By Patti Schmidt
PART 1 of 2
Two doctors believe they've discovered a new brand of illness and a new way for pathogens to make people sick. They also have an FDA-approved treatment that was effective in a small, preliminary clinical trial.
neurotoxic /nõr'ò tok'sik/, anything having a poisonous effect on
nerves and nerve cells, such as the effect of lead on the brain and
nerves. -The Mosby Medical Encyclopedia
There are many theories and much disagreement about what causes Chronic Fatigue Syndrome (CFS), Multiple Chemical Sensitivity (MCS),
fibromyalgia (FM) and some other chronic multi-symptom illnesses.
Some science points to abnormalities in the immune system's
viral-fighting pathways; other research to a cascading combination of
genealogical, environmental, and health-and personality-related
events and factors that begin with a predisposition and a "bug" and
ends with someone who's chronically ill. And despite a rash of
recent scientific evidence to the contrary, some out-of-touch
physicians still insist sufferers are just depressed.
While some blame stress and societal ills for the widespread fatigue,
depression, joint pain and cognitive problems common to these
illnesses, recent research suggests these problems may instead be
linked to toxins generated by cells gone awry-that many people are
chronically ill due to biotoxins in their system they cannot
Two scientists – family practice physician Ritchie C. Shoemaker and EPA
neurotoxicologist H. Kenneth Hudnell, Ph.D., – have collected data to
back up this "neurotoxin-mediated illness" theory, and they've
developed both a simple way to test for neurotoxins and a treatment
protocol featuring an effective, FDA-approved prescription medicine
that flushes toxins safely from the body.
Shoemaker's website features information and research as well as a
way to measure toxin exposure potential. After answering a brief
health questionnaire about symptoms and some questions designed to
eliminate confounding factors, it takes just five minutes and $8.95
to take the online Visual Contrast Sensitivity (VCS) test, which
measures the impact of neurotoxins on brain function.
Data from the questionnaire and vision test are analyzed immediately
to determine if users are likely "positive" or "negative" for
neurotoxins. The website doesn't make an official diagnosis, but
gives a push in the right direction. Users can then take the test
results to a physician so they can be treated if necessary.
The two say they have data to support the claim that 90 percent of
the people who test positive for neurotoxins improve following their
"If you have the VCS deficit, the potential for biotoxin exposure,
and don't have other exposures or medical conditions that could
explain the deficit, our data indicate that the response to
toxin-binding therapy is over 90 percent," says Ritchie C. Shoemaker,
M.D., the physician who helped develop the theory and the treatment. The story of how a small-town family practice physician and a civil
servant who works for the EPA came up with that theory- and how they
found a treatment for the 10 million Americans they claim it can
help- is at least as interesting as the theory itself.
Ritchie Shoemaker always planned to have a rural primary care
practice. He graduated from Duke University Medical School in North
Carolina in 1977, courtesy of the National Health Service Corps,
which paid for his medical education in return for a stint serving
under-served areas of the U.S. In July of 1980, following a Family
Practice residency in Williamsport, Pa., the NHSC sent him to its
clinic in Pokomoke City, Md.
"I could hardly believe that the government was going to pay my way
through a few years at Duke Medical School, in order to do something
I already wanted to do," he said.
Pokomoke City was then a thinly populated small town situated along
the Pokomoke River, a tributary of the 200-mile long Chesapeake Bay.
The Pokomoke itself flows South from Delaware, 80-miles long and just
50 yards wide in some places.
At the time they settled there, Shoemaker and his young wife JoAnn
were newlyweds. Taking great pleasure in the idyllic setting, they
became involved in civic activities; had a daughter, Sally; and began
protecting the unique ecology of the Lower Eastern Shore, building
and restoring wetland ponds, wetland gardens and a mile-long nature
"This was everything I had ever wanted," said the doctor. " I had
the love of a spouse and family, the love of my practice and of my
land. I was happy."
In 1996, the first reports of "sick fish" in the river began
appearing in local newspapers. It wasn't long afterward that some of
his friends and patients began complaining of flu-like symptoms. "They had nasty headaches, diarrhea, rash, cough, persistent muscle
aches and failures in short-term memory," says Shoemaker.
His intuition, backed by a solid grounding in science (he was a
biology major in his undergraduate days) told him the sick fish and
the sudden illness among his patients were related. When someone
brought him a dead fish, fresh from the Pokomoke, the curious young
doctor put it under a microscope.
