ProHealth health Vitamin and Natural Supplement Store and Health
Log In  |  My Account  |  View Cart  View Your ProHealth Vitamin and Supplement Shopping Cart
800-366-6056  |  Contact Us  |  Help

|
|
|
|

Trending News

Gut Bacteria, Artificial Sweeteners and Glucose Intolerance

Culprits of Autism Identified: Toxins, Gut Bacteria, Nutritional Deficiencies, and Vaccines Made wit...

Vitamin E intake critical during 'the first 1,000 days'

Turmeric compound boosts regeneration of brain stem cells

Lower risk of mortality over thirteen year period in association with higher levels of vitamin D

Reverse Mitochondrial Damage

Use of Broad-Spectrum Antibiotics Before Age 2 Associated with Obesity Risk

VIDEO: Beautiful Clouds - Relaxation and Meditation

CoQ10: The Longevity Factor

Elevated plasma biomarkers of chronic inflammation in Gulf War illness

 
Print Page
Email Article

Neurotoxins: Diagnosis and Treatment Information for Chronic Fatigue Syndrome, Fibromyalgia and other

  [ 1544 votes ]   [ 2 Comments ]
www.ProHealth.com • March 26, 2003


By Patti Schmidt

PART 2

Patti Schmidt is an award-winning writer and PWC (Person with CFIDS), a former CFIDS support group leader, co-founder of the Greater Philadelphia CFIDS Alliance, and is an officer of the Board of Directors of the CFIDS Association of America. Ms. Schmidt has written about a wide variety of topics relating to coping with the disease and seeking out effective treatment.

The first part of this two-part series explained how two scientists, Maryland family practice physician Ritchie C. Shoemaker and EPA neurotoxicologist H. Kenneth Hudnell, developed their "neurotoxin-mediated illness" theory explaining why many multisystem illnesses like Chronic Fatigue Syndrome (CFS), Multiple Chemical Sensitivity (MCS), fibromyalgia (FM), Sick Building Syndrome (SBS) and Lyme Disease are making people sick these days. Hudnell and Shoemaker believe they have both a biomarker for neurotoxic illness and an effective treatment. (The first part of the article can be read online at http://www.ImmuneSupport.com/library/showarticle.cfm/id/3990/.)

The first article also detailed the clinical trials in which they tested the theory; the new, simple, inexpensive way they test for neurotoxins; and described their treatment protocol, which features an effective, FDA-approved prescription medicine that flushes toxins safely away. The two became convinced that many of these illnesses are neurotoxic when clinical trials found their treatment for Pfiesteria - cholestyramine (CSM) - also helped many of those patients improve. Pfiesteria, the toxic dinoflagellate Pfiesteria piscicida, is the cause of many major fish kills and fish disease events all over the Eastern seaboard, especially North Carolina and Florida.

As part of my research for this series, I agreed to go through Dr. Shoemaker's diagnostic and treatment protocols. I've been ill with CFIDS, FM, Irritable Bowel Syndrome (IBS) and a few others for more than 20 years, so I had little hope that his treatments would "cure" me. But CSM, often prescribed to lower cholesterol levels, has a long safety record, so it probably wouldn't hurt me, either. But then Dr. Shoemaker's diagnostic process found something unexpected, putting a whole new spin on things; And suddenly, the world was a very different place for me.

The Diagnosis

Dr. Shoemaker's office is located in Pocomoke City, Maryland. First I sat in a medium-sized, cheerful front office and filled out medical information and insurance forms. Within minutes, I was led to a small, clean exam room. I took out my notebook and a tape recorder. Dr. Ritchie Shoemaker entered the room suddenly. He read my medical history and health questionnaire and it was immediately clear from his comments that the challenge of figuring out and treating these diseases is what drives him. We spent the next two hours going over my history, symptoms and his theories. (See part one for theory details.) To help me visualize how his theory works, he begins drawing on a roll of white paper stretched taut on the patient's examining table between us.

