Category Archives: Mold and CFS

How To Make Sure An Invisible Disease Stays That Way

Update to CFS – The Invisibled Disease – by Khaly Castle

Would you like a dose of outrage?  Try this.  30 years later, and we have proof.  Not proof that this illness is real.  Not proof that it is biological.  We know these things.  No, I’m talking about proof that the research community at large IS NOT INTERESTED IN RESEARCHING THIS ILLNESS.  NOT EVEN A LITTLE BIT.

Originally published and completely written by Erik Johnson on September 8, 2015, “CFS – The Invisibled Disease” recounted the history of how a syndrome was made to disappear before our very eyes.

Erik’s article documents the events that culminated in the creation and subsequent undermining of the Chronic Fatigue Syndrome.  He says:

Two teachers from the Truckee teachers lounge happened to be in Peterson’s office when CDC epidemiologist Gary Holmes was there.  They asked to see him for something that was on their minds.   Gerald and Janice Kennedy, along with Irene Baker, wanted to know why the flu-like illness could rage through the school, but the teachers IN that lounge were the only ones who didn’t recover.

Gerald Kennedy spoke of his speculation that perhaps the fumes from the copy machines made the difference, or perhaps something bad in the filters from the heating system.   Could a toxic exposure be responsible for allowing the virus to take hold?

Gerald recounted, “I remember telling him (CDC epidemiologist Dr. Gary Holmes.)  about the filters. You could tell he though we were a bunch of loonies.  That was early into it, and we were still thinking, Well, maybe we ARE crazy.  But you would think we would be questioned, at least, and there weren’t a lot of questions.  He just nodded his head.  He seemed to have already made up his mind about us.”

Now… think about it.  What did Irene, Gerald and Janice ask for?

Did they say “Please Dr. Holmes, help us with the horrible virus”?

No, they wanted to know what it was about that room which made the difference.

Here’s the bitter irony:  Over the last few weeks, history has almost exactly repeated itself.  Same players, same location, same results, 30 years later.

On Sunday, August 7 2016, Simmaron Research hosted a patient update event in Incline Village, Nevada.

Dr. Daniel Peterson, one of the original two doctors at the Incline outbreak, was present, as were Drs. Hornig, Knox, and several others.

Also in attendance were the CDC, represented by Dr. Elizabeth Unger, and Truckee High School, represented by Erik Johnson, PROTOTYPE appointed by Dr. Cheney, who came armed with a load of documentation from the original outbreak, and who made the same request that was made 30 years ago by Irene, Gerald and look into what was there at inception.

Erik Johnson took the opportunity at this meeting to offer documentation -from the outbreak that started the syndrome CFS-to researchers present at the Update.  He also offered to take anyone who was interested, including Dr. Unger, on the CFS History Mold Tour, as described in this blog:

Simmaron’s “Patient Update”, August 7 2016.  Dr. Unger from the CDC in the foreground, with Dr. Daniel Peterson standing behind and slightly to the left:

Simmaron Unger Peterson

Erik Johnson, prototype and survivor of the Incline Village inception of the Chronic Fatigue Syndrome.  Peterson and Unger still in the background:

Simmaron Unger Johnson

Erik Johnson sitting and chatting with Dr. Elizabeth Unger, who is holding the documents that were just given to her AT THIS MEETING by Erik Johnson:

Simmaron Johnson Unger 2

Dr. Elizabeth Unger of the CDC looking through the documents given to her by Erik Johnson, while Dr. Peterson hovers closely:

Simmaron Unger Peterson documents

To be fair, the only researcher present who showed interest in the documentation Erik brought…was Dr. Unger from the CDC.  The folks at Simmaron were dismissive, and actually told Erik that he was being rude.  There you go.  I think we all suspected that researchers weren’t the slightest bit interested in what patients have to say.  But how despicable for researchers who were actually there at the inception of a syndrome to completely brush off their own appointed prototype, who presented solid documentation from that time period which never was given consideration.

As far  as Dr. Unger goes….

Here’s the solid proof that there is no interest in pursuing real research into the Chronic Fatigue Syndrome.


Dear Erik,

Thank you for your message. I have read the information you provided about mold at Lake Tahoe. I have made inquiries at CDC about how mold exposure is approached and have learned methods are not particularly reliable. I appreciate your offer to provide more information, but it is not necessary at this time.
Best wishes,
Beth Unger

In closing, I (Khaly Castle) find the entire CFS research community to be contemptible.  Whether or not a researcher finds anything is not the issue.  Whether or not a researcher can be bothered to LOOK is the primary qualification for being a researcher.



Documentation provided to Dr. Unger and others included the following:

Truckee, California. Coincident with, and reported as part of an outbreak of CFS in northern Nevada and Califor-nia [13, 17, 24], nine of 10 high school teachers who used a single, small, poorly ventilated conference room became ill sequentially. All nine teachers required a leave of absence, and two retired. Eight teachers remain ill 5 years after the onset of the outbreak. The one unaffected teacher spent less time than the others in the conference room, often doing his wor…k outdoors. The conference room was one of four rooms serviced by an all-water heating system installed in 1985. It functioned by using variable air flow over a coil filled with hot water. The fresh-airv ents were sealed with no other sourceo f fresh air available. There were no functioning windows or air con-ditioning. A spirit duplicator and two coffee machines were in the room. The onset of illness was generally sudden, evolving over 1 month, and fatigue was the predominant symptom. Headaches, myalgias, and dyspnea were other common com-plaints. Photophobia was often noted, with difficulty keeping the eyes open even in darkness. Many individuals experi-enced recurrent sinusitis. The prevalence of severe fatigue is noted in figure 1.
Clin Infect Dis. 1994 Jan;18 Suppl 1:S43-8.
Concurrent sick building syndrome and chronic fatigue syndrome: epidemic neuromyasthenia revisited.
Chester AC, Levine PH.
Georgetown University Medical Center, Washington, D.C.
Sick building syndrome (SBS) is usually characterized by upper respiratory complaints, headache, and mild fatigue. Chronic fatigue syndrome (CFS) is an illness with defined criteria including extreme fatigue, sore throat, headache, and neurological symptoms. We investigated three apparent outbreaks of SBS and observed another more serious illness (or illnesses), characterized predominantly by severe fatigue, that was noted by 9 (90%) of the 10 teachers who frequently used a single conference room at a high school in Truckee, California; 5 (23%) of the 22 responding teachers in the J wing of a high school in Elk Grove, California; and 9 (10%) of the 93 responding workers from an office building in Washington, D.C. In those individuals with severe fatigue, symptoms of mucous membrane irritation that are characteristic of SBS were noted but also noted were neurological complaints not typical of SBS but quite characteristic of CFS. We conclude that CFS is often associated with SBS.
PMID: 8148452 [PubMed – indexed for MEDLINE]





From Erik:  “When the schools were first examined, it was using AIR SAMPLING.. back when it wasn’t known that it would miss Stachybotrys.  And back then finding ONE SPORE of Stachybotrys meant “Run for your life”.”

CFS: The November Factor

Guest Blog by Erik Johnson

Now that it’s that dreadful time of year again, let me tell you about the November Factor, a phenomenon that was reported immediately in both the Lake Tahoe and Lyndonville outbreaks of ME/CFS – a season where people seem to fall apart for no apparent reason.

The best doctors can come up with is “Seasonal Affective Disorder”, lack of sunlight and stress of the holidays.   But I think there’s a bit more to it, based on what I saw at the inception of CFS.

It’s a a long read, but bear with me. I’m going somewhere with this.

From Jean’s Desk – The November Factor
By Jean Pollard

( Previously available at the following url, but has been taken down:…/…/novemberfactor.htm)

Published in Lyndonville News, November 1999

I have been  trying to think of what to discuss in my article this month. I am sitting  here going crazy with our schedule, trying to fit in the CFS patients, and  it occurred to me that the reason we are so busy is that it is October.

Suddenly, wham…I realized that IT IS OCTOBER. You may or may not know what  that is, the November Factor. This little known observation for us in the  scheduling end of a CFS medical practice will tell you that this phenomenon  is REAL. I totally believe that this is real, and so do other offices who  deal with patients. A relapse generally occurs for most patients during this  time period of October-November.

Many years ago, hmmm…, around 1987, we  noticed a huge amount of calls from patients around the fall saying they  felt terrible. They had done OK over the summer months, but suddenly they  felt terrible and had more severe symptoms or even new ones.

We sat down one  day, each with our coffee, tea, or Pepsi, around a table and went over every  conceivable reason why people with CFS start to relapse in the fall. We  considered the weather, people turn their furnaces on in the cold weather.  The sun is now lower in the sky and the clocks are turned back…creating a  darker atmosphere, and very little sunshine or Vitamin D exposure. Perhaps  more infections since people are cooped up in their houses and are generally  exposed to more contagious agents, no more fresh air, etc. Nothing seemed to  fit.

To this day, we still are dogged by this phenomenon. Also, in the  spring around March and April, this also occurs but not to the degree that  autumn seems to bring. I, personally, feel that it is a real factor in the  illness of Chronic Fatigue Syndrome and I lie awake at night wondering what  the precipitating event is that causes these relapses. It does happen.