"The link was the river," Shoemaker says in the book he wrote about
these events, Pfiesteria: Crossing Dark Water. "Each one of them had
spent time working or playing in the slow-moving Pokomoke during the
summer of 1997."
He had no idea that what was under that microscope would change his
life and put him at the uneasy nexus where politics, ecology and
Meanwhile, Shoemaker's research collaborator Hilton Kenneth Hudnell,
PhD, a calm, soft-spoken neurotoxicologist, was building a civil
service career at the Environmental Protection Agency.
Ken Hudnell grew up in North Carolina, where the Neuse and Trent
rivers join at New Bern. In a twist of fate, the Neuse was where
Pfiesteria-related fish kills were first found – the very same
organism thought to produce the devastating effects Shoemaker
observed under his microscope and in his clinic.
"It's not the same river system that I played on while growing up,"
says Hudnell today. "Back then there were few fish kills, and people
didn't associate human illness with them. My nemesis was seaweed
growing on the bottom and clogging my outboard motor. Now in many
places, the seaweed has been choked out by surface blooms of
cyanobacteria-blue-green algae- due to pollutant runoff from massive
hog farms upstream from New Bern."
A one-celled dinoflagellate, Pfiesteria piscicida is colloquially
known as the "fish killer" in areas where it has wreaked its havoc on
the local ecosystem.
Pfiesteria wasn't the first dinoflagellate that caught Ken Hudnell's attention. After majoring in chemistry and psychology at the University of North Carolina at Chapel Hill, he moved to the Virgin Islands for three years to start a diving business.
"I soon learned that you don't eat certain types of fish that feed
around the reefs," he remembered. "Those fish ate a dinoflagellate
called Ciguatera and accumulated their toxins. When people ate the
fish, they got violently ill. Many recovered completely after a few
days, but others remained chronically ill. Now I know why – they had
biotoxin circulating in their bodies that they couldn't eliminate." His experience with ciguatoxins and other biotoxins in the Caribbean
compelled Hudnell to return to the U.S. to enter graduate school. "I wanted to understand the relationships between neurobiology, toxic
exposures and human illness," he said.
Hudnell received a graduate degree from his alma mater and is an
adjunct professor there now. His work at the EPA's National Health
and Environmental Effects Research Laboratory, which involves using a
battery of neurobehavioral and electrophysiological tests to measure
sensory, motor and cognitive functions in people affected by toxic
exposures, has been recognized with two of the agency's Science and
Technology Achievement Rewards.
At the EPA, Dr. Hudnell developed a theory explaining the worldwide
increase in biotoxin-related events: human activities and natural
events impact the earth's water, land and air, altering the habitat
and promoting the development and spread of toxic organisms. Those
toxic organisms, in turn, impact man as well as the ecosystem we all
have to share.
It's an interdependent circle, which features mankind using up land,
air and sea resources, all the while ignoring the symptoms of
burgeoning environmental problems that place us in peril.
Two hundred and fifty miles north, Ritchie Shoemaker was
independently coming to the same conclusions. Chronic illness, he
was beginning to believe, was partly a result of the damage we've
done to the ecosystem.
Take Lyme disease, for example: As millions of people in the city
moved to the suburbs- and then further out into the countryside when
the suburbs became crowded- they altered the habitat to one favored
by mice and deer. Houses and new landscaping provided food and
cover, and eliminated the predators of a growing deer population.
Deer and mice are tolerant hosts, allowing ticks to complete their
life cycle by providing a reservoir of blood-borne pathogens for the
ticks to deposit into a human who happens to be in the "wrong" place
(like his back yard), at the wrong time, leaving behind a tell tale
trail of acute or chronic illness. If we hadn't destroyed their
original habitat, in other words, we may never have gotten close
enough to become a temporary feeding trough for the tick.
The doctor and the scientist met when Shoemaker, hungry for more data
on Pfiesteria, called Hudnell at the EPA one July morning in 1998.
"At 10:15 a.m., I read that Ken had found Pfiesteria patients showed
a visual contrast deficit that lasted a year or more," remembers
Shoemaker. "By 10:17 a.m., we were on the phone and working
Hudnell's early work as a UNC undergraduate led him to the VCS
literature. He developed a VCS test on an oscilloscope screen early
in his graduate studies there, soon after it was first reported in
the scientific literature that the visual system was more sensitive
to mid-size bar patterns than to smaller- or larger-size bar patterns. "I realized that this meant there were different processes in the eye
and brain for detecting different aspects of a visual pattern, and I
wanted to understand how they worked," he said. "Later I found that
those processes were differentially susceptible to disruption by
various toxins and disease processes."