Some of Dr. Shoemaker's questions are a bit odd, including, "Have you ever felt a sudden, sharp pain like a lightning bolt or a feeling like an ice pick stabbing you?" But odd or not, once while driving to work years ago, I got an intense pain in my heart and thought I was having a heart attack. I detoured to my physician's office just minutes away and was diagnosed with costochondritis, an inflammation of the ribcage's costochondral joints. I know FM patients often experience that. Do I have light sensitivity or a metallic taste in my mouth, he asked? Yes, I'm sensitive to light, I told him, and the weird tastes I get sometimes in my mouth seem more like either mayonnaise or pennies to me. He checked ‘yes’ for that one, too.

Shoemaker hears complaints of strange tastes often from his neurotoxic patients. He asked me a group of hypothalamic-related questions: Do I ever have mood or appetite swings, profuse sweats, night sweats or an inability to control my body temperature? All of them, I say. Divide 7 into 91, he said, looking for how I handle numbers. I'm surprised and a little humbled when I can't do it, even after he gave me extra time. Most neurotoxic patients have these symptoms, too.

Do I suffer from excessive thirst, frequent urination or a susceptibility to static electrical shocks? Yes to all three, I answered, especially the shocks. But I'm curious: what do those things have in common? Is a tendency to give people electrical shocks tied to illness somehow? What do all of these things signify? Shoemaker answered the shock question first: Hormonal deficiencies cause neurotoxic patients to lose water, and as salt becomes more concentrated in their blood, sweat glands respond to protect the blood from excessive salt by excreting it in sweat. In fact, cystic fibrosis patients are diagnosed by the amount of chloride in their sweat, and often neurotoxic patients have even more chloride in their sweat than cystic fibrosis patients. The salty sweat dries on the skin, making it a very large, efficient conductor of electricity. I'm happy to know why this happens, but I had no idea it had anything to do with my health problems.

As he examined me, then has an assistant take 12 vials of blood, he answered my other questions. He ordered several tests, including levels of ACTH (adrenocorticotrophic hormone), cortisol and ADH (antidiuretic hormone). He also wanted to know my osmolality (the amount of salt in my blood). He also tested for MSH (melanocyte-stimulating hormone) and leptin levels (see part one of this series for a detailed description of how MSH and leptin effect patients with neurotoxic illness); ordered an HLA-DR by PCR (human immune response gene testing, done by polymerase chain reaction); and tested for androgen levels, including total testosterone, androestenedione, dehydroepiandrosterone sulfate (DHEA-S),* and MMP-9, the enzyme that delivers inflammatory elements from the blood into the brain, lung, heart and joints. He also ordered a Tumor Necrosis Factor (TNF) level test; a plasminogen activator inhibitor-1 (PAI-1) test; and a test to see if I have a Coag Negative Staph infection.

MMP-9 levels are increased by the immune system's response to biotoxins, and it delivers inflammatory elements into joints, lungs, heart and brain. Shoemaker's research shows that patients with high MMP-9 are often the ones who also have Unidentified Bright Objects (UBOs) on their MRIs. He believes it may be that UBOs come from ischemia (lack of oxygen), inflammation or from the same kind of demyelination that Multiple Sclerosis (MS) patients suffer from. But after treatment with Actos and CSM, MMP9 levels fall and UBOs disappear. Shoemaker believes every neurotoxic patient should know their MSH and leptin levels. Leptin initiates MSH production. The damage to the MSH production pathway (also known as leptin resistance) that's seen in neurotoxic patients is a marker for biotoxic illness. He says he answers the question, "How long will I be sick, doctor? with this: "As long as your MSH is low, you'll continue to have symptoms." MSH controls peripheral cytokine production, thought to cause inflammation throughout the body. An MSH deficiency allows cytokine production to go wild. MSH also controls defenses in mucus membranes in the nose and GI tract, which is why Shoemaker tests for Coag Neg Staph, an opportunistic colonizer found in the deep recesses of the nose. In the gut, research has yet to define the mechanism that allows people to lose nutrients into stool, often referred to as "leaky gut," and which creates the IBS symptoms like bloating, gas and cramps, diarrhea and constipation that neurotoxic patients often suffer from.