For  those of you out there reading this, I would love your input as to what you  think plays into this. Does it happen to you? Your children? We always thought the school issues played a big part in these relapses because the kids are going back to school after having a respite for the summer from the  stress and anxiety of school connected woes…homework, up early, extracurricular activities associated with school events, socializing,  dating, etc. However, the spring produces the same problems and the kids have been in school all year (except for those home tutored of course).  Adults, however, have not had that hiatus from school. They have already worked all year around…so the fall or spring should really have no bearing on their symptoms. But it does. It drives me crazy trying to put the pieces of that puzzle together. There is an answer, but what is it?

“The November Factor”: Dr. Bell on ME/CFS & the Flu that Isn’t Flu

By Dr. David S Bell, MD, FAAP* • • March 30, 2011


If robbery is taking without permission, CFS could be the greatest thief of all.

Certainly much has been stolen – the energy to go to work, to play with your children; the ability to enjoy reading a book; the luxury of a refreshing sleep. And, like true, great crimes, the victim sometimes does not even realize that a robbery has been committed.

It is as if the thief in a department store steals the surveillance camera along with the jewelry. The thief of CFS steals not only energy, it may rob the victim of the ability to perceive loss. And the mechanism is simple: Energy is quietly replaced with guilt.

Because the victim feels guilty about experiencing fatigue, the robbery goes unreported. Is it any wonder that this is a controversial illness?

The gift of human nature is the perception of who and what we are. We see ourselves either accurately or inaccurately dependent upon personality and the myriad of factors we call life. We see and feel, relating these experiences to our image of who we think we are. Because fatigue is something to be ashamed of in our society, it may go unreported.

The thief makes off with the priceless essence of our life and replaces it with a plaster statue of guilt. CFS becomes a thief of identity as well as activity. It is possible to say “I am an athlete,” or “’I am a devoted parent.”

When CFS has crept out the back door with energy and hope in a burlap sack, these statements are no longer possible.

It makes no difference whether they were accurate to start with. Even if a fantasy, they were a real fantasy for us. With CFS, even fantasies and dreams are stolen. It is like the movie The Dark Crystal, where the small victims are placed in an evil machine that sucks out their ‘vital essence’. CFS is the thief of the ‘vital essence’.

CFS will do to medicine what quantum mechanics has done to physics. The laws, once considered inviolable, are turned on their head.

Just as we were comfortable with the simplistic notions of physics before relativity, doctors are comfortable with the simple notions of medicine now. It really makes little difference that these notions are incorrect, except to those who are not helped by modern medicine.

When CFS becomes accepted and understood, the simplistic mechanisms will be replaced by theories that are able to explain what is now considered subtle. And, of course, with this understanding will come effective treatments – not just those to improve the symptoms of CFS – but those that will revolutionize medicine.

An example of an illness assumed to be straightforward but is, in fact, bewildering, is the ‘flu.’

A person will say, “I was well until a year ago February when I got the flu.” Or “In the months before I got sick I kept getting the flu.” Or “My immunity must be low because I have had the flu three times this winter.” And of course, when the doctor has no idea of what may be causing your symptoms, comes the standard, “I think it is the flu.”

The longer I study medicine the less I understand about the flu.

Jason Ewing was in his mid-thirties, and apart from being a little overweight, appeared like many up-and-coming executives who trooped into the company offices in the morning, brief case swinging at his right side. He had a promising career until two years ago when he developed a typical case of the flu. Actually, as with many persons with CFS, there was one minor difference. This flu had more-than-usual exhaustion associated with it.

It is a detail frequently overlooked, and it has always been difficult to tell whether there really was more exhaustion with this first flu or whether now,  two years later, the fatigue is remembered more prominently.

But at the time Jason took time from work and returned, still not feeling well, a week later. He had not even bothered to see his doctor during the illness because ‘it was just the flu.’ Two weeks later he had crept almost to the point of recovery, and paid it little attention. He was at work when the flu came back a second time.

Jason noted with clarity that this second flu episode was identical to the first.

Not just a similar illness, but the same illness. And now we are getting into strange territory. If a person gets a cold, we assume runny nose, cough, sore throat. But, like ice cream, colds come in many varieties – hundreds in fact – and they are all slightly different.

For example, one cold starts off with a scratchy throat, swollen glands, a little nausea and intense sneezing which lasts a day. But this cold is not the same as that of the neighbor down the street, sore throat and headache but no sneezing. We can call them both colds, but the pattern of symptoms is slightly different, and indeed with viral studies we can see that the initiating virus is also different. But what Jason noticed was that whatever the first virus had been, the second one felt exactly the same.

It would be hard to describe the specific combination of 20 symptoms that made up this particular ‘flu’. It would be like trying to describe an unknown ice cream flavor. In the ice cream store drooling Mocha Vanilla from the corner of your mouth, you say, “that’s it.” And it was a second one. It was separate from the first because he had recovered, implying that his body’s immune mechanism had conquered the first invader. He had returned to work and nearly forgotten about the flu three weeks before.

He went to the doctor and described the course and symptoms, and the exact similarity of the second course to the first. His doctor said that he could not get the same ‘flu’ twice, and that it must be a coincidence that the two were similar.

Jason nodded agreement; they had just made a pact to accept a statement, clothed in the language of science, that was obviously wrong.

There are many viruses that cause the illness we call the common cold. In fact the viruses that cause colds are of several different groups. Flu viruses are a little different, but sometimes it is difficult to say by the symptoms if something is a cold or the flu, because they overlap so much.

In general a cold is mild, one or two days of feeling crummy, and the flu is a week. The flu can be dangerous to older people because they develop secondary infections. And there is a vaccine to cover many of the strains of flu that appear during a given winter. There is the ‘Warsaw’ flu, the ‘Beijing’ flu, the ‘Moscow’ flu. It always seemed to me as a medical student that the different strains of flu were named for communist cities as if they were deliberate attempts at biologic warfare.

Each flu strain is distinct. If you had the ‘Hong Kong’ flu once, you would develop antibodies to this particular viral strain and recover. Then, because of blood cells called memory T-cells, you would remember this strain and not get it again, except in the rare instance after decades when the memory T cells become a little senile. That is why, in general, we get chicken pox or measles once in childhood and then do not get these illnesses again when our children have them.

It is difficult to measure or determine the specific strain of virus during an infection. The government will look for new strains in order to include them into the flu vaccine, but because they take several weeks and are costly they are not routinely done during a flu infection. You go to the doctor and he or she says “You have the flu. Please pay at the front desk.” (As an aside, have you ever noticed that the first ten visits for CFS are said to be due to a virus, and the next ten are said to be due to depression?)

So therefore it is not likely that Jason had the same flu twice in a row. And all of this would not have made any difference if everything got better and resolved.

Jason didn’t care much about T-cells and strain variation. Unfortunately, as he was recovering from this second bout he had a third, again with identical symptoms. There was a very particular set of discomforts that made up this flu and a particular malaise, and it came back full force.

He was treated with antibiotics – maybe it was a sinus infection – and again recovered, only to get it again a fourth time.

Over the next six months the process kept repeating with one significant trend. The episodes of this “flu” began coming closer and closer together and the recovery period shortened.

Six months after the initial episode, they were no longer separate bouts, but a constant illness with the symptoms of abdominal pain, flu-like aching, sore throat, joint pain, headache, blurry vision, trouble concentrating, and, of course, exhaustion.

Instead of being 35 and playing piggy-back with his children, Jason had CFS.

Jason’s six-month onset was not the most common for CFS, but then, again, there are many types of onset in this illness.

Jason’s particular onset, however, raises several important questions:

• Is the illness due to a flu-like virus?

• Is CFS due to an unusual virus that plays hide and seek for the first six months?

• Or does CFS have nothing to do with a virus at all?

Can flu-like symptoms be due to something other than an infection with a tiny microbe? The first time this question ever occurred to me was while I was an intern, working 36-hour shifts in the intensive care nursery. After being up all night and struggling to remember where I parked my car, I would notice that my lymph gland felt swollen and that I was coming down with the ‘flu.’ But after a coma-like sleep I would be recovered and ready to hit the next 36-hour shift.

Another of life’s ironies: They have now made it illegal for interns to work those hours because they would prescribe the wrong medications, put IV fluids in the wrong patients, and make other mistakes due to fatigue. But when a person is disabled with CFS and is constantly in that exhausted state, no one believes them, particularly the former interns.

The most common type of onset in CFS is the “acute onset” flu-like illness that does not resolve.

Yet even in this more frequent type, there are parallels with Jason’s flu. In the acute onset, there is a flu-like event, which after five days or so begins to resolve, just as one would expect with the flu. But after the initial resolution, almost to good health, the symptoms come crashing back and do not disappear again.

This implies that the illness is a little uncertain, it wavers a little at the beginning as if trying to make up its mind. “Shall I come down on Mrs. Peterson or not?” If this is so, it had a really hard time deciding about Jason.

A second unusual detail common to the onset of CFS is the severity of the fatigue during the initial episode of the apparent flu. Again, difficult to differentiate in retrospect, but in the initial illness, the fatigue seemed to be more severe than usual.

When I observed the outbreak in Lyndonville, I felt that this was one detail which set this flu apart from all the others. In fact I felt that you could even guess which people were destined to not get better – although I never hinted that at the time.

The belief I held was that there was a unique infection which caused CFS.

What is it about the flu that causes the symptoms that everyone knows only too well? The conventional explanation is that with an infection, viral or otherwise, chemical mediators designed to fight the infection are released into the blood stream. And it is the presence of these immune substances that actually cause the symptoms.

