to help. Pomegranate and oak ellagitannins also help, I have used these before for arthritis. Certainly reactive oxygen species play a large role in this, which are countered by antioxidants.

Phenibut helps a lot, but only for symptomatic relief. It is similar to baclofen and Lyrica, a GABA-B agonist. Phenibut reduces the release of 5-HT into the brain, and consequently reduces the immune reaction to it. It doesn’t deal with the cause of this, but it makes life manageable. It is not going to stop deterioration of the nervous system.

This has been an ordeal. When it gets bad, the brain fog, tinnitus, pressure & headaches are so bad that I can’t think. I have a difficult time with distractions, and even when there is absolute peace & quiet I find it hard to organize disparate bits of information, which is what this blog is all about. I am a programmer, and my whole career has been about mental focus and concentration. That is what has gone away. It is certainly scary, it is getting worse, and I know that 25% of those with true M.E. are bedridden and need care. It is easy to see how this could happen, and soon.

I will try to keep this blog going as long as I can, while I try to get a handle on this.

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

Part 1 in this series is here.

1. Background:The Honeywell Metropolis Works in Metropolis, Illinois is authorized by the Nuclear Regulatory Commission (NRC) to convert 150 million pounds of raw yellowcake from uranium mining operations to uranium hexafluoride (UF6), which is then shipped to the USEC uranium enrichment facility in Paducah, to produce nuclear fuel for nuclear power plants, and nuclear weapons production applications. This plant has a long series of UF6 releases and multiple environmental violations. Honeywell has engaged in union-busting tactics, and commenced a 13-month lockout of its union (United Steelworkers) in 2010-2011. They hired scabs to replace them, and the NRC granted it an unprecedented exemption to use poorly trained scabs in a nuclear facility to replace the locked-out union members. David Cote, Honeywell CEO, has a cozy relationship with President Obama, and Honeywell was the leading corporate contributor to the Democratic Party for the 2010 elections, even though he is a Republican. He is an outspoken supporter of the Keystone XL pipeline, which would ship oil from the environmentally destroyed tar sands region in Alberta, Canada, to Texas.

2. On May 10, 2012, Honeywell officials announced to the union members that they must clear the plant immediately. They privately said to the workers that this was due to “sabotage” of plant equipment. The NRC and the media reported that this was due to “equipment failure”. Most of the salaried employees stayed. NRC inspectors had been on hand at the plant since April.

3. May 12, it was reported on the union local Facebook page that private contractors from the Shaw Group had been called in. It was noted that Shaw gets paid twice as much as the laid-off union workers. Shaw Areva is the operator at the Savannah River site, at which the construction of a MOX plant was recently cancelled/put on hold, and which is to accept spent nuclear waste from Germany.

4. May 14, a UF6 release occurred at the plant. NRC inspectors did an on-site inspection.

5. May 18, a notice is published in the Federal Register of a change that Honeywell uses to measure radiation dosage for its workers, allowing up to 20 times more uranium exposure than previously.

6. May 21, NRC chairman Gregory Jaczko announced his resignation.

7. May 30, a much larger UF6 release occurred at the plant. The NRC later announced that it amounted to 21 pounds, but this was from a “review”, not a direct inspection.

8. May 31, reporter Mike Elk was physically restrained from asking Cote a question on Capitol Hill.

9. June 13, the increase in allowed uranium exposure officially took effect.

10. July 12, Honeywell announced that the plant will be shuttered indefinitely, as a response to Fukushima, to be upgraded as protection against earthquakes and tornadoes. It was reported that Shaw has no experience in such work, which should have been performed by union members.

11. January 2013, union workers began to be called back to work.

12. November 4, 2013, it was reported that the refrigerator in the control room at the Honeywell plant was contaminated with uranium.

13. March 7, 2014, Honeywell CEO David Cote was elected to the board of directors of the Federal Reserve Bank of New York.

14. May 14, 2014, the Huffington Post reported that commissioner William Ostendorff of the NRC had invested in Honeywell stock during the lockout.

