Category Archives: Blogs by Khaly Castle

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”.”

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.

History – REEVES CFSAC presentation 2009

Dr. William Reeves’ final presentation to the CFSAC was on May 27, 2009.  I remember watching it on live feed, and taking copious notes.  I found the notes just the other day when I was going through an old hard drive, and thought we could see how far we have come.  Or not.

Dr. Reeves’ presentation lasted approximately 40 minutes.   He prefaced it with an outline of what he would be discussing:

  • He would update us on  results of peer review
  • He would discuss the draft of the 5 year strategic plan, calling it a “complex topic”.
  • He  would explain the current CFS program, discuss the logic model that’s in the handout, go through the current version of the draft,  putting it into context with the peer review and stakeholders meeting, and the recommendations that this committee has made.

Dr. Reeves said the the “program objective is to devise control and prevention strategies, and improve the quality of life of sufferers.
We are not NIH, we are a complementary agency.”

He went on to say that the control strategy model is rather simple – that there is the population of the world, and in that population some have CFS.   Among those who have CFS, there is more than one subtype.

“We need to get these people to interventions. Their illnesses
need to be evaluated and managed. We must take subtypes into account. We must decrease the burden CFS poses on the
population, decrease impairment, and decrease economic impact.”

He said that the CDC needs to address the barriers to access to healthcare. But on the other hand, patients actually have to utilize that healthcare.

Thirdly, patients have to receive appropriate care.

“What do we think CFS is?” Dr. Reeves asked. “It’s a complex illness, with alterations in complex homeostatic systems.  It’s not the result of a single mutation or a single environmental factor. It comes from a combination of many factors: genetics, gender, stressors, immune stressors all interact.”

Reeves showed a slide with a diagram. He said, “This is our current model. You see the brain in the middle. Around the brain,
stress is involved, traumatic childhood stressors, allostatic load maladaptation to stressors, genes interact with one’s reaction to stress, autonomic nervous system, orthostatic intolerance, immune activation..”

He went on to say that all of these things go in both directions (meaning that these things contribute to causing CFS, but CFS
contributes to all of these things.) He then mentioned that acute and latent infections that may reactivate with various stressors, and
that diet and lifestyle are important, again in both directions.

(Of note is that the very first things he mentions in his model are childhood trauma and allostatic stress loads.  In other words, we do not know how to handle stress. The third thing he mentions is genetics, but he ties genetics to stress – not to susceptibility to a

Dr. Reeves moved on to discuss the CDC’s CFS research strategy.
He said that population studies “let us look at risk factors, the clinical course of illness, to be able to tease out subtypes. We measure
biomarkers in our population studies, as well as knowledge, attitudes, and beliefs.”

He said that the goals are the same in clinical studies. As far as laboratory studies go, he said that “nothing we do doesn’t have a lab

Dr. Reeves said that the goal of education activities is that “we have to change attitudes, knowledge, beliefs, and treatment patterns.”

Next, Dr. Reeves wanted to discuss the Logic Model that his team has developed. He said that the reason for a logic model is that it
‘allows you to put strategy and tactics into perspective, outline goal and measure success.”

In the logic model, there are inputs, outputs, and outcomes. He discussed them as follows:

Outcomes: “We want to reduce population morbidity and improve quality of life for patients.”

Inputs: “These are activities, what we actually do. It is not a trivial illness. Congress realizes and appropriates money to study it.
Advocates, academia and pharma, these are people we can partner with to do it.”

Outputs: “Knowing the burden of the disease, knowing the “knowledge attitudes and beliefs” of sick people, their families, physicians,  etc., education, the cfs website…”

“The only outputs we really haven’t gotten to yet is therapeutic targets.”

Dr. Reeves went on to discuss CFS publications. He said that there are 136 peer review publications, 4 manuscripts in press, 10
manuscripts in review. “This is how science is done“, says he. “Who reads them and who have they influenced?” he asked.

He said that there are about 3000 or so publications on Pubmed on CFS.   About 1600 in other journals reviewed by ISI. He noted that the “only group that has more in the world is the United Kingdom.”

Dr. Reeves then moved on to the Case Definition.
He said that the newly defined illness was first defined in 1988 (Holmes).  It was then redefined in 1994, and this definition is currently the international standard. (Fukuda).

He said this is the reference standard, but has it problems. Because of that, he said, an international group worked toward
streamlining this in 2000, and it took 3 years to streamline the 1994 definition into an operational guideline. (This is how we got what is
being referred to as the “Reeves empirical”, which basically eliminates all of the very sickest of us, and the original Incline Village
cohort….and yet includes people with mood disorders only.)