Part of the evidence for this is that when these substances are infused into healthy people they feel rotten, as if they had the flu. The flu virus and many other viral, and bacterial agents stimulate the production of these normal chemicals, which causes the symptoms. When the body’s immune mechanism destroys the infecting virus or bacteria the production of these immune mediators shuts down with a return to good health.

With Jason, the onset had begun as a typical viral infection followed by repeat episodes or relapses until a continuous illness developed. His course of CFS was then typical: There were good days and bad days, but no days without exhaustion, brain fog, and muscle and joint pain.

There were the usual problems with diagnosis, many specialists consulted, tests run. After 15 months the  diagnosis of CFS was made.

The time when the flu-like events coalesced into a continuous illness was around March of 1995. By summertime the symptoms followed a daily ritual that varied little.

• He would have four or five hours of up-and-around activity, headaches every other day, and so on.

• When he had a bad week, his activity would drop down to two to three hours a day and he would feel more ill.

• On a good week, sometimes coinciding with sunshine and a warm breeze off the lake, the activity could go as high as six good hours a day.

Summer eased on into fall, and into November.

Jason had a severe relapse in November, and felt the same as at the onset of his illness. Exactly the same.

His symptoms worsened to the degree that he was confined to bed for two weeks. He saw his physician who, predictably enough, said he had a virus and to take plenty of fluids and aspirin. On the next visit he was given an antibiotic just to be on the safe side. The flavor of this virus was the same flavor that had started his illness nearly two years earlier.

In this detail, Jason is not unique. CFS is an illness of relapses and remissions, and when patients describe relapses, they describe very similar events to those which occurred in their onset. It is not uncommon to hear, “It was like it was beginning all over again.”

It is because of this observation that the theory of a persistent infection, one that does not resolve, has been a steady thread through the tapestry documenting the history of CFS.

Viral and bacterial candidates come and go, but the proof has been hard to come by.

A second characteristic of Jason’s relapse that seems typical of CFS was its occurrence in November. In our office we call it the “November Factor.” For some reason, people with CFS get sick or sicker in late fall, and our telephone rings off the hook. I believe there is some connection between the unusual onset type and the worsening which occurs in November.

One possible explanation is that the patient has caught another bug. Kids are back in school, a perfect breeding ground for bugs of all sizes. They bring these bugs home, particularly this year’s variety and share them with their parents. The relapse is due to a worsening caused by an intercurrent infection, probably viral. This explanation implies that the relapses, and possibly the onset, are random, due to any old virus.

A second possible explanation is that summer is over and winter is setting in. Many persons with CFS feel better in the summer, perhaps because there is less stress, and more time sitting around on the porch in the warm August air. For young persons and schoolteachers, summer is a time of unsustained activity. That is, instead of eight straight hours of work, school or study, it is an hour here, a couple of hours there with rest in between. Therefore starting back to a day with eight straight hours of work or school can precipitate a relapse.

In this theory, the November factor is the resumption of sustained upright activity after a stress-free, relaxing summer. This possibility implies that a critical amount of sustained activity initiates a relapse, a common experience for persons with CFS.

A third possibility has to do with sunlight. Upstate New York, next to Lake Ontario, undergoes a change in November. The days become short with sunset at 4:45 PM by mid December. Worse yet, water vapor from the lake creates a perpetual cloud bank that drifts over Lyndonville and lingers for the next four months. Mid day is gray, bleak and cold, and all sensible adults have left for Florida.

Perhaps the lack of sunlight alters the brain’s melatonin and the addition of seasonal affective disorder is the November factor. Nearly everyone around here is depressed all winter, a fact that the chamber of commerce leaves out of the brochures. Our great joy in winter is a good nor’easter storm which blows the clouds up to Toronto and gives us several wonderful days of sunlight in which we can shovel snow. My lack of enthusiasm for winter here is more than compensated for by the arrival of the geese in the spring and the following months of cherry and apple blossoms that blanket the county.

There are other possibilities. With the coming of cold and bleak weather in November, people go into their homes, shut the windows, add plastic sheeting to

help insulate the windows and begin breathing more carbon monoxide. Carbon monoxide, despite being a deadly poison, is very interesting. It can cause a flu-like illness and prolonged neurologic symptoms very similar to CFS.

Oxygen makes many persons with CFS feel better, at least temporarily. Experiments with hyperbaric chamber treatments, where oxygen is pushed into tissues at high concentrations, have shown improvement in patients with CFS. High altitude sickness also shares many of the symptoms of CFS, again due to decreased oxygen availability to brain cells.

Could it be that the flu-like event is not due to an elusive virus at all, but instead to decreased oxygen availability to the cells? [Note: In 2007, Dr. Bell published Cellular Hypoxia in Neuro-Immune Fatigue – a book laying out his hypothesis that ME/CFS and FM may involve a dysregulation of cellular metabolism leading to the inability of the cells’ mitochondria to utilize oxygen normally.]

Medical science is amazing. The technological advances are astounding. We can rescue one pound preemie babies and transplant hearts, livers, and fingers. We

can diagnose retroviruses and have made great strides in treating AIDS. Few pediatricians can boast of seeing measles epidemics, and chicken pox will not be seen by the next generation of doctors. But try to explain something as simple as the flu.

Jason did well for the most part. The one time he got really sick was when I tried to treat him with fludrocortisone.

He got the same flavor flu-like event, initiating the relapse. It was not as severe this time, and it was not in November. He has been the only person treated with this medication who has had a relapse, but it again raises the question of whether the flu-like symptoms are due to infection or an entirely different mechanism. We stopped the medication, left him alone for two weeks and the relapse ended, albeit slowly.

It has now been almost five years since Jason began his journey, and he has improved slowly and steadily. He is up to eight hours of daily activity, and while the symptoms persist, Jason feels grateful that the crushing flu-like malaise has passed.

– Dr. David S Bell, MD, Lyndonville, New York, August 15, 2000


* This article is excerpted with kind permission from Dr. Bell’s classic book Faces of CFS – Case Histories of Chronic Fatigue Syndrome; © David S Bell, MD,

2000. It may be downloaded as a free eBook at Dr. Bell’s website

Re: Is ME infectious?
Post by Erik Johnson on Fri Aug 16, 2013 3:14 pm

I’m a survivor of the 1985 Lake Tahoe epidemic, a graduate of Truckee High School, and a Holmes et al “CFS definition patient-study group” participant as a prototype for the new syndrome of “CFS”

We have had a few more minor outbreaks since then, but nothing like the huge “Mystery Illness” incident that sickened thousands of people.

This strange illness is full of bizarre contradictions.
At times spreading like wildfire through groups of closely associated people, yet with people from these very groups seemingly unable to transmit it to anyone else.

I saw a pattern immediately. A strange “exception to the rules” in which the flu-like illness turned from noninfectious to wildly contagious.

The contagion occurred when people in the early “shedding phase” of viral illness were all in the presence of moldy buildings, particularly ones with Stachybotrys Chartarum.  Only then, was the disease easily passed from one to another.

The Truckee “teachers lounge” incident that caused Dr. Peterson to call the CDC, starting the path to the new syndrome, is a very well described example of this process.

I contacted the teachers at Elk Grove, and they found the very same “toxic mold” that we in Truckee did.

The clues are right there. Simply ask yourself, “If this were a purely viral illness, then why did the one teacher who made the effort to get out of that lounge manage to avoid becoming ill?”

-Erik Johnson
Clin Infect Dis. 1994 Jan;18 Suppl 1:S43-8.
Concurrent sick building syndrome and chronic fatigue syndrome: epidemic neuromyasthenia revisited.
Chester AC, Levine PH.
Georgetown University Medical Center, Washington, D.C.


Sick building syndrome (SBS) is usually characterized by upper respiratory complaints, headache, and mild fatigue. Chronic fatigue syndrome (CFS) is an illness with defined criteria including extreme fatigue, sore throat, headache, and neurological symptoms. We investigated three apparent outbreaks of SBS and observed another more serious illness (or illnesses), characterized predominantly by severe fatigue, that was noted by 9 (90%) of the 10 teachers who frequently used a single conference room at a high school in Truckee, California; 5 (23%) of the 22 responding teachers in the J wing of a high school in Elk Grove, California; and 9 (10%) of the 93 responding workers from an office building in Washington, D.C. In those individuals with severe fatigue, symptoms of mucous membrane irritation that are characteristic of SBS were noted but also noted were neurological complaints not typical of SBS but quite characteristic of CFS. We conclude that CFS is often associated with SBS.
PMID: 8148452 [PubMed – indexed for MEDLINE]

“This seemed to be evolving, before our eyes, from a flu-like illness into something else”
-Dr Paul Cheney

“… and it seemed to be spreading. Through the local hotel and casino, two area high schools, members of a girls basketball team.”
-Dr Nancy Snyderman

“That’s when we wondered, Hey, maybe we ought to call somebody. This is really unusual.”
-Dr Paul Cheney


I would like to call your attention to page 488 of Osler’s Web: Inside The Labyrinth of the Chronic Fatigue Syndrome Epidemic by Hillary Johnson, where a fabulous clue is reported.

Chapt 26 “Smoke and Mirrors”

After leaving Lyndonville, Dr Bell had been called in for meetings between parents and the school authorities of a grade school where a number of children had fallen ill, apparently with the “sick-building syndrome,”  a illness caused by toxins from building materials or other environmental sources.  “The parents claimed the school is poisonous,”  Bell said, “But…. SIXTEEN air-quality experts (have) looked, and they’ve found nothing. What is probably going on is an outbreak of Chronic Fatigue Syndrome.”