More to follow…

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


I came across this document while researching the radiological and health effects of uranium:

Mr. Larry Smith
Plant Manager
Honeywell Metropolis Works
P.O. Box 430
Metropolis, IL 62960


Dear Mr. Smith:

This letter refers to the inspections conducted from April 1, 2012 through June 30, 2012, at the Honeywell Metropolis Works facility. The purpose of the inspections was to determine whether activities authorized under the license were conducted safely and in accordance with NRC requirements. The enclosed report presents the results of these inspections. On May 3, 2012, May 25, 2012, and July 26, 2012, the findings were discussed with you and other members of your staff.

From the company website:

Metropolis Works is the only facility in the country that converts uranium ore into uranium hexafluoride (UF6). UF6 is an essential compound used to produce enriched uranium for use as fuel in nuclear power plants, which provide about 19 percent of America’s electricity. Metropolis Works is part of the Fluorine Products business within Honeywell Performance Materials and Technologies. (link)

Honeywell Uranium Hexafluoride Processing Facility, a uranium conversion facility, is located 3 km northwest of Metropolis, Illinois. The plant, Honeywell Specialty Chemicals in Metropolis, Illinois, has a nominal capacity of 15,000 tU uranium per year. The plant manufactures a variety of products, but about 80 percent of the plant’s work involves refining raw uranium ore into uranium hexafluoride. Across the Ohio river in Paducah, Kentucky, the Paducah Gaseous Diffusion Plant, can enrich the uranium hexafluoride into various levels for nuclear power or nuclear weapon purposes. (link)

So this plant is located near the southern tip of Illinois, across the Ohio River from the USEC uranium enrichment plant. Honeywell converts raw yellowcake into uranium hexafluoride. It is then shipped across the river, where the USEC plant utilizes the UF6 in enriching uranium for nuclear power plant fuel. Apparently there is also a role in the production of nuclear weapons.

It is the only facility of its kind in the United States.


On May 14, 2012, and again on May 30, 2012, there were accidental releases of uranium hexafluoride from this plant. According to the NRC document:

On May 14, 2012, the inspectors conducted an on-site inspection following a release of UF 6 during the preparation of a 48Y cylinder (Cylinder AC-123) for washing. The inspectors determined that in preparation for visual inspection of the internal surface, cylinder washing is normally performed by yard workers. At the time the release occurred, a salaried employee was performing the operation in accordance with the licensee’s procedure for washing UF6 cylinders. While preparing a cylinder for washing, the cylinder wash operator accidentally damaged the valve on the cylinder. The operator continued to prepare the cylinder for washing and while disconnecting the cylinder drain plug to insert a specialized wash adapter on the cylinder, released residual UF6 from the cylinder. From review of the procedure, the inspectors determined that the operator did not adhere to the written requirements of the procedure…

On May 30, 2012, operators were preparing a work site to make a line break to change out a pressure indicator on the auto sampler. The operators were establishing a second vacuum source using a Kinney pump on the first floor in distillation. The operators lined up the vacuum to the auto sampler, through the secondary sample cold trap using the Kinney pump on the first floor. The plant was in an annual shutdown and the cooling system for the cold traps was being serviced. Because the plant was shutdown, the cold traps were at ambient temperature, approximately 109 degrees Fahrenheit. When the operators started the Kinney pump and pulled a vacuum on the cold trap, it caused the UF6 in the cold trap to sublime releasing UF6. Approximately 21 pounds of UF6 was released exposing five operators who were treated at the dispensary with calcium gluconate and later released to return to work.

The graphic above, showing an atmospheric plume from the May 30 release, is from the web version of the HYSPLIT atmspheric dispersion model. I live in Maryland, near Baltimore.