While VCS testing had been used in neurotoxic exposure, Hudnell was
the first to use it to measure the effects of biotoxin exposure and
heavy metal toxicity, or as a marker for neurotoxic exposures like
Back at microscope in the summer of 1997, Shoemaker found a slimy
fish that was the first example he saw of just how much damage a
toxin-producing organism could do in the right set of circumstances.
In his search for answers, over the next few years he became
intimately familiar with the habits and neurotoxic illnesses of fresh
water and sea animals including fish, birds, alligators, turtles and
pelicans. He studied basic and esoteric subjects, including
predator-prey relationships of aquatic invertebrates; plants;
phytoplankton; the pathology of invertebrate organisms in marine and
estuarine environments; pesticide physiology; and the study of the
rhizosphere, the interface between a root and its immediate
He consulted experts in fields such as pathology; toxicology;
biochemistry; geochemistry; physiology; estuarine limnology; and even
membrane ionophore chemistry, the study of the passage of organisms
and molecules in aqueous solutions across membranes. He learned how
pesticides degrade in air, water and subsoils.
Given the intense political controversy that an environmentally
acquired illness like Pfiesteria created, he needed this knowledge to
piece together a mystery: Was there a link between the fish kills
and the illnesses his patients were suffering? Why didn't the body
rid itself of these toxins naturally? Do bacteria, fungi, algae and
other tiny organisms manufacture toxins that linger on in the human
body, long after the organisms themselves are dead?
Eventually, Shoemaker figured out that his patients had a new
illness, originally named Pfiesteria human illness syndrome in his
1997 article in the Maryland Medical Journal. The CDC renamed the
illness "Estuarine-Associated Syndrome" in 1998, and "Possible
Estuarine-Associated Syndrome" (PEAS) in 2000.
It took Shoemaker a few more years to put together his "chronic
neurotoxin-mediated illness" theory and some time after that to
gather the data to tell him his theory was sound. In the end, he
believes he and Hudnell have discovered a new brand of illness and a
new way for pathogens to make people sick. The two have continued to
gather data fleshing out the theory with more clinical and molecular
In the meantime, Shoemaker built up his medical practice, winning the
2000 Maryland Family Doctor of the Year Award and being named one of
five finalists for the National Family Practice Doctor of the Year
Award in 2002. At the same time, he battled state and local
bureaucrats who continued to tell people, "the river is safe,"
despite evidence to the contrary.
When Shoemaker went to the press with his theory and his data during
the outbreak in Maryland in 1997, the bureaucrats did everything they
could to ruin his reputation. One state official quoted in the local
newspapers accused him of "scientific malpractice," and claimed he
was "out of his field" when it came to the sciences.
Their refusal to see -and say -the truth simply drove him to work harder. When residents near the St. Lucie River near Stuart on Florida's East Coast suffered a rash of dinoflagellate illnesses in 1998, they listened to Shoemaker's theories of copper toxicity. Copper binds to pesticides, giving them easier entrance into organisms. If predators of dinoflagellates are more susceptible to the copper-pesticide toxicity than dinoflagellates, a decrease in the predator population could result in an increase in the dinoflagellate population. Also, if prey of dinoflagellates are killed at lower exposure levels than dinoflagellates, this might put pressure on the dinoflagellates to produce and release toxins in order to kill fish for a food source.
Then Florida officials earmarked $30 million to build lagoons that
filter runoff from copper-laden citrus groves, bought wetland farms
to restore them and dredged contaminated sections of the St. Lucie.
They levied a three-year, one percent sales tax to pay for these
The CSM treatment proved just as effective in Florida as it did in
Maryland. About 15 residents and investigators working on the St.
Lucie became ill with multiple systems symptoms and suffered a VCS
deficit. They responded well to CSM therapy given by four local
But like the guy who discovered that a bug causes ulcers, Shoemaker
found the medical community in Maryland reluctant to applaud his new
theory. In fact, it was met with active resistance, he said. For example, the head of ophthalmology at the University of Maryland
School of Medicine dismissed the value of visual contrast testing in
helping to diagnose Lyme disease by simply saying, "I don't think so."