MSH also controls pituitary function, which controls hormones. If you're deficient in MSH, you'll likely be deficient in ADH and prolactin, growth hormone, ACTH, LH (luteinizing hormone) and FSH (follicle-stimulating hormone), says Shoemaker. "Not all patients have all of these deficiencies, but it's unlikely that an MSH-deficient patient won't have at least one."

Luteinizing hormone plays an important role in controlling ovulation and in controlling the secretion of hormones by the ovaries and testes. Without androgens (male hormones like testosterone), the adverse effects of peripheral cytokines are multiplied. That dysfunction causes the rest of the hormones in your body to dysfunction, resulting in symptoms like low libido in both sexes; impotence in men and menstrual irregularities, endometriosis, sexual dysfunction and premature production of uterine fibroids in women. "Hormones may be why more women tend to get these illnesses," says Shoemaker. "It's a never-ending cycle that will continue until the source of MSH deficiency is corrected." When each of these feedback loops is damaged, each causes specific dysfunction. Lyme patients take Actos to correct the cytokine excess.

Working backwards to correct the MSH deficiency, we need to remove the damage to the MSH production pathway. That means that we need to block excessive cytokine production, which comes from fat cells. Enbrel, a drug for Rheumatoid Arthritis, suppresses cytokine production, but not cytokines produced by fat cells. Only Actos does that. Actos also blocks MMP-9, excessive leptin production and turns on uncoupling proteins which burn fat directly. That process, which causes weight loss, also mobilizes fatty acids, reducing insulin resistance that in turn lowers the adverse effects of cholesterol, triglycerides and blood sugar, thus helping us avoid heart disease and diabetes.

"All of this cytokine chemistry goes for naught if the person is still exposed to toxins," warns Shoemaker. "Then, regardless of which treatment you try, cytokines will increase." In other words, you must get rid of all confounding variables that might also be making you sick. That means that Lyme patients have to be treated for Lyme before they can be treated for the neurotoxic effects of Lyme; that the SBS patient must be removed from further exposure; and that Coag Neg Staph must be removed from the nose.

But back to the office visit: the Coag Negative Staph test isn't pleasant. To get a sample from deep inside your nose where the Staph organisms hide, he sticks a long Q-tip two inches up your nose. No one likes that test, but it's necessary because if it's a complicating factor, he must treat it first. Dr. Shoemaker also noted the results of a recent Complete Blood Chemistry, thyroid testing, and a few hormone tests like estrogen and estradiol that were ordered by my primary care physician, my gynecologist or a specialist. I asked what the significance is of sudden sharp pains, which he called neuropathic pains. "They reflect damage to nerves," Shoemaker replied. Many neurotoxic patients suffer from them, including CFIDS, FM and Lyme Disease sufferers. Light sensitivity, mood swings, sweats, and the other symptoms symptomatic of autonomic system dysfunction signify "hypothalamic neurotoxicity," otherwise known as CFIDS.

At the end of two hours, Shoemaker believes he has a complete picture of my medical history and previous diagnoses. He also notes my health questionnaire answers and the data from the physical exam. He asks about previous Lyme tests. All negative, I say. He frowns: do I know which tests were done? Find the reports, he says, because based on everything he's seen, he believes I have Lyme Disease.

I'm shocked; I'm not sure what to think. Then I remember that the University of Pennsylvania had tested my spinal fluid while looking for reasons for cluster headaches a few years back. Isn't that a sure sign of being Lyme-free, I ask? "You cannot rely on test results alone to make a Lyme Disease diagnosis," explains Shoemaker. "Not the Western Blot, not the Elisa, not the PCR test of cerebral spinal fluid. Lyme Disease is now considered a clinical diagnosis, which means a physician has to look at a patient's symptoms in order to make a diagnosis." I didn't know that. My head is spinning. I doubted that I'd been misdiagnosed because I'd seen some of the best doctors in the field. How could they each have missed something so obvious? I can hardly wait to get home to do some research.