UF6 is vary dangerous. When it mixes with water vapor from the air, it is split into uranyl fluoride and hydrofluoric acid, both of which are very toxic. This document referred to a UF6 release in Oklahoma in 1986:

When UF6 is released into the atmosphere, it reacts with the moisture in theatmosphere to form uranyl fluoride (UO2F2) and hydrofluoric acid (HF)… The HF is a corrosive and irritating acid vapor that can severely harm the lungs and skin if exposed in sufficient concentration. The UO2F2 forms a particulate, which is very soluble in the lungs, and can be carried away by the wind and deposited onto the ground. As the released material was dispersed, an individual offsite could have been exposed to the plume carrying these chemicals. The plume, where it was highly concentrated, was visible and could be immediately irritating to the lungs. The immediate effects from the exposure of these chemicals are edema of the lungs, skin irritation from exposure to HF, and renal distress due to heavy metal (uranium) intake…

UO2F2 is a soluble form of uranium. Thus, the predominant target organ for the acute uranium intake as a result of this release is the kidney, and the toxicity is primarily chemical rather than radiological. When the UO2F2 particulates eventually deposit on the ground, the chronic effects from the intake of uranium through various pathways are from chemical toxicity as well as radioactivity.

Uranyl fluoride is corrosive, as well as hydrofluoric acid. Uranium (-238) is considered to be weakly radioactive. But it is an alpha emitter, and accumulates in the skeleton. It keeps accumulating for up to three years after exposure. Therefore, long-term effects from radiological toxicity can be expected, as well as short-term chemical toxicity.

Uranyl fluoride is also a neutron emitter. The neutrons come from the action of alpha particles on fluoride. (link) Since uranium is a weak alpha emitter, uranyl fluoride is also a weak neutron emitter. But, since neutron radiation causes chemicals in cells to become radioactive, the bone marrow turned radioactive from the uranium in the bones could cause bone cancer, leukemia, and immune system damage in the long run.


I want to turn back to shortly before I started this blog. Around May 2, 2012, two radiation monitors in Colorado, close to each other, both suddenly registered readings thousands of times above background, at the same time. A day later, I got that familiar tingly feeling on my tongue.

A few days later, I suddenly found myself browsing Enenews. Two days had passed… I had no memory of those two days. Amnesia. Certainly the most bizarre symptom I have had since Fuku. I also had the overwhelming metal taste in my mouth, and I had flu symptoms for a few days. I attributed it to Fukushima, which was going nuts with radiation releases at the time.

I started this blog on May 18. Shortly after, more symptoms started appearing. Bumps on my abdomen, not really psoriasis that I am used to. My left eye started bulging out… I developed a pituitary tumor in January 2012, that caused my right eye to bulge out, and caused loss of vision in that eye. Now it started to appear in the left eye. Things were getting really bad.

Around May 31 and June 1, the symptoms started to increase again. I developed nystagmus, loss of coordination in my legs, arthritis was suddenly out of control. I would get bruises from bumping into walls. Warts started popping out on my skin. I got one on the tip of my nose. The plantar wart on my left foot is still there. Plus cold sores, teeth started loosening. I developed horrible proteinuria (a kidney condition), and the level of bubbles in my urine led me to think kidney dialysis was immediately called for. And about a week later, inverse psoriasis suddenly grew and covered my skin from the hips down to the feet. I am still struggling with this condition, but it is not nearly as bad now.

This was the time when I made this post:

There are too many symptoms to count. There is something wrong with my back, there is something wrong with my neck, there is something wrong with my chest, there is something wrong with my lungs, there is something wrong with my scalp, there is something wrong with my colon, there is something wrong with my kidneys, there is something wrong with my thyroid, there is something wrong with my eyes, there is something wrong with my teeth, there is something wrong with my gums, there is something wrong with my feet, there is something wrong with my bladder, there is something wrong with my fingernails, there is something wrong with my skin. I am racked with pain from head to toe. I can’t move a muscle without my body telling me there is something wrong somewhere.

I looked up videos and testimony from soldiers that were exposed to depleted uranium in the middle east. They had virtually identical symptoms as I had, kidney and skin problems, and cognitive problems, including amnesia. I attributed it to uranium poisoning from a plume from Japan, containing Fukushima radionuclides and uranium from an explosion at a Japanese chemical plant.

Now, with this new information at hand, I believe that the round of symptoms in early May were caused by a plume from Japan. The later escalation of symptoms could better be explained from the uranium hexafluoride release from Honeywell Metropolis Works on May 14, and especially the one on May 30.

There is the kidney damage from soluble uranyl fluoride, and the skin damage triggered from hydrofluoric acid. Plus a host of other things. The release was stated to be 21 pounds in the NRC document. I believe it was much more. The 1986 Oklahoma incident involved 29,000 pounds.