In his spare time, Shoemaker also wrote four books: Gateway Press,
in Baltimore, Md., published Pfiesteria: Crossing Dark Water, a
360-page tally of the outbreak in the waters of the Pokomoke, in
1997; Weight Loss and Maintenance: My Way Works, a 325-page
explanation of a weight loss mechanism with maintenance rates that
exceed 70 percent, in 1998; and Desperation Medicine, the 519-page
saga of his findings that neurotoxins are responsible for many
chronic illnesses, in 2001. His latest book, Lose the Weight You
Hate, is a 454-page update of his earlier diet primer which adds
recipes, an explanation of how neurotoxic illnesses contribute to
obesity and diabetes, and a discussion of the importance of genes and
how they effect weight loss.
Despite the disbelief, Shoemaker and Hudnell can point to data,
accumulated since the mid-60s, that visual contrast sensitivity
deficits exist in diseases like Type 1 diabetes, multiple sclerosis,
and in Alzheimer's and Parkinson's disease.
In fact, experts suspect that many diseases involve deficits in
visual perception, but there's little research relating toxic
exposures to differences in visual function before diagnosing disease. Visual contrast sensitivity testing assesses the quality of vision.
It differs from typical visual acuity testing in that it simulates
"real-world" circumstances, while routine visual acuity testing
measures eyesight under the best possible conditions.
"That's why measuring visual contrast sensitivity in patients who
report difficulty with their vision, yet see well on the conventional
visual acuity eye chart, is particularly useful," says Hudnell. The test is performed by showing the patient a series of stripes or
bars that slant in different directions. The patient must identify
which way each series of stripes is tilted. As the test progresses,
the bars become thinner and lighter. People with excellent contrast
sensitivity can discern the orientation of even very light, thin
bars; patients with neurotoxic damage cannot.
After chronic exposure to many organic solvents, VCS is the most
sensitive indicator of effects from many toxins, either because the
visual system is highly susceptible to neurotoxins or because even
small deficits can be measured, according to Hudnell.
"The visual system is the ideal place to look for evidence of
neurotoxicity," he says. "The retina is a microcosm of the brain; it
contains most of the cell types and biochemicals that are in the
brain. So the retina is as susceptible as the rest of the brain to
According to Hudnell, this "piece of brain," being near the front of
the face, is in close contact with the environment. Chemicals may be
directly absorbed from the air into the retina, so the potential for
exposure to neurotoxins is greater in the retina than in the brain. But unlike the brain, he points out, the visual system has few
functional outputs (pattern and motion detection, or color
discrimination, for example) and we can easily measure them. The VCS test measures the least amount of stimulation needed to
detect a stationary pattern.
"As neurologic function decreases due to toxicity, more and more
stimulation is needed to see the patterns," he explains.
The effect can be huge; the Pfiesteria cohort in one of Shoemaker and
Hudnell's studies showed a 60 percent loss of VCS on average relative
"When we see VCS drops like this following exposure, and see it
recover following treatment to eliminate the toxins, we're seeing an
indication of how strongly the toxins may be affecting the entire
nervous system," says Hudnell. "Of course, biotoxins don't just
affect the nervous system. They trigger release of inflammatory
agents in the body that can inflame almost any organ and cause
And that's where Shoemaker and Hudnell's theory begins, with
biotoxins in the body that some people – as many as 10 million
Americans – cannot naturally eliminate, resulting in many chronic
The two men believe these poisonous chemical compounds continually
circuit the human body, shuttling from nerve to muscle to brain to
sinus to G.I. tract and other organs, triggering the familiar
These symptoms are similar to those caused by infectious agents, and
so is the effect they have on nerve, muscle, lung, intestines, brain
and sinus, say the researchers.
Shoemaker and Hudnell say the compounds are manufactured by a growing
number of microorganisms that thrive in our ecosystem due to changes
in the human habitat.
"New biotoxins or toxin-forming organisms are being identified all
the time," notes Hudnell.
Some, like the deer tick that passes along Lyme disease, do so
directly. Toxin-forming bugs such as the fungi (Stachybotrys and
others) that cause "sick-building syndrome" and the blue-green algae
(Cylindrospermopsis and Microcystis) that poison people and animals
in most of the lakes in Central Florida, do their work by releasing
their toxins into air or water.