10/22/2015 –

Dr. Bell just confirmed to me that the school in question is the Tobin school:

So, Dr. Bell observed a cluster that appeared to be identical to the Truckee teachers lounge.

A circumstance which directly resulted in a chronicity of illness, whereas people just a few feet away “Dodged the bullet”,  where experts found nothing, despite our insistence that we could FEEL it.

Just as I have said ever since the instant I agreed to serve as a prototype for this syndrome, that we have a microcosm in these clusters that is available for easy analysis.  All we need to do is get CFS researchers to stick with it until we find out what exactly is different about these locations.

-Erik Johnson

Perhaps They Just Forgot

Guest blog by Erik Johnson

“Ground Zero for CFS” :

Fraught with meaning.  This conveys that there WAS a start point to this syndrome, a time and place that can be checked, to see how it all came about.

“Mold at Ground Zero for CFS”, Chapter 23 of Dr. Shoemaker’s book Mold Warriors adds a new dimension.

Not only is there a start point to the syndrome, but a CLUE as well.  Something a researcher can sink his teeth into.

I thought the “Sick Building” phenomenon that started CFS was an incredible thing, and since so many people said they wanted to solve CFS, believed they would want to hear about it.

Thanks to the new age of computer “social media”, I was able to make direct contact with hundreds of doctors, researchers, toxicologists, mold and CFS advocates.

Much to my surprise, the information I gave them about “Mold at Ground Zero for CFS” hit a dead-stop, every time;  A very odd way to show one’s interest in solving a mystery.

Mold at Ground Zero

As told in my chapter, I literally launched this syndrome by telling Dr. Cheney about the mold.  “I have an inexorably increasing reactivity to mold that grows progressively worse no matter where I live.”  But over the years, my reactivity grew more acute.  So did my chemical sensitivity.

In 1997, Dr. Peterson had told me “You have become a universal reactor. (to chemicals) Life is now intolerable for you.”  His only treatment option was Ampligen, and I couldn’t afford it.

With nothing else to try, I opted to try a “crazy” strategy of “Extreme Mold Avoidance”, and was quite surprised and pleased at the results.  My chemical sensitivities vanished.

Back at this time, “Toxic mold” was unknown but I felt certain that specialists in Multiple Chemical Sensitivity would want to know that mold could be as nasty of a chemical exposure as anything they were implicating.

I contacted quite a few MCS groups, who all responded very negatively, as they believed mold to be nothing more than an allergen. They were quite insulted that their “SERIOUS disease of MULTIPLE CHEMICAL SENSITIVITY” might be compared to a mere allergy, and were quite free in telling me just how wrong and mistaken I was to think I had a serious illness from “mere” mold.

Mold vs Chemicals?

One of these groups was the Chemical Injury Information Network.

I spoke on the telephone with Cynthia Wilson, who seemed interested when I explained that I am an Incline Village survivor and prototype for Chronic Fatigue Syndrome who “found a clue”, but as I described the toxic mold, her responses grew more impatient and aggressive.  Finally she exploded.  “It is CHEMICALS I tell you, CHEMICALS, damn it.  I am SICK AND TIRED of hearing people blaming each and every stupid irritant they discover.  There is no end to it.  CHEMICALS are the real cause, your mold allergy
is nothing more than a consequence.  The only reason I put up with listening to your story is that shortly before her death, my friend Cindy turned her attention to mold. BUT MOLD IS NOT THE CAUSE. IT IS CHEMICALS”   and hung up on me.

I hadn’t known until that moment that her friend and colleague, Cindy Duehring had just passed away.

I read about Cindy Duehring’s life and was amazed at her pesticide exposure, chronic progressive MCS, and that after all her years and writings about chemicals, at the very end of her life, dramatically switched her focus to mold.  I could tell by the way Cynthia spoke that for Cindy to do this was utterly baffling to her, seemingly a totally betrayal of everything she had formerly stood for.

It seemed to me that after building a safe house and exhausting all other exposures, the fact of still being “hit” pointed at something that must be transported  into her presence, but she couldn’t quite figure out what it was.

It sounded like we were on a parallel course, and just as I had done when my reactivity hit a point of picking out specific irritants, both found that a mysterious one stood out that was surprising and unexpected.  A specificity to “mold”.  Cindy’s story of reacting to her husband coming from work with fumes and chemicals clinging to him sounded very classic for how “mold reactors” perceive the problem, until they realize that mold appears to be a carrier, almost like a Trojan Horse, for these chemicals.

What a horrible shame that she figured it out, but wasn’t in time to devise a directed strategy toward this overlooked mold factor.

It is notable that the MCS groups all looked upon complaints of mold with such contempt. They were clearly unaware of toxic mold.

Ultrafine Particles

In 2002 I became aware of a toxicologist, Dr. Jack Dwayne Thrasher, whose work looked absolutely awesome. I read over his impressive body of work with mold.   He even seemed to think ‘ultrafine particles” might be important, which is actually one of the first things  we blamed during the 1985 Lake Tahoe Mystery illness, as we were being heavily bombarded with silver iodide “cloud seeding”.

cloud seeding begins

We thought these ultrafine particles might be affecting the environment. Protests were even held against cloud seeding, for no one knew what the consequences of being drenched with these minute silver particles would be.

I thought that surely here was the one that would take interest in my story and help me tell the world of the mold connection to Chronic Fatigue syndrome.

Yahoo groups were popular at this time, and I joined a group where he was an active member. I began to tell my story.

I told of my discussion with Cynthia Wilson and how I believed Cindy Duehring’s illness was similar to the progressive “Tahoe Mystery Malady” of those people who stayed in contact with toxic mold.  Dr Thrasher told me that he was an advisor to the Chemical Injury Information Network and a personal friend of Cindy Duehring.

“Then you know that she switched her focus to mold”, I grew excited. A breakthrough!

Here is where it got weird, for Dr. Thrasher had the same attitude as Cynthia Wilson.
Chemicals.. not mold.

I asked him, since he was a personal friend with Cindy and her husband, if he could ask for information she had assembled on mold, prior to her passing. There would undoubtedly be valuable clues. At the very least, perhaps her reasoning for this shift from blaming chemicals to a sudden “turnaround” on mold, which was so bizarre to her colleagues that it almost seemed that she had become a traitor to the MCS community.

Dr. Thrasher declined.  Not even Cindy Duehring’s interest in mold caught his attention.
Despite his own work with mold, he didn’t appear to believe it, and blamed chemicals instead. He told me I was mistaking formaldehyde exposure for mold exposure.

Stunned at Dr. Thrashers’ strange diversion away from mold, I exchanged stories with others in this group, in front of him so he would see more mold
clues, perhaps changing his mind.

A mother of autistic boy described a peculiar behavior, asking for help in figuring it out.
He absolutely would not go to a certain corner of the house.  This was taken by doctors to be some kind of emotional “fear” type behavior. But she said the odd thing is that when outside in the yard, he avoided the same corner.

Dr. Thrasher suggested that wood panels were releasing formaldehyde, causing his avoidance-behavior.

I questioned why such off-gassing would be limited to one corner, especially in such concentration that he could feel it outdoors, and offered up the concept that it was toxic mold.  For this level of avoidance was perfectly consistent with mine.

Dr. Thrasher stuck to his formaldehyde concept.  So I suggested this lady have her house tested by Dr. Gary Ordog, who was knowledgeable about mold illness.
She did, and that corner was positive for Stachybotrys.

Now, I realize that nobody likes to be proven wrong, especially in public, but still, I hoped that this demonstration would pique his interest in toxic mold and CFS.

It did the opposite.

Back to Truckee

Over the next few years, Dr Thrasher seemed bent on minimizing toxic mold, in favor of formaldehyde exposure.

During the Hurricane Katrina “Toxic Trailers” debacle, Dr Thrasher brought a great deal of attention to high levels of formaldehyde, yet at the same time, even as he mentioned mold, somehow managed to minimize it out of consideration.

I hoped that after Dr. Ritchie Shoemaker’s book Mold Warriors was published, Dr. Thrasher would reconsider.

But the events of 2008 showed that he had not changed his views.

I had watched this complex as it was built.  Prefabricated modules that were brought in on trucks and stacked by cranes, but the work wasn’t done by winter. The rain and snow drenched the unprotected modules.  I told my brother that this was bound to be trouble.  This looked like a mold disaster before the roof was even installed.

Yet here again, in a place where I predicted mold, could feel it outside, Dr. Thrasher diverted the tenants from mold and toward formaldehyde.  And this was in TRUCKEE, just on the other side of “Ground Zero for CFS”  It became clear to me that Dr. Thrasher had no intention of coming around to connecting mold and the syndrome.  Not only was he failing to mention it to these tenants,  he wasn’t going to say anything at all about knowing the story of how mold was an unspoken part of the equation at the inception of the syndrome.

A local survivor of mold from 1986 wrote a letter to the editor, explaining how this was mold rather than formaldehyde, but got no reply or response from anyone…  anyone except me.

The tenants became disenchanted with the formaldehyde hypothesis and hired another mold inspector, Jack Goshow, who shifted the focus back to mold.