Reeves said that the revision recommends standardized instrumentation to measure frequency, occurrence, and duration of symptoms.

(Doctors are having a hard time actually obtaining these instruments, or at least, Dr. Bell is, as he complained to the CDC).

Dr. Reeves then stated that provider knowledge, attitude, and belief is higher than 10 years ago.

Dr. Reeves moved on briefly to the peer review executive summary. He said that the CDC is using their comments to frame the
program, but that the bottom line was that the peers liked the current program and had endorsed the 5 year strategy.
He did make a comment on the criticism of the 2005 publication of operationalizing the 1994 Fukuda definition of CFS. His comment
was that the CDC leads the world in defining this illness, and that it was not an attempt to rewrite the 1994 Fukuda, just an attempt to
operationalize it.

Clinical guidelines was the next topic.
Dr. Reeves said that the biggest flaw in studies is that in cross-sectional studies, patients have only been sick 5 years. He said that the CDC was developing collaboration with the Mayo Clinic to use Rochester epidemiology, because local people use the Mayo Clinic from birth to death. That would give complete birth to death medical records on CFS patients, so that researchers could look back to see
what happened to some of these people as kids, what kind of traumas they may have had, and what happens to the clinical course
when they get it and go on. (Again the emphasis on the inability to process trauma).

Dr. Reeves then brought up the April stakeholder meeting – he said that “I’m not trying to be funny, but the response was very
impressive, given problems with travel/economy/illness.”
He noted that 8 people testified in person, and 30-something testified by phone. He said that leading up to that meeting and
subsequently, up until the present day, he had received around 350 or so emailed or written comments, many from some of the same
people who testified. He said that this does make it move difficult to say that 90 percent of stakeholders feel this way or that way,
because it’s all one person, basically.

He said that some of the issues that the stakeholders brought up were that:

  • Communications with the CDC had not been optimal.
  • The case definition was a high concern.
  • Pathology, biomarkers and sub typing, infectious agents, needed to be researched.
  • Management and treatment of the disease needed to be addressed.
  • Collaboration and data sharing needed vast improvement.

Reeves noted that these were the same types of comments that have been raised by the CFSAC, physicians, etc., so fair representation of concerns were addressed.

Next,  Dr. Reeves moved on to the topic of “moderators”, or things outside of what one can control, whether they be good or bad. First he mentioned some “good moderators”:

  • He said that funding had been quite available to the CFS research program.
  • He said that credibility is increasing, making research easier.
  • He said that from 1992 to 1999, funding was only 3 to 4 million per year, so they only focused on a few things, but that from 2000 to 2005, due to payback funding, “we were able to do the Wichita study, collaborate with the CFIDS Association of America, do a pilot national survey, funded one of the best post-infectious disease studies, and cytokine studies”.

Dr. Reeves said that now that payback is over, funding is decreased again.

The CDC has been doing a cross sectional study in Georgia, and have been following the CFS population there. There were a series
of workshops, he said, from 2000 to 2002, studies that show that the CFS construct is real, internationally. Across the board, he said,
in every country, the CFS construct is “Fatigue plus 8 magic symptoms, so the empiric underpinning is good”.

Then Reeves talked about “hindering moderators” or, as he put it, “what can one do with what one has. Economics is a problem for
everyone”.  He said that from 2000 to 2005, during payback, the budget averaged at about 7 million a year, but now we are back to
abut 3 to 4 million a year. He said that this represents a real 50 percent decrease, but then you have to factor in inflation.

Also, he noted, “we need to get more involved in more collaborations, working with others. Not just giving them money. We need to work together toward common goals with pharma, academia…”

Dr. Reeves then discussed the CDC’s Vision:
He said that he believed that the CDC had successfully focused on obtaining baseline information. So in moving forward, the strategy is
to focus on 4 goals:
(This is the 5 year plan)

1. Refine understanding of etiologic pathways to improve diagnosis and identify therapeutic targets. Reeves said that “Psychosocial,
clinical and biological markers must be identified.”  He also noted that we must identify risk factors, and used major depression disorder as “an extremely good example of this,another complex illness with subsets.”

2. Improve clinical management of CFS patients by providing evidence-based education materials that address evaluation and clinical management of CFS.

3. Clinical intervention trials.

4. Move CFS into the mainstream of public health concerns.

Finally, Dr. Reeves discussed upcoming activities, including an international workshop on clinical management. He noted that the “UK already has this integrated into their healthcare system”.

Reeves then mentioned that there is a CBT/GET trial in the process of being planned in Macon with the collaboration of the “UK group
and the Mayo Clinic”.


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