And although the pathogens differ, Shoemaker and Hudnell say the
biotoxins they produce all do their damage by setting off a similar
"exaggerated inflammatory response" in humans. While hiding out in
fatty tissues where blood-borne disease-fighters can't get at them,
they trick the body's immune system into launching attacks against
joints, muscles, nerves and brain.
There is increasing evidence to show these attacks are carried out by
a newly discovered group of molecules, the "pro-inflammatory
cytokines," and that the destruction they cause is linked to recent
surges in the rates of heart disease, obesity and diabetes.
Illnesses once blamed solely on diet and life-style choices are now
being shown to have an inflammatory basis.
And while infections cause a cytokine response from white blood
cells, especially macrophages, the cytokine response to neurotoxins
comes from fat cells.
"The body can turn off the macrophage cytokine response, so that the
achiness, fever, headache and fatigue of a cold will go away, but
there's no negative feedback that stops the cytokine response from
fat cells," says Shoemaker. "So the illness doesn't self-heal." The team's research found that through typing of immune response
genes, the HLA DR, they can show that individual susceptibility to
particular neurotoxins is associated with particular genetic factors
not found in others with a different neurotoxic illness or in
controls. In other words, they're beginning to crack the code to
show that some people are genetically predisposed to get certain
chronic fatiguing illnesses.
But the research that links these things – the exaggerated
inflammatory response, which may also involve an autoimmune response
by a process called "molecular mimicry" -and its link to heart
disease, for example, is in its infancy, so the medical community
Nonetheless, Shoemaker thinks these provocative discoveries will
eventually require researchers to confront the grim possibility that
these organisms have learned how to skew immune responses by using
powerful toxins to decimate the body's disease protection system. The diagnosis According to Shoemaker, a diagnosis of chronic, biotoxin-induced illness is based on biotoxin exposure potential, multiple system symptoms, the VCS deficit discovered by Dr. Hudnell, and no other reasonable explanation for the illness. "As opposed to illnesses which have no supporting tests or biomarkers like fibromyalgia, CFS, depression, irritable bowel disease, or just getting older, our approach gives the physician readily obtained hard data to use as a marker and, more importantly, as a monitor that changes dynamically with response to treatment," says Shoemaker.
Hudnell points out that new tests for cytokine levels, hormone levels and blood flow in the microvasculature of the retina help characterize how biotoxins induce chronic illness. The new HLA genotype tests (the DNA PCR assays -not the serology or transplant tests) also help identify people who are at risk for developing chronic illness from particular biotoxins because they're unable to eliminate those toxins.
"Patients must have a compatible history, the deficit in VCS, the HLA
genotype, an abnormal cytokine response, and the abnormal effects of
cytokines on hypothalamic hormones, especially melanocyte stimulating
hormone (MSH)," said Shoemaker. "All CFS patients should have the
MSH test done."
Shoemaker and Hudnell's data show that there's a group of CSM
treatment-resistant CFS patients who are coagulase negative Staph
(CNS) positive and who have high leptin levels. Leptin is a hormone
made by fat cells that signals the satiety center in the hypothalamus
that a person is no longer hungry.
Leptin stimulates the production of alpha melanocyte stimulating
hormone (MSH), which in turn controls production of endorphins (the
body's natural "opiates") and melatonin (which regulates sleep) in
the hypothalamus. CFS patients rarely have much MSH. Eradicating CNS does nothing to the high leptin and low MSH levels in patients with "end-stage CFS," says Shoemaker, but it certainly does in patients who are diagnosed acutely and treated aggressively, preventing irreversible damage to the MSH-manufacturing pathway.
"We must recognize that the process by which CFS develops may
include an acute neurotoxic event which includes upper respiratory
symptoms," says Shoemaker.
Shoemaker believes that the secondary cytokine damage from neurotoxic
exposure changes the mucus membranes in the nose, allowing
biofilm-forming, slow-growing CNS to release hemolysins (once called
delta toxins) that in turn activate a powerful cytokine response.
The boost in cytokines disrupts the leptin-MSH production link. This
classic, positive feedback system increases cytokines and CNS and
"While the data is certainly compatible with this model, I haven't
asked for volunteers to put CNS in their noses to watch for
subsequent development of CFS," says Shoemaker jokingly.
