Gulf War Syndrome

Gulf War Syndrome

Persian Gulf War syndrome (GWS) or Persian Gulf War illness (GWI) is an illness reported by combat veterans of the 1991 Persian Gulf War typified by a range of medically unexplained symptoms. It has not always been clear whether these symptoms were related to Gulf War service, or the occurrence of illnesses in Gulf War veterans is higher than comparable populations.

Gulf War Syndrome Symptoms

Symptoms attributed to this syndrome have been wide-ranging, including chronic fatigue, loss of muscle control, headaches, dizziness and loss of balance, memory problems, muscle and joint pain, indigestion, skin problems, shortness of breath, and even insulin resistance. Brain cancer deaths, amyotrophic lateral sclerosis (also known as Lou Gehrig's disease), multiple sclerosis, and fibromyalgia are now recognized by the Defense and Veterans Affairs departments as potentially connected to service during the Persian Gulf War.

Gulf War Syndrome Government Research

Since the end of the Persian Gulf War, the U.S. Department of Veterans Affairs (VA) and the British Ministry of Defence have conducted numerous studies on Persian Gulf War Veterans. The latest studies have determined that while the physical health of deployed veterans is similar to that of non-deployed veterans, there is an increase in 4 out of the 12 medical conditions reportedly associated with Persian Gulf War syndrome - fibromyalgia, chronic fatigue syndrome, eczema, and dyspepsia. They have also concluded that while mortality was significantly higher in deployed veterans, most of the increase was due to automobile accidents.
In the United States in 2008, the federally mandated Research Advisory Committee on Gulf War Veterans' Illnesses released a 452-page report, indicating that roughly 1 in 4 of the 697,000 veterans who served in the first Persian Gulf War are afflicted with the disorder.
The report implicated exposure to toxic chemicals as the cause of the illness. The report states that "scientific evidence leaves no question that Persian Gulf War illness is a real condition with real causes and serious consequences for affected veterans."
The tables below apply only to coalition forces involved in combat. Since each nation's soldiers generally served in different geographic regions, epidemiologists are using these statistics to correlate effects with exposure to the different suspected causes.
U.S. and UK, with the highest rates of excess illness, are distinguished from the other nations by higher rates of pesticide use, use of anthrax vaccine, and somewhat higher rates of exposures to oil fire smoke and reported chemical alerts.
France, with possibly the lowest illness rates, had lower rates of pesticide use, and no use of anthrax vaccine. French troops also served to the North and West of all other combat troops, away and upwind of major combat engagements.

Excess prevalence of general symptoms

Symptom	U.S.	UK	Australia	Denmark
Fatigue	23%	23%	10%	16%
Headache	17%	18%	7%	13%
Memory problems	32%	28%	12%	23%
Muscle/joint pain	18%	17%	5%	2% (<2%)
Diarrhea	16%		9%	13%
Dyspepsia/indigestion	12%		5%	9%
Neurological problems	16%		8%	12%
Terminal tumors	33%		9%	11%

Excess prevalence of recognized medical conditions

Condition	U.S.	UK	Canada	Australia
Skin conditions		21%		4%
Arthritis/joint problems		10%		2%
Gastro-intestinal (GI) problems				1%
Respiratory problem		2%		1%
Chronic fatigue syndrome		3%		0%
Post-traumatic stress disorder		9%		3%
Chronic multi-symptom illness		26%

Gulf War Syndrome Possible Causes

Nerve gas medication and insect repellents

In 2008, a paper published in the ''Proceedings of the National Academy of Sciences'' suggested that excess illnesses in Gulf War veterans could be explained in part by their exposure to organophosphate and carbamate acetylcholinesterase inhibitors. A federal report released in November, 2008, agreed, stating that exposure to two substances "are causally associated with Gulf War illness":

• pyridostigmine bromide, an acetylcholinesterase inhibitor intended to protect against nerve agents., and
• pesticides and insect repellents (often acetylcholinesterase inhibitors)

Chemical weapons classified as nerve gases are also strong acetylcholinesterase inhibitors.

Oil well fires

During the war, many oil wells were set on fire, and the smoke from those fires was inhaled by large numbers of soldiers, many of whom suffered acute pulmonary and other chronic effects, including asthma and bronchitis. However, firefighters who were assigned to the oil well fires and encountered the smoke, but who did not take part in combat, have not had GWI symptoms.