Potrblog noted elevated radiation readings in his blog around this time. St. Louis is in the affected area:


We noticed elevated AIRBORNE radioactivity after a super cell thunder storm moved near our location. The heaviest part of the storm had passed approximately 15 minutes prior to the readings you will see in the video.

These are the highest airborne radioactivity readings we have ever measured in Saint Louis.

There was also a high radiation event in South Bend, Indiana around this time. This is also in the affected area. It is possible that these radiation anomalies were from Fukushima, but they could also have come from Honeywell, or both. It is hard to know. But it cannot be said that there weren’t elevated readings at that time.

The mysterious and strange things that went on at the Honeywell plant, the NRC, and the background politics of the issue will be described in Part 2 of this post.

UPDATE: I have included this excellent talk by Dr. Doug Rokke, the former head of the Pentagon’s depleted uranium project. The symptoms described here are identical those who suffer from exposure to depleted uranium in the middle east, except that there is the additional poison, hydrofluoric acid, involved.

Talk – Dr. Doug Rokke – Depleted Uranium (DU)

Every answer about WIPP provokes more questions.


The popular theory that has been advanced as to the cause of the WIPP plutonium and americium release, which is apparently believed by the Department of Energy (DOE), is that a switch was made from inorganic kitty litter (clay or diatomaceous earth) to organic kitty litter, as an absorbent in containers of nuclear waste from Los Alamos National Laboratory (LANL). Nitrate salts were also added, and the combination of these substances caused a chemical reaction that caused an explosion in one of more containers.

This theory was advanced by James Conca, but has not been confirmed. No chemist, including Conca, would ever have OK’d such a thing. And the change was not approved by the New Mexico Environment Department.

Here Don Hancock, an expert from the watchdog group SRIC weighs in:

Bull Shit! Radioactive "Leak" blamed on "Organic" Kitty Litter at WIPP

The kitty litter theory seems to be ridiculous. Why would they do such a thing? Clay is inert, and binds to plutonium with a strength that science has not fully explained. Organic ingredients emit gases when they decompose, and the addition of nitrate salts cause a chemical reaction. Cost? What could be cheaper than the ingredients of plain kitty litter?


But it came out that the agent responsible for the chemical reaction might have been an organic-based pH balancer. This is making a little more sense, but not much more.

The emails trace LANL’s approval of two products requested by contractor EnergySolutions, which packages LANL waste, to neutralize the pH balance of drum contents sent to WIPP.

The products contain organic ingredients known to be incompatible with the nitrate salts present in the LANL waste containers – “a bad combination,” according to Cole Smith, a chemist in NMED’s Hazardous Waste Bureau.

EnergySolutions asked LANL managers for approval in a May 2013 email to switch to one of the products. LANL approved the change a month later – despite product warnings clearly stating that the product is incompatible with metallic nitrates and “strong oxidizers,” such as nitrate salts, both of which are found in the LANL drums.

Nitrates and organic matter are known to oxidize, a reaction that generates heat.

The other product mentioned in an email was a new liquid to neutralize acids and bases in the drums. When Zeke Wilmot, EnergySolutions industrial hygienist, asked in an August 2013 email for approval to use the product, he notes that “criticality safety issues are not my area of expertise” and “it may be advisable to have LANL personnel weigh in on these issues as well.”

A subcontract technical representative for LANL environmental programs responded to Wilmot and approved the change in a September 2013 email copied to eight other people. The approved product also contains an organic ingredient.

“It wasn’t the most fantastic choice because nitrate salts in combination with organics is a bad mixture,” said Smith, who also serves on the NMED team that writes the permit for WIPP.

“That might be the problem right there,” said William Quintana, head of the New Mexico State University chemistry department. “Nitrates are oxidizers. Every chemist knows that.” (link)

There is some question as to whether a criticality occurred at WIPP, that is, a nuclear chain reaction. This could have contributed to the explosion, and created more radioactive materials to be released, activation products, which are produced by the interaction of neutrons with the containers and other materials underground in the WIPP mine. There were no measurements made of these isotopes, so we don’t know whether this happened or not.