I felt this was a terrible loss of an opportunity to make progress on solving Chronic Fatigue Syndrome, because Dr. Thrasher was familiar with my story, had worked with Dr. Shoemaker, was right  there on the spot in Truckee, and so far, had been the only mold researcher I had seen to even mention the possibility that ultrafine particles might be important.

Ever since 2008 I have used this apartment complex as a “demonstrator” on the “CFS History Mold Tour”.  Many of the ones I have taken there can’t make it across the parking lot, let alone get inside Tracy Penner’s front door.

Lack of Communication?

As told in Khaly Castle’s blogs, after the Whittemore Peterson Institute was built, I made many trips up there to educate them about “Mold at Ground Zero for CFS”, and offered to take Dr. Judy Mikovits… and any who were willing.. to come to “The Mold Tour”

So far, no takers, although they are all very much aware how my story has been confirmed.  I even gave them copies of Dr. Shoemaker’s book Surviving Mold.

The years crept by. All the CFS and mold researchers continued playing with their various concepts, plodding along, and still showing no interest in just going back to where CFS started.. and ask a few questions of those who were there.

With all this in mind, IMAGINE MY EXCITEMENT when this came out.

Wow.  Here it is.  Dr. Thrasher has FINALLY taken an interest in “mold and CFS”, even co-authoring a paper with Dr. Brewer, who is a scientific advisor for the Whittemore Peterson Institute – ALL of whom know the mold history.

Surely now they would want to put all the pieces together.

Shortly after Dr. Brewer’s paper came out, he was asked where he first heard of mold.  Oddly enough, he said the idea never crossed his radar until the RealTime test came out.  How very strange that Dr. Brewer was completely surrounded by people who all know the story of Mold at Ground Zero for CFS”.. all of whom I had ASKED to pass this story along to researchers, and yet, if what Dr. Brewer says is true, not a single one of his associates told him.

I wonder why they didn’t?  Perhaps they just forgot.

Now, as everyone who has read my story knows, the crux of “Extreme Avoidance” is to decontaminate after passing through “plumes”, so as to keep minute amounts of some incredibly nasty stuff out of my sleep zone.

One of the first stories I told Dr. Shoemaker in 2002.. ironically at the same time I was pursuing Dr. Thrasher to be the one who would help me unveil this paradigm to the world… was of a lady who had tried everything in the book to get better from CFS.
Then she suddenly got better “for no reason”  This was as mystifying to her as it was to everyone else.  She said it was totally baffling, for NOTHING had changed.   Except this.
“My husband retired, and is hanging around the house all day, driving me nuts”

Wow. There it was.  Her husband was no longer going somewhere and bringing “the stuff” home on his clothing.  A scenario that perfectly fits my decontamination protocol scenario.

And perhaps what Cindy Duehring apparently became aware of, but her epiphany came too late to do anything about it.

A darken’d and tempestuous day…it was.

In 2011 I took a trip out to Reno, Nevada, to meet the man who saved my life..Erik Johnson, the Mold Warrior.  The trip was cathartic in many ways.  Erik took me on “The CFS History Mold Tour”, which encompassed most of the critical locations involved in the inception of CFS as named by the CDC.  I can’t even begin to tell you what that was like emotionally.

We also made a trip to the WPI.  It was quite a shock to find out later that the very day we were there, Judy Mikovits was being fired.

But just recently, I’ve had a bit of a further shock.  It’s been pointed out to me that, according to the Heckenlively/Mikovits book “Plague”, Dr. Mikovits had a mold problem of her own:

“ Annette Whittemore fired Mikovits over the phone at around 4:30 p.m. on Thursday, September 29, 2011. It was an uneventful day prior to the Lombardi brouhaha. Mikovits had left the Whittemore Peterson Institute about a half hour earlier after going to the lab to tell her research associate Shanti Rawat that she would be taking the next day to move David’s posessions out of the Condo they had been renting the past ten months from the Whittemore’s as her Riverwalk condo was being repaired from mold. Mikovits would then bemoving her things back to the Riverwalk as her lease was up September 30.”(page 144)

This becomes extraordinarily interesting when you revisit the blog I posted after the trip to Reno.  I’ve pasted it below.  The original publication date was May 21, 2012. 

A small section of the original blog has been removed because, though it was intended to pay homage to an author of a certain book that describes being within the maze of CFS history, the author objected.  I replaced that section with these words:  “Our trip started at the top of Mount Rose, looking down on Lake Tahoe and Incline Village.  It was beautiful.” 

Nothing else has been changed, added, or deleted.

In particular, take a look at  the section titled “The Sideshow”.  You’ll see why I received the second major shock regarding the timing of that visit when I saw the description of Dr. Mikovits’ day on page 144. 

It is also interesting to note that Erik had been educating Dr. Mikovits in the story of how mold was an unknown component in the 1985 Tahoe Mystery Illness since the 2009 IACFS/ME conference in Reno, and had given Dr. Mikovits a copy of Dr. Ritchie Shoemaker’s 2010 book, “Surviving Mold” the year before the date of our visit to WPI, in an attempt to engage the interest of CFS researchers into a major factor that had been overlooked.

CFS – THE MOLD TOUR (Published 5/21/2012)


For a few years now, I’ve been living a lifestyle based around mold avoidance.  By “based around”, I mean that my daily routines, my living quarters, my life decisions, and even the location that I have chosen as home base – all incorporate the premise that mold is my kryptonite and must be avoided at all cost.  This premise has kept me upright for a good long run.

The Background

In 2007, I was bedridden, and had been for a while.   I was suffering migraines on an almost daily basis.   I was having seizures.  I had full Parkinson-like symptoms.  My gallbladder was on the verge of coming out, I’d had 8 consecutive kidney stones, my teeth were exploding in my mouth, and I had an appointment to get my thyroid irradiated.  My cognitive abilities were probably at the 3rd grade level.  I was definitely not smarter than a 5th grader.  My idea of a vacation was migrating to the couch.

One day, I posted what became a fateful piece on a message board.  I said, “Maybe my house is killing me?”. That statement drew a response that saved my life, from Erik Johnson.  He said, “Now you’re talking my language”.   That kicked off a friendship that has endured through thick and thin, and a subsequent road map out of hell.

Here was a survivor of Incline Village,a Cheney-appointed prototype for the illness cluster there, which infamously earned the attention of the CDC and the name “Chronic Fatigue Syndrome” – a man who was as sick as they come, and who was now out climbing mountains.  I decided that whatever he did to achieve that kind of turn-around was what I would do.  It didn’t matter what it was.  It could have been “stand on your head an hour a day and count backwards in Arabic”, and I would have done that.  As it turned out, it was mold avoidance.

Over time, I got to know Erik’s story.  He talked of particular areas in Incline Village, around lake Tahoe, in Reno….and the teacher’s lounge at Truckee High School, as all having the toxic effect that he avoids.   He said that the effect is still there.  In the fall of 2011, having reached a high enough level of health to even entertain such an idea, I decided to take a trip out to Reno to see for myself.   After all, this man had put me back on my feet.  I wanted to see “inception”.

The Journey

I left Albuquerque feeling well, excited to be making this trip.  I flew into Reno, with a six hour layover in Phoenix.   By the time I got to Reno, everything I was wearing and all of my luggage was contaminated.  My computer was contaminated.   The Phoenix airport felt awful, and the second hop from Phoenix to Reno had me squirming with pain.   I felt like I was getting superblasted with toxins.   By the time I got to Reno, I could hardly stand myself.   When I met Erik, he couldn’t stand me, either.  I was thoroughly doused with toxins.  The first order of business was a decon shower and a change of clothes.  Everything I brought had to stay outside.   In particular, the green hoodie I wore on the entire trip was lethal.   Day one was all about cleanup.

But, after the decon and the clothes change, my own health took an immediate bounceback.  As hard as I got hit, the idea of keeping my immune system response dampened down with constant avoidance protocols paid off.  I was functional.  Welcome to Reno.

The Sideshow

The next few days were a whirlwind of activity, including multiple exposures to toxic assault.  A walk with Erik through downtown Reno and along the riverwalk was an amazing adventure, simply because we threaded our way through plumes and exposures to people who were cross-contaminated.   We moved as if in unison, in that strange dance that moldies do…simultaneous shifting from one side of the street to the other to avoid a blast of badness coming from a building, backing away from a counter where the clerk was emanating cross contamination, and then…”Did you feel that?  Look at your hands, your veins are popping.  So are mine.”   Wonderful validation.

A trip to the WPI and a tour of the campus was interesting.   At the time, the WPI was still looking good, although unbeknownst to me at the time, my visit was on the same day that Judy was being fired.   The building was beautiful, a real testament to forward-thinking and high hopes.   However, the impression was that of a ghost-town.   I met Annie at the reception desk, and introduced myself as another CFS sufferer who had achieved a large level of health through mold avoidance.  The building itself felt good to me.  However, near the counter there was a lingering cross-contamination, a “gift” that somebody had left behind.  It was enough to make me back away.

The Main Event

One whole day was devoted to a tour of CFS History, which equates to the same thing as “The Mold Tour”.  Before getting into details, I have to tell you that this trip changed my life on two levels.

On one hand, it was like visiting the scene of a horrible event that changed the history of my “people” forever.   I imagine the feeling was similar to visiting a concentration camp that one’s parents were interred in, or visiting the scene of a violent crime that resulted in the death of a family member.  It hit me to the core, in a way I didn’t expect.  Here was where people suffered greatly, where a town ostracized their own desperately ill citizens, where the CDC came and effectively issued our death sentence.  Here was where a catastrophe got swept under the rug.  Here was where the paradigm of concerted and overt lassitude on the part of the government was framed as policy, and where everything that has broken my life began.  Here was the epicenter of the wormhole, the same wormhole that has generated an inescapable tractor beam that has sucked me into its event horizon, years later and miles away.