Anthrax vaccine

During Operation Desert Storm, 41% of U.S. combat soldiers and 57-75% of UK combat soldiers were vaccinated against anthrax. The early 1990s version of the anthrax vaccine was a source of several serious side effects including GWI symptoms. Like all vaccines, it often caused local skin reactions, some lasting for weeks or months. While the Food and Drug Administration (FDA) approved the vaccine, it never went through large scale clinical trials, unlike almost all other vaccines in the United States.
One study found that deployed Persian Gulf War Syndrome patients are significantly more likely to have antibodies to the experimental vaccine adjuvant squalene (95 percent) than asymptomatic Gulf War veterans (0 percent; p<.001), which raises the possibility that squalene was used experimentally (squalene is not approved for use as an adjuvant in the United States) in the Anthrax vaccine given to soldiers prior to deployment in the Persian Gulf War to better induce immunity.
The potential implication that the Anthrax vaccine given to soldiers immediately prior to the Gulf War was correlated with Persian Gulf War Syndrome prompted the Department of Defense to task the Armed Forces Epidemiological Board (AFEB) to review Asa, Cao, & Garry's methods. The AFEB found several shortcomings that called into question the validity of the results; namely questionable positive controls, the unproven specificity of the ASA assay, and the potential that the researchers were not blind in their knowledge of patient illness/wellness.
The Department of Defense published a study in 2009 which found no relationship between squalene antibodies and symptoms. The researchers concluded "We found no association between squalene antibody status and chronic multisymptom illness. The etiology of Gulf War syndrome remains unknown, but should not include squalene antibody status."
Research into the vaccine used after 1997 suggests that specific vaccine lots used in immunization during the Anthrax Vaccine Immunization Program program initiated in 1997 likely contain squalene because " the incidence of antibodies in personnel in the blinded study receiving these lots was 47% (8/17) compared to an incidence of 0% (0/8; P < 0.025) of the AVIP participants receiving other lots of vaccine."
Even after the war, troops that had never been deployed overseas, after receiving the anthrax vaccine, developed symptoms similar to those of Persian Gulf War Syndrome. The Pentagon failed to report to Congress 20,000 cases where soldiers were hospitalized after receiving the vaccine between 1998 and 2000.
Despite repeated assurances that the vaccine was safe and necessary, a U.S. Federal Judge ruled that there was good cause to believe it was harmful, and he ordered the Pentagon to stop administering it in October 2004. The ban was lifted in February 2008 after the FDA re-examined and approved the drug again. Anthrax vaccine is the only substance suspected in Persian Gulf War syndrome to which forced exposure has since been banned to protect troops from it.
Subsequent anthrax vaccines, however, have met with approval. On December 15, 2005, the Food and Drug Administration, released a Final Order finding that the current anthrax vaccines are safe and effective. The anthrax vaccine currently used is not the same vaccine that was issued during the First Gulf War.

Chemical weapons

Many of the symptoms, other than low cancer incidence rates, of Gulf War syndrome are similar to the symptoms of organophosphate, mustard gas, and nerve gas poisoning. Persian Gulf War veterans were exposed to a number of sources of these compounds, including nerve gas and pesticides.
Over 125,000 U.S. troops and 9,000 UK troops were exposed to nerve gas and mustard gas when an Iraqi depot in Khamisiyah, Iraq was bombed in 1991.
One of the most unusual events during the build-up and deployment of British forces into the desert of Saudi Arabia was the constant alarms from the NIAD detection systems deployed by all British forces in theatre. The NIAD is a chemical and biological detection system that is set up some distance away from a deployed unit, and will set off an alarm automatically if an agent is detected.
During the troop build-up, these detectors were set off on a large number of occasions, making the soldiers don their respirators. Many reasons were given for the alarms, ranging from fumes from helicopters, fumes from passing jeeps, cigarette smoke and even deodorant worn by troops manning the NIAD posts.
Although the NIAD had been deployed countless times in peacetime exercises in the years before the Gulf War, the large number of alarms was, to say the least, very unusual, and the reasons given were something of a joke among the troops.
The Riegle Report said that chemical alarms went off 18,000 times during the Gulf War. The United States did not have any biological agent detection capability during the Gulf War. After the air war started on January 16, 1991, coalition forces were chronically exposed to low (nonlethal) levels of chemical and biological agents released primarily by direct Iraqi attack via missiles, rockets, artillery, or aircraft munitions and by fallout from allied bombings of Iraqi chemical warfare munitions facilities.
Chemical detection units from the Czech Republic, France, and Britain confirmed chemical agents. French detection units detected chemical agents. Both Czech and French forces reported detections immediately to U.S. forces. U.S. forces detected, confirmed, and reported chemical agents; and U.S. soldiers were awarded medals for detecting chemical agents.
Some, including Richard Guthrie, an expert in chemical warfare at Sussex University, have argued that a likely cause for the increase in birth defects was the Iraqi Army’s use of teratogenic mustard agents. Plaintiffs in a long-running class-action lawsuit continue to assert that sulphur mustards might be responsible. Both chemical agents, at the exposure levels required to cause such birth defects, would be likely to produce elevated levels of cancer not seen in Gulf War veterans. Khanisiya was the location of an Iraqi chemical weapons storage facility bombed during the first Gulf War.
There is also speculation that residual chemical agents from the Iran–Iraq war caused environmental contamination and chronic exposure amongst the troops, consistent with the increased observation of birth defects amongst the Iraqis bracketing the period of the Gulf War.