One of the pH neutralizers used was Spilfyter Kolorsafe acid neutralizer, which was used exclusively after April 2013. The material safety data sheet for this product indicates:

Section 7. Handling and Storage

Avoid high heat and/or freezing conditions. Keep container tightly closed. Suitable for general chemical storage under normal warehouse conditions.

NOTE: If this product is stored at temperatures >150 °F or at elevations above 5000 feet, gas may form, increasing the pressure within the container, causing the container to bulge. If bulging occurs, remove the container from the work area and slowly open the container to release the gas.

Be sure to wear proper personal protective equipment.

The product is not supposed to be stored at elevations over 5,000 feet, because it may release gas. Los Alamos is at an elevation of 7,300 feet.


So this theory make a little more sense, it is not quite as stupid as the switch to organic kitty litter, but it is still stupid. At least there is a plausible motive for it.


Mitigating the internal chemistry of these drums, once filled, would have been (and is now) expensive, time-consuming, and potentially dangerous. For all these reasons it must have been unpopular with LANL management, especially once an agreement (the “Framework Agreement”) was made (and widely publicized in the local press) to get these and other drums totaling 3,706 cubic meters of TRU waste off “The Hill” by June 30, 2014. Governor Martinez was prominently identified with this plan, the details of which (and political context of) this organization is not in a position to fully assess.

Suffice it to say that we doubt the value of the Framework Agreement and the wisdom of process that was followed to get it.[3]

Completion of this Agreement was also specifically written into the (very brief and vague) LANS annual Performance Evaluation Plan (PEP) for fiscal year (FY) 2014 as a contract requirement (“Successfully, and cost effectively, complete Framework Agreement commitments to the New Mexico Environmental Department…”, p. 7 here).

In FY13, LANS was docked one year of contract award term (worth about $2 billion in gross income) for failure to meet contract requirements – primarily for having to shut down most of PF-4’s operations starting in June of last year. (PF-4 operations have not yet fully restarted, the topic of the next Bulletin.) The previous year (FY2012), LANS received a “one-time waiver” from the recommended consequences of its failure that year to meet the minimum award term extension requirements, in part because a quarter-billion-dollar security improvement project was mismanaged. More details of what turned out to be a highly controversial ruling by Acting NNSA Administrator Neile Miller at the time are on this page. Ms. Miller no longer works for the government.

Part of the LANS management fee is also dependent on successful completion of the Framework Agreement. As matters stand now, LANL will miss the (quite artificial) deadline and has caused an accident and ongoing safety hazard that places several program management objectives at LANL and WIPP at risk – a strong black mark under several performance measures.

For all these reasons, LANL was under considerable pressure to process and ship its legacy nitrate salt wastes. Perceived or real “production pressure” is a common cause of accidents in the DOE weapons complex, as elsewhere. (link)

So there was a financial motive involved. The private corporation Los Alamos National Security (LANS), which runs LANL, was under pressure to meet a deadline, and would have suffered financially by not meeting it. What does it matter if 200 million people have to breathe plutonium? It’s all about money. Of course, it’s too late now.

So there are still 368 drums at WIPP from this waste stream that are at risk of exploding. Also 57 containers are in a tent at Los Alamos (how reassuring, a freaking tent), and 116 have been shipped to WCS in Andrews, Texas. WCS is little more than just a hole in the ground.


Don Hancock above mentioned that it has not been confirmed that the waste involved came from Los Alamos, but the DOE believes it has. He mentioned Idaho National Laboratory (INL) as a possible source for the waste.

The top of the following graphic shows the isotope measurements for the WIPP release, measured at Station A. The bottom shows the average isotope concentrations for the LA-MIN02-V.001 waste stream from Los Alamos, which has been identified to be the source to the plutonium and americium release.

The WIPP measurements show there was 2 times as much Americium-241 released as Plutonium 239+240. The waste stream analysis shows that there was 92 times as much Plutonium-239+240 in the waste as Americium-241.

That is a huge difference in the isotopic ratios. There is 184 times as much americium as would have been expected from the average amounts in the waste stream.