On the other hand, it was extreme validation.  It was validation that everything Erik had told me about the level of toxic assault in the area was true.

Reno itself is no picnic as far as toxic assault goes.  Erik lives there, and I immediately saw what his concept of “extreme avoidance” entails.   It doesn’t mean living in the desert.  It means living right in the middle of a city full of opportunities to get slammed.   It means maintaining a pristine living space, honoring decontamination protocols, and wending your way through “normal” activities on a daily basis, and cleaning up the mess it makes with your extreme protocols.

Our trip started at the top of Mount Rose, looking down on Lake Tahoe and Incline Village.  It was beautiful.

But the air was a little foul. Not in smell, but in feel. I could sense swelling at the base of my skull, a souring of brain activity.  It wasn’t a place I wanted to be.

The next stop on the tour was the library in Incline Village.   We got out of the truck and walked into the library.  As we rounded the corner to the reception desk in the middle of the building, I felt some very familiar symptoms, quite rapidly.   Brain compression hit within moments of approaching the area, along with a narrowing of vision, rapid heartbeat, and agitation.   I couldn’t wait to get out of there.   Erik grinned at me.  He knew I’d react that way.  We didn’t stay long.

We visited the building that housed Dr. Cheney and Dr. Peterson in the days of inception.   Erik described to me how he sat in that very office, stunned to the core when Cheney asked him to be prototype for the illness that the CDC was framing as “Chronic Fatigue Syndrome”.   He didn’t want it.   The responsibility was daunting.  The enormity was staggering.  But then he realized that as prototype, researchers would listen, would come and explore the toxicity of the area, would follow the clues that he and others in his cohort could point to.  He had no idea how wrong he was.

He also described to me how that very office, those very  handrails, were  where patients would stagger to and push off from, to propel themselves to the next handhold, as they came out of the office.  The staggering gait, the inability to convert brain-commands to neural action, were all described in Osler’s Web.   These things, over time, have been reframed somehow as “fatigue”.   It was not on any scale of fatigue.

We worked our way through Incline Village and through King’s Beach towards Tahoe Vista.   There were intermittent stops on the way, some that were interesting historically and others that were just downright toxic.   I won’t go into detail, as the main event was yet to come.  The tour is worth taking for any CFS patient.  It was a remarkable journey, both from a “grounding” perspective and from a neurotoxic perspective.

It was time to head toward the piece de resistance, Truckee High School.   Upon our arrival, Erik warned me to follow him, that sometimes one had to be careful about which way one approached the building.   He said that the wind can blow the effect right out of the building and walking into the wind may be a bad idea.  I followed him closely as he remembered his high school days there, and how he had to sit outside at every opportunity.   Our approach was uneventful, but as soon as we opened the door to the high school, I went into neural  shut-down mode.  The inside air pushing its way out was filled with a forceful toxic assault.

We crept inside, approaching the hallway that contains the infamous teacher’s lounge.  As we got closer and closer, my heart rate jacked up enormously, and my vision closed in.   My peripheral vision was shot, and I could only see through a tunnel.   My head began to spin a bit, and the veins on the backs of my hands popped noticeably.

As we rounded the corner, with the lounge in sight, I turned around and headed back out.  I could not take one more step forward.  It was too much.  Whatever was wrong with that place, whatever it was that contributed to all those teachers’ illnesses, was still there.   Erik walked me out and back to the truck, and we went up into the mountains for some fresh air.  It was only moments before I was back to normal.  We had a pleasant walkabout and a good dinner, and went back to Reno.

The Takeaway

It’s been more than two decades…creeping up on three….since the outbreak of illness in Incline Village.   It is beyond my comprehension that in all this time, not one researcher has gone back and listened to this story.  Other than patients who have come to do the tour, nobody has explored these pockets of toxicity.   There are still survivors.   The story  can still be told.  And, whatever is wrong with that area is still there.   Erik doesn’t offer mold as the cause of CFS.   He has never once said that.   His clues don’t negate viral impact.  There WAS viral impact in that cluster.   But some recovered, while some went on to enjoy a lifetime of CFS.  What was the differential?

At this rate, we’ll never know.

Life of Brain (blood barrier, that is)

(This is a repost of an article written by Khaly Castle with Erik Johnson, and originally published on 10/6/2012 at Blog)

Some things in life are bad.  They can really make you mad.
Other things just make you swear and curse.
When you’re chewing on life’s gristle, Don’t grumble, give a whistle.
And this’ll help things turn out for the best…Eric Idle, Monty Python’s Life Of Brian

The blood-brain barrier (BBB) is a highly effective biological mechanism, a metabolic and cellular barrier located in the capillaries of the brain.  Its primary function is to prevent the passage of nonessential molecules from the bloodstream to the neural tissue while allowing other substances through.

Delivery of medications and chemical treatments directly to the brain has been a holy grail of science.   The hindrance has, of course, been the BBB.  Nanotechnology is enabling remarkable strides in this field, allowing us to explore the possibilities of nano-induced medication transport, nano-enhanced visual imaging of brain tumors, nanorebooting of blood flow after brain injury, and more.  The emerging field that involves interaction between nanomaterials and living systems is known as “bionanointeraction”.

We know that the high surface energy of nanoparticles is an attractant for VOCs (volatile organic compounds).

This is the trick that is being capitalized upon by science to transport medicines to the brain…use of the surface excitability of nanoparticles to “glom onto” other substances and carry them into the target area.

This is a really good, basic, and graphic little video of how the surface excitability of nanoparticles works:

We know that mold can biosynthesize nanoparticles.

In one of our previous blog pieces, “And now for something completely different!”, we discussed mold and its ability to produce nanoparticles.

In nanotechnology, it has been discovered that by using the natural processes of biological systems, Aspergillus fumigatus can be used as a nanoparticle factory. The synthesis process was quite fast and silver nanoparticles were formed within minutes of silver ion coming in contact with the cell filtrate, claims the Bhainsha study from 2006, Extracellular biosynthesis of silver nanoparticles using the fungus Aspergillus fumigatus

If mold is in fact capable of biosynthesizing nanoparticles and metabolizing them, then that compounds things even more. We know mold is capable of biosynthesis, because scientists are using that technology to create “nanofactories”. There’s no reason to think mold would only do this in captivity.

We know that in this day and age, mold has a lot more access to metal particles than it used to.

Heavy metal contamination from burning oil, aerosolized household chemicals and pesticides, heavy metals and inorganic ions in our waste material which becomes processed into fertilizer via sewer sludge, industrial off-gassing…all have contributed to a toxic planet.

All of these things come into play in order to conceptualize this:

What if mold has adapted?   What if it is evolving to meet its survival needs in the industrial atmosphere created by man’s machinations?  Fungi, after all, have been in the business of evolving for well over a billion years.  What if some molds have mutated to allow them to withstand formerly intolerable metal particulates, and convert them to nanoparticulates?

If you’re still with me so far, consider the following theorizations by Erik Johnson.   Based on the above, I found them to make perfect sense and to fit well with what my illness experience has been.

  1. If a mold only produced nnps while obtaining metal particles, this could account for how the illnesses can mysteriously arise and disappear for “no reason”. Nanoparticle production would vary greatly.
  2. If the mold which produces the nnps is a toxin-producer, the attached VOC would be of the associated mycotoxin, or the toxin produced by that particular mold.
  3. But if the mold is NOT virulent, and just using Fentons (a bio-chemical process)to degrade materials… the resulting illness might be from whatever VOC was scrubbed from the air and transported into the brain instead of mycotoxins.

How would this manifest itself as illness expression?  Well, depending on the mold and what it came into contact with, there could be outbreaks of similar and yet slightly different illness.  According to Erik:

In hospitals, the nurses would have an inexplicable reaction to gluteraldehyde glommed onto the nnp.

In FEMA trailers, the “illness” would be the attached formaldehyde.

In Sheep Dip Farmers who get Myalgic Encephalomyelitis, it would be the OP pesticides they are using on moldy sheep.

In office buildings, reactions to the chemicals in carpet…. MCS galore!

More food for thought from Erik:

The common denominator between seemingly unrelated chemical exposures is that when mold is involved, novel pathogenesis is being seen.

In the past, mold did not have materials of such high density to process, so their Fentons would never have been so strong.

Which may account for the sporadic way this happened in the past, but has become quite common now.

The mold might sit there, toxic to bacteria, yet fairly benign against our normal human immunity, until metal particles sweep in on the winds, precipitate in the rain, channel to a mold colony, spew out nanoparticles, and suddenly turn the same mold colony into the “altered antigenic toxin spewing demon from Hell“, throwing out a means by which nearly any VOC that is there to be attracted by its surface energy, then suddenly allows these toxins to sail right on into the brain.

Stay tuned for the next installment.  Nature may have provided us with the means to perceive and identify this danger.

The Bleed

(This is a repost of an article written by Khaly Castle with Erik Johnson, and originally published on Blog on 9/21/2011.)

Aerotoxic Syndrome is a fairly recent term, to describe a fairly recent phenomenon – long or short term illness that is attributed to cabin air that has been contaminated with atomized chemicals.