But the team has found particular genotypes of the immune response
genes in HLA-DR that show marked consistency within a diagnosis group
and marked disparity in other diagnostic groups.
Shoemaker won't yet say that the HLA DR genes or the abnormalities in
the leptin/MSH pathway are the "Holy Grail" of CFS research, but will
admit that there are unique HLA genes in his CFS patients; that his
Sick Building Syndrome patients have at least three unique triplets
of gene biomarkers; his Post-Lyme patients have two; and that these
gene-types are quite different from each other.
Is CFS an illness that includes a genetic susceptibility to
particular neurotoxins, which trigger cytokines associated with
carrying CNS, that produce nerve, hormone and immune system
dysfunction in the ventromedial nucleus of the hypothalamus? Maybe,
"If our study shows that replacement of MSH improves many (or most!)
of the abnormalities of CFS, I'll believe that," says Shoemaker. That study will be done after the animal studies required by the FDA
are completed. They hope it will establish an effective MSH dose and
the most effective method of MSH delivery, as well as confirm that
symptoms reoccur when MSH is stopped, and then again show benefit
when an effective does is reinstituted.
They'll do baseline VCS tests and MSH levels first, and will attempt
to show that high levels of plasminogen activator inhibitor-1
(PAI-1), tumor necrosis factor alpha and leptin improve after
A longer trial is planned, pending initial results. That study,
which will be done when funds are obtained, will also attempt to show
that high levels of PAI-1 and leptin improve after treatment. Shoemaker believes PAI-1 is likely to be responsible for the extra
clotting and vascular disease frequently found in CFS patients, and
that once leptin levels fall, CFS patients who have gained weight
will be able to lose it.
Before you can take the CS exam at Dr. Shoemaker's web site
(http://www.chronicneurotoxins.com), you have to register and get a
log-in identity and password, as well as answer symptom and medical
history questionnaires. Then you can buy a VCS test for $8.95, or a
package with several tests and treatment protocols for $49.95. The preliminary test (a free questionnaire) assesses the symptoms
commonly associated with biotoxin-induced illness, as well as your
potential for exposure.
"Many symptoms of and potential exposures to biotoxins are not yet
well known by physicians," says Shoemaker, "So they're easily
After you take the test, your results are available immediately.
They can also be sent to your physician. If your physician isn't
familiar with the theory or protocol, the website mentions a list of
referral physicians across the nation, or you can request to see Dr.
Shoemaker in his Pokomoke City office. (A second part to this
article will detail the author's diagnostic and treatment experiences
at Dr. Shoemaker's clinic.)
The treatment protocol
Cholestyramine (CSM) is an FDA-approved medication which has been
used to safely lower elevated levels of cholesterol for more than 20
years. It isn't absorbed; if it's not taken with food, it binds
cholesterol, bile salts and biological toxins from bile in the small
intestine, and then the CSM-toxin complex is excreted harmlessly. Science – or Shoemaker and Hudnell -doesn't have definitive answers
yet as to exactly how or why CSM clears neurotoxins from the body,
but a double-blind, placebo-controlled, cross-over clinical trial of
eight Pfiesteria patients positive for biotoxins showed that those
who took a placebo remained ill, but improved following CSM
treatment. Data from 30 others he's gathered since matches the
original study data.
Shoemaker says while some patients notice immediate improvements,
Lyme disease patients who've been sick for more than five years
usually require toxin-binding therapy for 4-8 weeks, he says. "Most patients improve in two weeks, some with complete abatement of
symptoms, but depending on the amount of toxin in your body, it may
take longer," says Shoemaker.
He believes the response of these patients to CSM therapy shows the
underlying common theme of neurotoxin-mediated illness, and that the
proof that toxins were responsible for the illness is found when
patients recover, i.e., have no symptoms following treatment with his
"The proof of neurotoxin effect comes from watching the biomarkers
change with treatment and relapse with re-exposure," says Shoemaker.
"There's very strong evidence, especially in the Sick Building
Syndrome patients." Hudnell agrees.
"The best evidence that biotoxins are causing the illnesses comes
from cases with repeated illness," says the toxicologist. "When you
see patients with chronic illness recover vision as symptoms resolve
while being treated with a drug that can do nothing but remove
compounds from circulation, then see vision plummet and symptoms
return following re-exposure to sources of toxins, and finally see
re-recovery with re-treatment, sometimes for three or four cycles,
you become convinced that it's the toxins causing the illness."