Lyme Disease

Soon, genetic testing results confirm that Dr. Shoemaker was right about my genotype; additional results were also compatible with Shoemaker's preliminary diagnosis of Lyme Disease. I had no confounding exposures, i.e., nothing else that would explain these symptoms. (The Lyme was probably what caused the CFIDS, FM, IBS and other illnesses.) In the meantime, my research confirmed that Lyme Disease was a clinical diagnosis, and that there were two scientific camps: one that believes that as little as a three week-long course of antibiotics would eradicate Borrelia burgdorferi (the bacterium responsible for causing Lyme Disease) and another that believes chronic Lyme Disease patients needed much longer antibiotic treatment. Naturally, insurance companies are in the short-term camp.

According to the LymeTruth organization's website (http://www.lymetruth.org/), serological tests may not detect up to 60 percent of cases of Lyme disease. In some areas, 100 percent of
deer ticks harbor Lyme disease spirochetes. More than 50 percent of infected humans never notice a rash or a bite; I did have a rash in the 1980s that no doctor was able to diagnose, but it wasn't the typical "bullseye" rash Lyme patients get. I contacted several Lyme experts. One went over my medical history in detail with me, and we found 13 indications of Lyme Disease, including an incident of Bell's Palsy in 1977 and meningitis in 1986. A recent significant improvement while taking Amoxicillin was also an indicator - it's one of the best Lyme killers.

I had chronic Lyme Disease. It was probably why I first got CFS, and was also probably the reason for the last - and worst - of my many relapses, the one that finally knocked me out of the working world. Shoemaker was confident I had chronic Lyme Disease before he got the test confirmation because his research has shown that people with my specific group of symptoms, diagnoses and exposure (i.e., where I'd lived) all shared the same genotype, a "15-6-51," and a "1-5." (Differential association of HLA-DR genotypes with chronic neurotoxin-mediated illness: Possible genetic basis for susceptibility, R Shoemaker, presented Nov. 11, 2002 at the American Society of Tropical Medicine and Hygiene's 51st annual meeting. Abstract available at
http://www.chronicneurotoxins.com/learnmore/latestAbstracts.cfm) That research hadn't been available to my other physicians previously, so they never knew to run that test. The research is still preliminary as well.

But Shoemaker notes that it's not surprising that individual susceptibility to illness caused by toxins made by invertebrates is controlled genetically. (An invertebrate is any animal lacking a backbone.) The immune response genes, including HLA-DR, along with immunoglobulins and white blood cells called T cells, are only found in vertebrates. It's also not surprising that deficiencies of the immune response to those toxins result in illnesses in some patients with exposure, but not in other patients with the same exposure who don't have the same immune response gene defect.

"Basically, if you get bit by a tick and develop Lyme Disease, you will develop chronic Lyme Disease if you have those genes," says Shoemaker. The "1-5" genes also predict I would develop low MSH, which is why I have chronic pain and chronic fatigue, pituitary abnormalities and alterations in gut and nose function. "The '1-5' genotype will give you MSH deficiency regardless of which toxin you're exposed to, if you also have one of the genes for susceptibility to the toxin you're exposed to," says Shoemaker.

Shoemaker's current research is finding ways to replace MSH in MSH-deficient neurotoxic patients. (See his website at http://www.chronicneurotoxins.com for details.) He also says the Lyme tests that were done on me didn't meet CDC criteria. "No one would have diagnosed you with Lyme Disease [before]," he said. That's because in 1994 a group of experts decided that you must have 5 of 10 bands present on the Western Blot Lyme test to be positive for Lyme. I didn't have all 10, but most "Lyme-literate" physicians would also consider some of the other symptoms I've had, like the meningitis, and diagnose me with Lyme anyway because research shows many Lyme patients don't have all 10 bands. "The difficulty is, the bands they chose were based on a European Borrelia, which guaranteed Lyme was rarely diagnosed," Shoemaker points out.

My local Lyme support group leader agreed with that assessment and told me that many patients still remain undiagnosed, just as I was. He also said he gets calls every week from patients previously diagnosed with CFIDS or fibromyalgia who find out they've had Lyme for some time. (See my sidebar for more information about how to determine if you've been adequately tested for Lyme Disease. If you have any doubts, make sure a "Lyme-literate" physician examines you
and your health history in detail.)