Depleted uranium

Depleted uranium (DU) was used in tank kinetic energy penetrator and autocannon rounds on a large scale for the first time in the Gulf War. DU munitions often burn when they impact a hard target, producing toxic combustion products.
The toxicity, effects, distribution, and exposure involved have all been the subject of a lengthy and complex debate.
Because uranium is a heavy metal and chemical toxicant with nephrotoxic (kidney-damaging), teratogenic(birth defect-causing), and potentially carcinogenic properties, uranium exposure is associated with a variety of illnesses. The chemical toxicological hazard posed by uranium dwarfs its radiological hazard because it is only weakly radioactive, and depleted uranium even less so.
Early studies of depleted uranium aerosol exposure assumed that uranium combustion product particles would quickly settle out of the air and thus could not affect populations more than a few kilometers from target areas, and that such particles, if inhaled, would remain undissolved in the lung for a great length of time and thus could be detected in urine. Uranyl ion contamination has been found on and around depleted uranium targets.
DU has recently been recognized as a neurotoxin. In 2005, depleted uranium was shown to be a neurotoxin in rats.
In 2001, a study was published in Military Medicine that found DU in the urine of Gulf War veterans. Another study, published by Health Physics in 2004, also showed DU in the urine of Gulf War veterans. A study of UK veterans who thought they might have been exposed to DU showed aberrations in their white blood cell chromosomes. Mice immune cells exposed to uranium exhibit abnormalities.
A 2001 study of 15,000 February 1991 U.S. Gulf War combat veterans and 15,000 control veterans found that the Gulf War veterans were 1.8 (fathers) to 2.8 (mothers) times more likely to have children with birth defects. After examination of children's medical records two years later, the birth defect rate increased by more than 20%:

"Dr. Kang found that male Gulf War veterans reported having infants with likely birth defects at twice the rate of non-veterans. Furthermore, female Gulf War veterans were almost three times more likely to report children with birth defects than their non-Gulf counterparts. The numbers changed somewhat with medical records verification. However, Dr. Kang and his colleagues concluded that the risk of birth defects in children of deployed male veterans still was about 2.2 times that of non-deployed veterans."