In another study of 51 post Lyme disease patients treated with CSM
after a tick bite, both those who tested positive and those who
tested negative to Lyme had the same number of symptoms after
treatment as matched controls. Shoemaker says that data from more
than 500 other patients he's seen since matches the study data. Prior to treatment, the chronic Lyme disease patients had a
statistically significant VCS deficit. Following treatment, all
patients' clinical syndrome was gone; and their VCS scores and the
number of symptoms were the same as that of the controls.
Some of these Lyme disease patients, especially those who'd been sick
longer then three years, suffered what Shoemaker calls "a symptom
intensification reaction" early in CSM therapy, similar to, but more
intense than, the Herxheimer reactions experienced previously during
antibiotic treatment. The reaction was reduced with pioglitazone
(Actos) therapy or prevented by pretreatment with Actos, which
downregulates proinflammatory cytokine production by fat cells. Patients who weren't reexposed to another tick bite didn't relapse,
though follow-up was stopped at 18 months.
There are other diagnoses- chronic Ciguatera seafood poisoning,
Possible Estuary Associated Syndrome, brown recluse spider bites and
mycotoxicosis-that were thought to involve biotoxins, but for which
there was no known, effective treatment. Shoemaker has treated
patients with these illnesses successfully with cholestyramine, too. Over the years Hudnell has done studies that linked environmental
exposure to neurotoxicants like airborne solvents and metals to
adverse neurologic effects in humans, including VCS deficits. But
there was no treatment for it.
"There was nothing I could do to help them, and the impairments were
permanent," he said. "So I was ecstatic when we found that a simple
treatment, taken for a short period of time, could benefit so many
people who had suffered severe chronic illness due to biotoxins." News spreading Others have gotten excited about this research: Paul Cheney has used the VCS test and a modified version of the protocol to treat patients at his Bald Head Island Clinic in North Carolina.
Chuck Lapp, director of the Hunter Hopkins Center in Charlotte, NC,
also plans to put one of the machines in his office. "A number of my patients have complained that I wear loud, patterned clothing, and that it bothers their vision when I wear a patterned tie, so I think there may be something to this," he said.
There are also almost 50 physicians in a nationwide referral network
who are familiar with the VCS test and the treatment protocol; for
more information, contact the website for the name and number of the
doctor nearest you.
In June, Hudnell and Shoemaker presented data from their latest
studies on Sick Building Syndrome and Post Lyme Syndrome at the
8th International Symposium on Neurobehavioral Methods and Effects in
Occupational and Environmental Health in Brescia, Italy, where Dr.
Hudnell chaired a session on biotoxins. Shoemaker co-chaired. Next, they plan to conduct human studies that will more definitively
characterize the proinflammatory cytokine basis of chronic,
biotoxin-induced illness, and describe the permanent damage that they
think has occurred in the hypothalamic-pituitary-adrenal (HPA) axis
of those who had the highest exposure levels for the longest periods
They also want to do the animal studies and human trials needed for
FDA approval of hormone replacement therapy that they think will help
those with permanent damage. To that end, Dr. Shoemaker has
established a not-for-profit corporation, the Center for Research on
Biotoxin Associated Illness (CRBAI).
"If the research is to get done, CRBAI needs to raise funds through
grants and donations from private organizations and individuals
because there is virtually no Federal funding of research in this
area," said Shoemaker.
In the meantime, he still sees patients every day in his Market
Street office, many suffering from chronic, neurotoxic illnesses.
Both Shoemaker and Hudnell routinely get calls from all over the
world asking for advice on toxic outbreaks and how to treat them.
New patients are still taking the tests on the website and beginning
So as physician William Osler advocated long before the advent of the
biotoxin-mediated illness theory, to find the proper diagnosis,
Ritchie Shoemaker listens to the patient.
"Recognizing the pattern of a neurotoxic illness is as subtle as
being run over by a steamroller, once you learn how to ask the right
questions," he says.
Physicians need to learn to ask the patient a few more questions in a
new order-in essence, take an organized neurotoxin history, he says. "All our biomarkers and all our data and all our nice molecular
models simply provide an academic foundation for what the bedside
physician already knows to be true," insists Shoemaker. "The toxins
Editor's note: To read part 2 of this article series, click on the following link: http://www.immunesupport.com/library/showarticle.cfm/id/4291/searchtext/neurotoxins/