New Possibilities

Driving home from Shoemaker's office, there was a moment when I realized a new diagnosis opened up new treatment possibilities. Suddenly, the world was a very different place. At various points during the antibiotic treatment, if I experience a severe Jarisch-Herxheimer reaction (an immediate worsening of all symptoms while taking antibiotics, essentially a "die-off" reaction caused by a cytokine storm of TNF and MMP-9), Shoemaker will prescribe Actos to stem the tide. I'm instructed to call immediately if I start to feel much worse. Since Actos blocks cytokines, it's a pretreatment before taking CSM, which can also cause increased cytokines if the patient isn't adequately pretreated.

Actos is a drug usually given to diabetics. The difference between Shoemaker's approach to treating Lyme is that he'll give oral antibiotics, like the oral Amoxicillin I took, a chance to do the job, but if the patient is still having symptoms, then he uses the Actos/CSM protocol to give the antibiotics an even better chance. "The response of a patient to Actos/CSM is predictable - if the Lyme organism is dead you'll improve," he says. "If there are still Lyme organisms actively circulating, however, then the patient must be treated with additional antibiotics, justifying the extra cost and risk." If still symptomatic after round two of antibiotics, then Shoemaker tries another CSM/Actos regimen. He's perfectly convinced that Lyme is both an infectious and a neurotoxic disease, so it makes sense to pulse these drugs alternatively, giving the drugs a chance to work on both.

The first time we tried the CSM/Actos regimen, it didn't work - it made me feel worse slowly. Since I had been improving on Amoxicillin prior to that, a return to low energy, napping in the afternoon and all of the other symptoms I'd suffered didn't make me confident. But Shoemaker assured me that the return of those symptoms meant I still had Lyme organisms circulating, so we switched to another antibiotic, Doxycycline. Within a few days, I felt better. Within a week, I was back to feeling great. I've been on the Doxycycline for almost a month now, and soon we'll try another CSM/Actos treatment. If the oral antibiotics don't continue do the job, we'll try intravenous ones. If the antibiotics have done their job well, the Actos/CSM treatment will draw the neurotoxins out of my body, allowing it to heal on its own.

The other day for the first time in many years, I woke up feeling refreshed and energetic, ready to tackle the world at 7 a.m. What a difference from before, when I'd have to start the day slowly, hoard my energy and hope that I'd have enough to read or write a bit by noon or 2 p.m. Maybe I'd get a second wind later in the evening and be able to write, read or think a bit, but many days, I didn't have any energy at all and was unable to accomplish much of anything.

I'm not sure how 20 years of CFIDS has damaged my body, or what effect that damage will have on my Lyme Disease treatment. But I'm feeling better now than I have since-well, I can't even remember feeling this good, it's been so long. I've had so much energy, I moved into a new apartment recently and had everything put away and organized within three weeks. I'm actively writing every day, socializing and living an almost-normal life. I'm carefully pacing myself, following a strict drug regimen and otherwise taking good care of myself.

I can't be sure what the future holds, of course. But I have more hope of recovery than I've had for a long time.

* See http://www.naples.net/~nfn03605/dheacfs.htm for an interesting hypothesis on DHEA and CFS patients.


SIDEBAR: Research teams find neurotoxins in CFS patients

Two corollaries to Shoemaker and Hudnell's work made news recently; now Shoemaker and his team are not the only ones finding neurotoxins in CFS patients.

Recent research by Dr. Yoshitsugi Hokama from the University of Hawaii at Manoa discovered high levels of ciguatoxin, a potent neurotoxin, in CFS patients' blood. The finding was announced at an international symposium on toxins held in Japan in November 2002; the preliminary research was sponsored by an association for CFS.

Hokama's study found that many CFS patients had higher levels of ciguatoxin than cancer or hepatitis patients or people with acute ciguatera poisoning.

"Chronic ciguatera poisoning has already been suggested as a scientific model for CFS," said Dr. Hokama.

But when the research was published, Shoemaker said Dr. Hokama's development "opened up the thinking of the CFS community to the importance of biotoxins and chronic symptoms."

In 1999, ciguatera was the second illness that Ken Hudnell and he had tried the VCS testing and CSM protocol successfully on. They also presented a paper in 2000 which detailed their protocol for diagnosing and treating ciguatera poisoning.