According to Wikipedia, with the exception of the Boeing 787, the air in a jet or turboprop cabin is supplied by “bleed air” from the aircraft’s engines. By most accounts, the air is approximately half bleed air, and half recirculated air. Although most aircraft cabins have filters for the recirculated air, the bleed air is not filtered.

Bleed air has the potential to be contaminated by a multitude of chemicals, not the least of which is TCP (tricresyl phosphate), from the synthetic lubricant oils used. This can happen when there is a seal leak, or when reservoirs are overfilled. TCP is an organophosphate, deemed to be linked to neurological damage when ingested.

According to a 2009 article in the Wall Street Journal titled “Up in the Air: New Worries About “Fume Events” on Planes” the FAA recorded over 900 “fume events” between 1999 and 2008. “But some airline-worker unions believe that contamination events are underreported by airlines and pilots.”

In the last blog post, (And Now For Something Completely Different) we talked about the toxin potential to human health that appears to be inherent in nanoparticles.  Basically, the surface excitability of a material that is reduced to nanosize is greatly enhanced, giving nanoparticles the ability to “glom onto” biotoxins and other particles, and transport them to the human brain.

We talked about “Steering Immunostimulation By Particle’s Size: Nanoparticles and Human Health”, which deals with the idea that the human immune system differentiates between viral and bacterial pathogens based on size, and as a result, pathogens or toxins that are introduced to the system in nanosize are treated to a viral immune response.

We also talked about the fact that molds can act as nanoparticle factories, metabolizing nanoparticles and then spitting out plumes of even smaller nanoparticles, and in some cases how the mold toxins themselves have been attached to the new smaller nanoparticles.

This makes toxic mold a particularly compelling model for this hypothesis, as not only is it adding its own toxic elements to the nanoparticle soup, it is actually capable of breaking nanoparticles down to even smaller size and emitting them in plumes, even further increasing the potential for this dynamic.

But let’s bypass the mold factor completely for a moment.  It’s an added factor that makes the nanoparticle delivery system even more confounding and dangerous, but even without it,…. Houston, we have a problem.

There are numerous studies out there that one can pull up regarding nanoparticle content in aircraft engine emissions.  Most agree that, as one study put it, “aircraft engines emit a considerable amount of insoluble sub-0.1 μm sized combustion aerosol particles” Petzold, Aviation Particle Emissions and Airport Air Quality, June 14, 2005.

That being the case, let’s bang that against the 2007 annual report issued by The Committee on Toxicity, a committee that evaluates chemicals for their potential to harm human health, for various government departments and regulatory authorities in the UK.  This report covers a variety of toxic topics, including nanoparticles, the COT addendum to joint statement of the committees in Toxicity, Mutagenicity and Carcinogenicity on Nanomaterial Toxicology.

Item number 11 is of particular interest:

For pharmaceuticals it has been shown that incorporation into nanoparticle formulations can greatly influence the biodistribution (and hence toxicity) of included chemicals. Indeed the intention behind many such formulations is to facilitate drug delivery across tissue barriers. There is little evidence that the biodistribution of other chemicals not physically included in the original formulations, but accidentally present in the body at the same time as the nanoparticles, can be so influenced.

However there is at least a theoretical possibility that freshly generated nanoparticles with reactive surfaces could significantly bind and alter the biodistribution of other xenobiotics. Such effects would not represent nanoparticle toxicity per se, but would represent a consequence of co-exposure.

”Reactive surfaces could significantly bind and alter the biodistribution of other xenobiotics”

This is exactly what we’ve been talking about.  If, for instance, TCP would normally have to be ingested in quantity in order for its neurotoxic effect to establish damage in the human body, but instead was delivered directly to the brain via binding to nanoparticles, then we are talking about a whole new and potent delivery system of xenobiotics – One that would not require “massive quantities” to see effect.

So while it may not appear that enough xenobiotics were being introduced into your airplane cabin via the “bleed air”, the fact that nanoparticles can grab these toxins and upload them to the brain, bypassing normal avenues of immune response, changes the game completely.

This is the exact same mechanism that we were talking about in the last blog, except that we were talking more about biotoxins from mold.  As Erik Johnson pointed out in one of his communications to the W.H.O., the Saratoga Springs manual noted surges of fungal pathogenesis that could not match what they knew about mycotoxins.  Dr. William Croft called the effects “radiomimetric”.  In the case of Aerotoxin illness, we have a different toxin possibly being subjected to the same hypothesis of delivery to the human brain as we did with mold toxins in the last article.

Dr. Sarah Myhill, CFS/ME expert in the UK, is also the medical advisor to the Aerotoxic Association.  She goes into more detail in her paper Aerotoxic Syndrome – The Poisoning of Airline Pilots, Cabin Crew, and Passengers, that is possible on any airflight, where she discusses the effects of bleed air and its contamination with not only TCP, but an accompanying range of volatile organic compounds and heavy metals from the engine itself. 

All of this is dire enough.  What we are proposing is simply the additional nanoparticle factor.  If we take what we already know about fume events and factor in the nanoparticle delivery-mechanism potential, we may be looking at a ready explanation for why toxic assault is happening at such increasingly devastating levels.

Again, this paradigm is not being proposed “instead of” XMRV, or instead of any other current pathogen trail.  There is no reason to think that there is only one dynamic at play here.

But Erik Johnson observed the effect of transcendent-toxic-pathogenesis at the inception of CFS, noted its uncanny similarity to Aerotoxic syndrome, and the application the nanopathology hypothesis appears to possess potential to demystify at least some portion of these otherwise inexplicable phenomena.

This effect still screams for research. It may be a dynamic that reaches far beyond CFS and encompasses a new look at human health issues on a very broad scale.

And now for something completely different!

– Monty Python

(This is a repost of an article written by Khaly Castle with Erik Johnson, and originally published on 9/15/2011 at Blog)

Steering Immunostimulation By Particle’s Size: Nanoparticles and Human Health

What on earth does that mean?

Let’s talk about a paper that was prepublished in “Blood – Journal of the American Society of Hematology” in March 2010, entitled “Particle size and activation threshold:  a new dimension of danger signalling”, Rettig et al.  (For more detail, please click on the link to read the entire paper.)

This research article starts by describing the innate immune system in basics.  The innate immune system works by detecting danger signals, or molecules that originate from invaders and disturbed or abnormal cells.

It goes on to document the three forms of nucleic acid that are recognized by the immune system, and how they are recognized by Toll Like Receptors.  When those receptors are activated, the immune response is initiated.  Cytokines and co-stimulation molecules are produced, and certain homing and chemokine receptors are upregulated.

Then, the paper shows that there is a difference in how the innate immune system responds when the “invader” is reduced from micro- to nano-particulates.

This is a major concept to get one’s head around.

The “Particle size” paper documents that nanoparticles, but not microparticles, induce interferon-alpha production in human cells.  Research suggests that the plasmacytoid predendritic cells (pDC), which are critical mediators linking the innate and adaptive arms of the immune system, selectively take up nanoparticles, while monocytes require a larger amount of “danger signal” to be fully activated.

Both pathways stimulate the immune system the same way..but the difference seems to be that nanoparticles induce an interferon-alpha response, while microparticles induce production of TNF-alpha.

A little bit about nanoparticles:

In nanotechnology, a number of physical phenomena occur when the size of a system is reduced to nanoscale.  Quantum effects become dominant when the nanometer size range is reached.  This is  known as the “quantum realm”. There can be an increase in surface area to volume ratio, and acceleration of ion transport.   The properties of materials change as nanosize is reached and the percentage of atoms at the surface of a material becomes significant.

Although nanotechnology is a subject of bitter debate amongst scientists regarding the safety of usage, there are a multitude of studies which indicate that there are dangers to both the environment and to human health.  Most of these dangers are due to the high surface-to-volume ratio, which can  make the particles very reactive.  Nanostructured Materials, by Jackie Yi-Ru Ying.

For instance, a recent study looked at the effects of zinc oxide nanoparticles on human immune cells, and found that the smaller the nanoparticle, the more increased the cytotoxicity.  Mechanisms of toxicity involve the generation of reactive oxygen species, with monocytes displaying the highest levels, and the degree of cytotoxicity dependent on the extent of nanoparticle interactions with cellular membranes.  Hanley et al, The Influences of Cell Type and ZnO Nanoparticle Size on Immune Cell Cytotoxicity and Cytokine Induction.

Some interesting factoids about mold and nanoparticles…


Aspergillus fumigatus is a common mold that is typically found in soil and decaying matter.  It readily becomes airborne.  It is one of the most common Aspergillus species to cause illness in individuals with compromised immune systems.  For these people, Aspergillus fumigatus can become pathogenic, causing a range of symptoms and diseases.  It also produces cytotoxic mycotoxins.

In nanotechnology, it has been discovered that by using the natural processes of biological systems, Aspergillus fumigatus can be used as a nanoparticle factory.  The synthesis process was quite fast and silver nanoparticles were formed within minutes of silver ion coming in contact with the cell filtrate, claims the Bhainsha study from 2006, Extracellular biosynthesis of silver nanoparticles using the fungus Aspergillus fumigatus

….and sewer sludge

When legislation went into place to curtail the practice of dumping sewage waste into the ocean, a new practice emerged.  Sewer sludge got renamed fertilizer, and got dumped on farmer’s fields under the guise of recycling.