In a study of U.K. troops, "Overall, the risk of any malformation among pregnancies reported by men was 50% higher in Gulf War Veterans (GWV) compared with Non-GWVs."
In the Balkans war zone where depleted uranium was also used, an absence of problems is seen by some as evidence of DU munitions' safety. "Independent investigations by the World Health Organization, European Commission, European Parliament, United Nations Environment Programme, United Kingdom Royal Society, and the Health Council of the Netherlands all discounted any association between depleted uranium and leukemia or other medical problems." Since then, there has been a resurgence of interest in the health effects of depleted uranium, especially since it has recently been linked with neurotoxicity.
Increases in the rate of birth defects for children born to Gulf War veterans have been reported. A 2001 survey of 15,000 U.S. Gulf War combat veterans and 15,000 control veterans found that the Gulf War veterans were 1.8 (fathers) to 2.8 (mothers) times as likely to report having children with birth defects.
Although not identifying Gulf War syndrome by name, in June 2003 the High Court of England and Wales upheld a claim by Shaun Rusling that the depression, eczema, fatigue, nausea and breathing problems that he experienced after returning from the Gulf War were attributed to his military service.
A 2004 British study comparing 24,000 Gulf War veterans to a control group of 18,000 men found that those who had taken part in the Gulf War have lower fertility and are 40 to 50% more likely to be unable to start a pregnancy. Among Gulf War soldiers, failure to conceive was 2.5% vs. 1.7% in the control group, and the rate of miscarriage was 3.4% vs. 2.3%. These differences are small but statistically significant.
In January 2006, a study led by Melvin Blanchard and published by the ''Journal of Epidemiology'', part of the "National Health Survey of Gulf War-Era Veterans and Their Families", stated that veterans deployed in the Persian Gulf War had nearly twice the prevalence of chronic multisymptom illness (CMI), a cluster of symptoms similar to a set of conditions often called Gulf War Syndrome.
On November 17, 2008 a congressionally appointed committee called the Research Advisory Committee on Gulf War Veterans' Illnesses, staffed with independent scientists and veterans appointed by the Department of Veterans Affairs, announced that the syndrome is a distinct physical condition. The committee stated that the condition was likely caused by a drug given to troops to protect against nerve gas, known as pyridostigmine bromide, and pesticides that were used heavily during the war.
It said other possible causes could not be ruled out. The committee recommended that Congress increase funding for research on Gulf War veterans' health to at least $60 million per year.
Tests of 5 Gulf War Veterans in 2007 and analyzed by Wayne State University Medical staff revealed the 5 Veterans studied have severe chromosome damage. The damage uncovered is 10 times the level found in the normal population. The chromosome damage is similar to that seen when exposed to Alpha radiation and could be related to Depleted Uranium munitions exposure. Further, more widespread tests need to be conducted before conclusions can be drawn from this research.

Evidence against

Similar syndromes have been seen as an after effect of other conflicts — for example, 'shell shock' after World War I, and ''post-traumatic stress disorder (PTSD)'' after the Vietnam War. A review of the medical records of 15,000 American Civil War soldiers showed that "those who lost at least 5% of their company had a 51% increased risk of later development of cardiac, gastrointestinal, or nervous disease."
A November 1996 article in the New England Journal of Medicine found no difference in death rates, hospitalization rates or self-reported symptoms between Persian Gulf veterans and non-Persian Gulf veterans. This article was a compilation of dozens of individual studies involving tens of thousands of veterans. The studies did find a statistically significant elevation in the number of traffic accidents suffered by Persian Gulf vets vs. non-Persian Gulf vets.
An April, 1998 article in Emerging Infectious Diseases found no increased rate of hospitalization and better health overall for veterans of the Persian Gulf War vs. Veterans who stayed home. James D. Knoke and Gregory C. Gray, Naval Health Research Center, San Diego, California, USA, Emerging Infectious Diseases 1998 Oct-Dec;4(4):707-9, Hospitalizations for unexplained illnesses among U.S. veterans of the Persian Gulf War.
The US Institute of Medicine, released their conclusions in a September 2006 report further casting doubts on the validity of Gulf War Syndrome, writing that although roughly 30% of service men and women who served either have suffered or still suffer from symptoms, no single cluster of symptoms that constitute a syndrome unique to Gulf War veterans has been identified.
While an increase in birth defects has also been attributed to Gulf War Syndrome, a study on members of the Mississippi National Guard deployed to the Persian Gulf, conducted in 1996 found that of a total of 55 births, five children were born with birth defects.
The study concluded that “The rate of birth defects of all types in children born to this group of veterans is similar to that expected for the general population.” In another study of 75,000 births conducted by the New England Journal of Medicine, 7.45% of the Gulf War veteran children were born with birth defects, compared to 7.59% for children of veterans not deployed in the Persian Gulf

Iraq War

Many U.S. veterans of the 2003 Iraq War have reported a range of serious health issues, including tumors, daily blood in urine and stool, sexual dysfunction, migraines, frequent muscle spasms, and other symptoms similar to the debilitating symptoms of "Gulf War Syndrome" reported by many veterans of the 1991 Gulf War, which some believe is related to the continued United States' use of depleted uranium.
New research from the United Kingdom, published in the medical journal the Lancet compared the health of thousands of service personnel who served in Iraq with the health of thousands who did not, stated:

"If we had found an increase in morbidity after the Iraq war equivalent to that before the Gulf War we could say that these changes were not related to the occurrence of symptoms; all we can now say at this stage is that our new data add to the evidence that there was some relation between the specific pattern of medical countermeasures used in 1991 and ill health."