"I have two patients who were tested by Dr. Hokama who had positive titers to ciguatoxin; he put them on six weeks of CSM therapy and retested them. I'm told that none had ciguatera afterward," said Dr. Shoemaker.

Ciguatoxins are potent biological toxins, probably of dinoflagellate origin (like Pfiesteria), found in the flesh of marine animals. They're capable of producing powerful neurological symptoms like
pain, tingling or numbness, and central nervous system symptoms like headache and autonomic dysfunction. They can also produce immune system, bowel, liver, heart and muscle problems.

Dr. Hokama is a pathology professor at the University of Hawaii at Manoa's John A. Burns School of Medicine. He's written hundreds of peer-reviewed publications about various fish toxins.

Hokama's assay, the Membrane Immunobead Assay test, tests a patient's blood serum using a monoclonal antibody for ciguatera toxin. His assay is the first to test for one of the eight known ciguatoxins.

"Trying to find ciguatoxins in blood had been impossible previously," notes Dr. Shoemaker.

While this assay has been available for a while, some in the molecular toxicology field have criticized it because it picks up a part of the chemical structure in ciguatoxin that's found in many
other compounds. The ciguatoxin assay, therefore, is sensitive for ciguatoxin, but not specific for it.

"Ciguatera remains far more common than I had thought, with the distinctive HLA genotype 4-7,8-53 present in 20 percent of the normal population and in more than 90 percent of patients with chronic ciguatera illness," said Dr. Shoemaker.

Shoemaker sees Dr. Hokama's finding as evidence that as technology progresses, we'll likely find proof of more toxins that can damage humans.

"Until we can definitively identify individual biotoxins in human tissue, we'll just have to use the tools of neurotoxin detection, including Visual Contrast Sensitivity (VCS) tests, watching symptoms and cytokine responses, and looking at HLA susceptibility and hypothalamic markers," he said.

An association for CFS's announcement of this research is available at
http://www.ImmuneSupport.com/library/showarticle.cfm/id/4088/

Dr. John Ramsdell, head of the NOAA Marine Biotoxin program in Charleston, SC, has been looking at mice and brevetoxin, another neurotoxin. Brevetoxin is associated with "red tide," the
fish-killing organism that has been a problem in many tropical locations such as Jacksonville, Fla.

He treated some of his mice with regular mouse chow and gave them brevetoxin. The mice died quickly. Then he gave the mice cholestyramine (CSM at 60 mg/kg three times per day by gavage) for one week and then gave them brevetoxin again. They all lived.

"He's now looking at cytokine levels and brevetoxin levels in [blood] serum and he will look at taurine levels in CSM-treated mice versus control mice," said Dr. Shoemaker. "As we've seen with leptin, mice aren't men, so it's possible that there are different mechanisms of toxin behavior in mice. But finding protection from a toxin's effects is pretty exciting."

An abstract of Ramsdell's paper is available at www.chbr.noaa.gov/CoastalResearch/Manuscripts/ manuscripts%20101502.pdf.

SIDEBAR TWO: FOR MORE INFORMATION

Dr. Shoemaker

To get more information on Dr. Shoemaker's theories, take Visual
Contrast Sensitivity tests or to make an appointment to see him or an
associate, see his webpage at http://www.chronicneurotoxins.com.

Lyme Disease

One of the top physicians treating Lyme is Joseph Burrascano. MD. His
treatment program for Lyme is available at
http://www.ilads.org/burrascano_1102.htm

For general information on Lyme Disease, try:

* The Lyme Alliance at http://www.lymealliance.org/

* LymeTruth at http://www.lymetruth.org/

* LymeNet at http://www.lymenet.org/

* Lyme Disease Information and Support of the North Shore, Mass. at
http://www.lymesite.com

* Lyme Disease Association, Inc. at http://www.lymediseaseassociation.org/

For information on common misdiagnoses, see http://www.mercola.com/2001/jul/25/lyme_disease.htm

For information on the pitfalls of Lyme Disease testing, see:

* The Lyme Alliance website, which contains Tom Grier's very helpful
articles at http://www.lymealliance.org/research/grier/grier.php. Of
special note are the ones titled, "Why The Controversy Over
Diagnosing and Treating Lyme Disease." and "Laboratory Tests."