According to the EPA, sewer sludge consists of “volatiles, organic solids, nutrients, disease-causing pathogenic organisms, heavy metals and inorganic ions, and toxic organic chemicals from industrial wastes, household chemicals, and pesticides.”  In other words, you name it, it’s in there, including nanoparticles.  And, Aspergillus fumigatus is a common byproduct of sewer sludge.

For more reading on this, try starting with The Real Dirt On Sewer Sludge, by Wendy Priesnitz

What does this have to do with CFS?  Maybe nothing.  More likely, maybe everything.

When  I say CFS, I mean the entity that got named CFS…the Incline outbreak.

Here is an excerpt from a recent communication between Erik Johnson, Incline Village survivor, and the W.H.O.:

During the 1985 Incline Village “mystery illness” it seemed that common household molds were suddenly having a devastating effect on all of us.

Everyone knew it, everyone noticed this, but it was ENTIRELY attributed to changes in the immune function of patients due to infection, and NEVER on the possibility that something in the ambient atmosphere might have potentiated the toxicity of fungal-products from common molds.

I have been telling everyone for 25 years that I have had BETTER results by treating mold “as if it were Plutonium” than anything I have seen from the most aggressive chemotherapy aimed at viral or bacterial infections.

This is how I came to be known as “The Mold Warrior”.
”Mold Warriors” by Dr Ritchie Shoemaker. Chapt. 23 “Mold at Ground Zero for CFS”.

In my military career as a launcher specialist for “The Neutron Bomb”, I was trained to look for what DOESN’T happen after a neutron strike: A LOSS of immune function which leaves one susceptible to nearly anything, as opposed to consequences arising as a normal consequence from normal infection.

That is exactly the type of effect that I witnessed during the 1985 Tahoe Mystery Malady:   An inexplicable loss of immune function that appeared to correlate to environmental locations.

I have read that fungi serve as “bionanofactory” for biosynthesis of nanoparticles.

It seems to me that mold does not normally have access to fine metallic particulate matter which can be processed into “ultrafine” nanoparticles, as “modern pollution” did not exist.

These metallic nanoparticles are known to affect the microglial cells and induce CP450-decoupling” with the subsequent production of Reactive Oxygen Species, which is entirely consistent with CFS.

The activities of humans have dramatically changed the potential for contact between fungi and ubiquitous airborne metallo-particulates.

If mold is capable of what the article below [refers to this article .] says mold is doing… and is converting ambient atmospheric fine metal particles into even smaller nanoparticles… the global environment is in deeper trouble than anyone suspects.

The inception of Chronic Fatigue Syndrome just might have been the cautionary warning for nanoparticulates that nobody heeded.
– Erik Johnson

In further communications with the W.H.O., Erik Johnson made the following statements:

In the Saratoga Springs manual, the hints of a sudden surge in fungal pathogenesis is mentioned in several places where the effects matched nothing in THEIR mycotoxin literature. Dr William Croft, who published the first peer reviewed abstracts on trichothecene toxicity in the United States, said the effects were “radiomimetic”.

IAQ experts Pierre Auger and Harriet Burge agree that T2 (trichothecene) mycotoxins fall short of achieving this level of illness.

My own experiments with mold samples suggests that there are special times when this effect blazes forth with an intensity and magnitude that causes a “hit and run” effect upon the neuro-immune system which baffles physicians trying to identify a toxic substance.

To the best of my ability to discern, these times correspond to the ion-shift of the atmosphere.

Several years ago, I saw an abstract which described the capability of certain molds and bacteria to act as biosynthesizers of nanoparticles.

My speculation is that the mutation discovered by Dr Shoemaker has resulted in the conjugation of this resistance-property by various powerful “toxin forming” molds, which are now capable of withstanding the antimicrobial effects of human-introduced ubiquitous metal particulates, and processing them into extremely hazardous “nano-plumes”.

This resistance trait emerged in the late 1970’s, just prior to the incredible surge in unexplained-illness such as Gulf War, Fibromyalgia, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, as well as massive increases in autism, Parkinsons, MS, and ALS.

The CFS epidemic strangely centered upon north Lake Tahoe, and oddly spared an almost identical demographic at south Lake Tahoe, only twenty miles away.

I believe that the emergence of “CFS” in such an otherwise pristine area represents the “canary” of a much larger ambient environmental alteration.

The reasons for which might be a special condition of application of ultrafine silver particles to this specific region.

During the 1980’s, the local ski resorts embarked upon an illegal and untested campaign of intense cloud seeding with silver iodide. Many environmentalists were concerned that in addition to the approved mountaintop dispersers that were strategically placed upwind, that private aircraft were covertly targeting every storm from and potential precipitation heading toward the resorts.

My speculation is that this intense seeding is responsible for gradually increased resistance in the microbial terrain of north Lake Tahoe, which combined with the newly potentiated indoor toxic molds, resulted in “spot colonies” of extremely hazardous molds which emitted nano-plumes and manifested in unprecedented immune suppression that ALLOWED people in these environments to acquire the opportunistic infections which might otherwise have been warded off, resulting in “clusters” of unexplained illness and the inception of the Chronic Fatigue Syndrome.
-Erik Johnson

Further Food for Thought

From the Fresno Bee:  Shower of toxic particles threatens Valley air by Mark Grossi, July 14, 2010

(Last I checked, the link was broken, but it was  There is reference to the entire article with a partial reprint here:

A mysterious shower of microscopic chemicals near a Fresno shopping center could be the first evidence of a broad, undetected assault on the lungs of San Joaquin Valley residents.

If confirmed in other Valley cities, it means many thousands of people are daily breathing these cocktails of chemicals — known as ultra-fine particles — that corrode and damage lungs.

The plume in Fresno probably spreads over many square miles, not just the Fashion Fair area where they were discovered, said UC Davis atmospheric scientist Anthony Wexler, who detected the pollution.

Sensitive, expensive equipment is needed to detect and study ultrafine pollution. Science is only now defining the possible problem.

Wexler revealed Fresno’s midday rise in microscopic pollution last month at an air-quality conference, saying he and others will continue studying them to determine the source and extent of the plume.

Researchers also must figure out what’s in the particles and more clearly define the possible health threat. It may be years before local, state and federal officials can develop a cleanup strategy.

The particles are so small that 1,000 of them would fit across the width of a human hair. For years, science has known that such particles exist, but they are thousands of times smaller than previously studied particles in dust, soot and diesel smoke.

Health problems from such pollution were detailed last month in a study on allergic asthmatics, whose lungs are inflamed to the point that only a small amount of pollen, animal hair or other allergens can trigger a crippling attack.

The findings from Dr. Andre Nel, a UCLA medical researcher, were published by the American Journal of Physiology-Lung Cellular and Molecular Physiology.

“If there is a surge in ultra-fine pollution particles, it makes twitchy airways even more twitchy,” he said. “It results in a much lower threshold of allergens to create an asthmatic response or an attack.”

These specks can come from volcanoes or ocean spray, but they also come from printer toner, vehicle exhaust and chemical reactions in the air. Fresno’s particles may come from traffic and other pollution vapors.

The site near Fashion Fair is not far from Highway 41, Shaw Avenue and many businesses and restaurants, so there could be many different contributors to the pollution.

Wexler said he suspects the particles form after pollution gases accumulate in the air each day, though there could be a particular source spewing the particles.

But he said it’s a good bet that the problem is not just isolated in the Fashion Fair area. Thousands of Fresno residents may be exposed to the particles.

Is this midday rise in pollution occurring in other Valley cities? It’s possible, said Wexler. This kind of pollution also has been detected in other places, such as Pittsburgh, which has problems with particle pollution.

The Valley is known nationally for particle pollution. In the American Lung Association’s latest rankings, Bakersfield and Fresno-Madera were the country’s two worst places for short-term bouts of particle pollution.

The ranking applied to fine-particle pollution, which includes the smallest specks that Wexler discovered near Fashion Fair.

Researchers in Southern California say the tiny particles contain 1,000 or more different substances. The particles tend to grow larger, accumulating many toxic chemicals from the air.

In the UCLA study, Nel showed the chemical debris corrodes and injures the lungs, and the body responds with inflammation. He said it could possibly cause problems for even those with healthy lungs, but he has only studied asthmatics.

For asthmatics, Nel said conventional treatment does not address the problems created by pollution. He said science would have to alter medications, using the kind of antioxidant chemicals found in broccoli and other natural sources to combat the lung injuries.

Nel said such a treatment needs to be developed soon because there is evidence that ultra-fine pollution is becoming a problem in many places, and asthma is on the rise worldwide.

”The particles are increasing in the industrialized Northern Hemisphere,” he said. “They are being spread on the wind from city to city, country to country and even continent to continent.”

The reporter can be reached at or (559) 441-6316.

Let’s put it together and see what we get.

Is mold capable of acting like a nanofactory, spitting nanoplumes into the air?  And can these nanoplumes carry nanoparticles that are subsequently laced with biotoxins such as tricothecene toxins?  Have nature and mankind collided to create a perfect delivery system for highly toxic particles to be shuttled across cell walls and through the blood/brain barrier?  If so, that would certainly create an immune system open to the uptake and residence of name-your-pathogen.

It certainly seems to be a paradigm screaming for research.

And just for fun, try this:

Silent Spring

“The words of the prophets are written on the subway walls
And tenement halls”
And whispered in the sounds of silence – Paul Simon, Sounds of Silence