While there are individual differences in the drums, and since we don’t know how much Plutonium-241 was released from WIPP, it is possible that the WIPP release came from this waste stream, though it really seems unlikely, and the container had to have been an “outlier” that did not reflect the average proportions of isotopes in the waste. If it turns out that more than one container contributed to the WIPP release, this becomes wildly improbable.

Maybe this is has all been a smokescreen to obscure the presence of much more dangerous high-level waste from a site like INL or Hanford.


Well, this is what it is all about. We have seen what cesium-137 from Fukushima is doing to Japan. It will be active for 300 years. Plutonium-239 will be active for 241,000 years.

The ALI limits in the publication Medical Management of Internally Radiocontaminated Patients (p. 44) show that americium-241 and plutonium-239 are dangerous at one-33,000th the amount of cesium-137. One 55-gallon drum of cesium-137 could conaminate the USA for 300 years:

Dividing this volume by 33,000 gives us the volume of seven 00 capsules:

Seven 00 capsules of WIPP plutonium could irradiate the USA for 241,000 years

Fukushima activity is on the rise. Health update.

Fukushima activity is on the rise. These sludge results are around 3 weeks old, but iodine-131 in Tokyo hasn’t been this high since January, and Gunma hasn’t been this high since last September. Increased fission is happening. Certainly both rain and air radiation detections have been elevated lately in North America – there have been significantly elevated readings in Arkansas, Michigan, and Ontario.

The Chiba sludge readings are late… they changed to a once a month publication, and that is even late.

A update about my health issues: Around April 1 I developed a very bad case of the flu. I had a high fever and was in and out of delirium for days. At the same time, I developed these weird symptoms, with fingertips pruney and puckered like just having gone for a swim in the pool. I also had red patches under my cuticles, and some fingernails turned pink and purple. I have psoriasis, but this is not psoriasis.

I was having a severe psoriasis flare at the time I got sick. And it got worse. But after two weeks, the psoriasis suddenly started going away. At the same time, I developed nystagmus in my left eye. The nystagmus was uncomfortable, and I suddenly was experiencing blurred vision in this eye.

I believe that this secondary condition is something called ADEM, or acute disseminated enchephalomyelitis. It is a temporary condition, which is rare in the US, and somewhat less rare in developing countries like India. It is a demyelinating disease, which means that the immune system attacks the myelin sheath that covers nerve axons. It reduces the conductivity of the electrical transmission of nerve impulses. “Disseminated” means it affects both the central nervous system and the peripheral nervous system. It occurs after infections or vaccinations. But it is temporary, frequently goes away within a few days, and almost always is gone within three months.

The reason that this is interesting is that disseminated encephalomyelitis is a symptom of stage 3 of chronic radiation sickness. Weakened immunity is also a symptom of this. What made my psoriasis suddenly go away was a sudden drop in levels of interleukin-22 (IL-22). This cytokine is involved with immunity against viruses and bacteria.

ADEM itself gives flu-like symptoms, and also it is like a case of fibromyalgia from hell, where your head is swimming, and you can’t concentrate on anything.

Well, around the first of the month, I developed uveitis, or inflammation of the eye, along with blurred vision. This is a symptom of ankylosing spondylitis, which has a completely different immune profile than psoriasis. The nystagmus went away and was replaced by eyelid twitching. I made an appointment with an ophthalmologist for this, because uveitis carries the risk of blindness. I think it was last Saturday morning when I looked in the mirror and shuddered… because it looked like I was getting Bell’s palsy in addition to an inflamed eye. This is probably my low point since 3/11/11.

But the weather was nice, and I managed to lay out in the sun at the beach for a couple days. This usually heals me. When I went to my appointment, 5 days after I made it, the uveitis was gone. It went away as fast as the psoriasis did.

My eyeglass prescription for my left eye had changed though. I have been wearing eyeglasses for 52 years, but it never has changed so suddenly and drastically before.

I am still coughing, and I still have ear infections (otitis media). I’m not out of the woods yet. And since my immune system now goes through a revolution every two weeks, I’m not sure what to expect next. I still don’t want to look in the mirror.