After 10 years of research worldwide, overseen by the veterans' lawyers and funded by the UK's Legal Services Commission, no evidence was found which established any specific cause for the range of the health problems of over 2,000 British troops who were seeking disability pensions for Gulf War Syndrome.

---

This article is licensed under the Creative Commons Attribution-ShareAlike License. It uses material from the Wikipedia article on "Gulf War Syndrome" All material adapted used from Wikipedia is available under the terms of the Creative Commons Attribution-ShareAlike License. Wikipedia® itself is a registered trademark of the Wikimedia Foundation,

Vagus nerve infection

An Interview with Michael VanElzakker Ph.d

Van Elzakker’s hypothesis could explain several of the mysteries associated with chronic fatigue syndrome

Michael VanElzakker’s Vagus Nerve Infection Hypothesis (VNIH) for Chronic Fatigue Syndrome may be the most intriguing hypothesis to come along in the last twenty years.  If it’s correct it could explain several mysteries including how a virus might trigger the disease and then seemingly disappear, why the Lipkin study failed to find an active infection, why cytokine studies have trouble finding evidence of the ‘never-ending cold’, why when antivirals work they often take so long to do so.

• One Theory to Explain Them All? The Vagus Nerve Infection Hypothesis? 

It’s raised a lot of interest. Now Michael VanElzakker ‘sits down’ and answers some questions about it.

Background

What is your background? When did you get interested in this subject and start  developing this hypothesis? 
I am a neuroscientist. I mostly focus on posttraumatic stress disorder (PTSD), which I consider to be very different from CFS and a separate arm of my research interests (although there are many interesting overlaps between the views of CFS and PTSD within our culture).

A sick friend prompted his interest in this disorder

However,  I got my bachelor’s and master’s at the University of Colorado – Boulder, at a time when the Psychology & Neuroscience department there was very focused on psychoneuroimmunology-related phenomena. Some of the many research programs there related to neuropathic pain, cytokines, and the vagus nerve. All it took was for someone who was thinking about CFS to be exposed to these different literatures and to start fitting them together.
I started thinking about CFS because I have a sick friend. She got sick back when CFS was viewed even more skeptically than it is today – I remember one MD referring to it as “yuppie flu.” I knew that my friend was not malingering – why would she be? She had to put her life on hold. It was pretty devastating.
The focus on the vagus nerve is simply because that organ is responsible for symptoms during “normal illness” that strongly overlap with CFS symptoms.

Testing the Theory

Apparently imaging techniques are not able yet to find localized infections in the vagus nerve. How far are they from being able to that? Is there interest in developing those kinds of techniques?
You reported that  PET scans have shown ‘promise’ in identifying activation of the microglia – a prominent part of your theory. (The VNIT proposes chronic microglial activation causes the vagus nerve to send signals to the brain that result in flu-like symptoms.)  It seems that we could settle the VNIH theory right now if PET scans showed clusters of infected areas around the vagus nerve. How effective are PET scans at doing something like this now?
I’ll answer these two questions together. As far as the effectiveness of PET scans finding local vagus infection: We don’t know. That’s part of what my group is trying to work on. There are a lot of technical problems that will require pilot testing.

Most PET scans are done of the brain. VE would like to do one further down in the vagus nerve area

One of the big problems is that PET scans cost thousands of dollars per hour. It’s difficult to convince funding agencies to give us money to pilot test a method so that we can even begin to ask questions about a hypothesis that may or may not be accurate. But I’ve got some really good people on my team and we’re working on it.
There’s interest because of this hypothesis, but most imaging of the vagus nerve thus far has been at the level of the brain, trying to understand the mechanism of vagus nerve stimulation for epilepsy or depression. We’re trying to image it farther down.
If someone made an animal model of the hypothesis, that would help raise interest. I laid out a protocol in the paper for creating an animal model; I hope somebody with a rat lab takes the idea and runs with it. I’m not jealously guarding these ideas, I put them in the paper in the hopes that other groups would work on them too.
You suggested that future CFS research  use radiolabeled antibodies to localize clusters of specific virus types. This is done to find tumors. Is it possible to radiolabel antibodies so that they pick up clusters of infection in the body?
Yes, it is. But there are several problems to this with regards to the VNIH of CFS. One is that antibodies are specific, but CFS could be caused by a number of different pathogens. So, we could flood someone’s body with radiolabeled antibodies against HHV-6, but maybe in that specific case, their symptoms are caused by HHV-4 (Epstein–Barr).
Another problem is that some of the pathogens that might be most likely to cause CFS are found in the vast majority of humans. So, radiolableled antibodies against HHV-1 would find a signal in most people, but only cause CFS if the viruses are in a vagus (para)ganglion. And the vagus nerve is so highly branched, that could be all over the trunk. Another problem is that antibodies cannot always get inside ganglia, which are immunoprivileged. But despite all of that, I still think it’s a research program that is worth pursuing.