* http://www.lymesite.com/reliable_testing.htm

For information about the "conspiracy" see: http://www.jersey.net/~joebur/conspire.htm

Editor’s Note: Part One of this article was published in Healthwatch Volume XI, No. 4, 2002, and can be read online at http://www.ImmuneSupport.com/library/showarticle.cfm/id/3990/.



Please Discuss This Article:   Post a Comment 

ciguatoxin neurotoxin epitope in CFS
Posted by: DrEnlander
Apr 24, 2009
The CFS experiment did not show Ciguatoxin reaction but an epitope that resembled it. We performed an experiment in 2002/2003 where we used a competitive MIA with crude fish ciguatoxin and CFS with synthetic JKLM ciguatoxin epitope. It suggested similarities in structure with ciguatoxin. It was not the fish toxin itself, however the idea that a neuro toxin may play a part i the diagnosis of CFS was fascinating ref; Chronic Phase Lipids in Sera of Chronic Fatigue Syndrome (CFS), Chronic Ciguatera Fish Poisoning (CCFP), Hepatitis B, and Cancer With Antigenic Epitope Resembling Ciguatoxin, as Assessed With MAb-CTX Y. Hokama, G.A. Uto, N.A. Palafox, D. Enlander, E. Jordan, and A. Cocchetto Journal of Clinical Laboratory Analysis 17:132–139 (2003) regards D. Enlander MD New York
Reply Reply

How is the author doing now?
Posted by: jacoline
Mar 29, 2010
Very interesting article. When you suffer from chronic illness, the causes and treatment are such a mystery. I also suffer from chronic lyme, CFS and FM, and wonder how the author is feeling now.
Reply Reply
 
Free Chronic Fatigue Syndrome and Fibromyalgia Newsletters
Subscribe to
Our FREE
Newsletter
Subscribe Now!
Receive up-to-date ME/CFS & Fibromyalgia treatment and research news
 Privacy Guaranteed  |  View Archives

Save on Vitamins and Supplements

Featured Products

Ultra ATP+, Double Strength Ultra ATP+, Double Strength
Get energized with malic acid & magnesium
Optimized Curcumin Longvida® by ProHealth Optimized Curcumin Longvida® by ProHealth
Supports Cognition, Memory & Overall Health
Vitamin D3 Extreme™ by ProHealth Vitamin D3 Extreme™ by ProHealth
50,000 IU Vitamin D3 - Prescription Strength
Ultra EPA  - Fish Oil Ultra EPA - Fish Oil
Ultra concentrated source of essential fish oils
FibroSleep™ by ProHealth FibroSleep™ by ProHealth
The All-in-One Natural Sleep Aid

Natural Remedies

IBS, Crohn’s Disease, Colitis, and Other Digestive Disorders IBS, Crohn’s Disease, Colitis, and Other Digestive Disorders
Why Berries Offer a Rainbow of Health Benefits Why Berries Offer a Rainbow of Health Benefits
Running on Empty? Fuel Up with NADH Running on Empty? Fuel Up with NADH
Protect Against Sun-Induced Skin Aging From The Inside Out Protect Against Sun-Induced Skin Aging From The Inside Out
The Brain Boosting and Fatigue Fighting B-12 The Brain Boosting and Fatigue Fighting B-12

FIBROMYALGIA RESOURCES
What is Fibromyalgia?
Fibromyalgia 101
Fibromyalgia Symptoms
Fibromyalgia Treatments
| CFS RESOURCES
What is CFS?
ME/CFS 101
ME/CFS Symptoms
ME/CFS Treatments
| FORUMS
Fibromyalgia
ME/CFS
ADVANCED MEDICAL LABS
WHOLESALE  |  AFFILIATES
GUARANTEE
CONTACT US
PRIVACY
RSS
SITE MAP
ProHealth on Facebook  ProHealth on Twitter  ProHealth on Pinterest  ProHealth on Google Plus
Credit Card Processing