Treatment

Herpesviruses apparently love to set up house in the sensory ganglia, but you suggest that antiviral drugs might have trouble getting to them and destroying them there. Why is that?

Antivirals may take much longer to work in ME/CFS because they have difficulty accessing the vagus nerve where the viruses are present

Similarly to how the central nervous system has a blood-brain barrier (BBB), peripheral nervous system ganglia are immunoprivileged. According to the hypothesis, the frequent failure of drug therapy and also one’s own immune system to eliminate infections within vagal ganglia and paraganglia is just like how some drug doses and antibodies do not penetrate the BBB.
You noted that behavioral/stress management therapies such as CBT are moderately effective in about 30% of people with chronic fatigue syndrome, and that CBT resulted in lower viral loads and improved immune functioning in HIV. Why would this be?
Stress causes a cytokine response. So, if someone who doesn’t like public speaking is giving a presentation, their immune system is generating a cytokine response. If such a person even thinks about giving a presentation, they are likely to generate a cytokine response.
People with CFS have an authentic reason to be concerned about any activity that requires physical exertion, and it’s called post-exertional malaise: worsened symptoms after exertion.
According to the vagus nerve infection hypothesis (VNIH), there is a physiological reason behind post-exertional malaise: Exercise provokes muscle tissue to produce the proinflammatory cytokine IL-6, which would then exacerbate the ongoing  local cytokine response within vagus nerve ganglia or paraganglia. That’s the hypothesized mechanism behind post-exertional malaise.
The CBT practitioners in the infamous PACE study were focused on avoidance/fear of activity because they began with the assumption that CFS is psychological. They think the fear of activity itself is the cause of CFS; I’d say that fear of activity is justified, but like all fear, it can become dysfunctional. For the vast majority of their patients, CBT did not help. The three out of ten that found some slight improvement may have used CBT to figure out exactly what level of activity they should be worried about. So, the moderate improvements they reported in a minority of patients were probably related to stress reduction.
In patients with HIV, reducing something like stress that taxes the immune system is bound to help a little bit.
I understand that this is a really charged topic among CFS advocates, and there is a lot of misinformation out there. Just to be clear, cognitive-behavioral therapy (CBT) does not get at the root cause of CFS. CBT offers coping strategies and is not a cure. But I can’t think of a single medical condition that isn’t exacerbated by stress. CFS is no different. Having a chronic illness is stressful and it makes one’s life complicated and there’s a grieving process. CBT is for those parts of the illness. It’s intended to help people solve problems and to challenge dysfunctional patterns. If you’re seeing a CBT practitioner who views CFS as a psychologically-based illness and is approaching your CBT that way, fire them. Find someone else.
While CBT can help people with serious and chronic medical problems, it should be used as an adjunct and not a primary treatment. It would be crazy, for example, for a doctor to prescribe CBT instead of chemotherapy for cancer. But chemotherapy is a known, empirically tested treatment for cancer. CFS doesn’t have such a thing yet.

Behavioral practices like CBT that reduce stress can be helpful in immune mediated diseases such as HIV and ME/CFS, but are adjunct, not primary therapies

Without a cure, the next best thing is to focus on quality of life. I am very much focused on finding an explanation for CFS, which would then lead to a cure. I have hypothesized that CFS is a neurological illness triggered by a foreign pathogen infecting the vagus nerve. But the fact is that stress has profound impact on immune system function. CBT for CFS patients can reduce stress, which is one mechanism of action to improve symptoms.
I should also say – CBT sometimes gets conflated with graded exercise therapy as well. Some studies have combined these two techniques but they are not the same thing. In the paper I gave an example of a treatment regimen that included graded exercise therapy.
Again, to be clear, if the VNIH is correct and some combination of glial inhibitor, antivirals and vagus nerve stimulation can be used to quell symptoms, then and only then does it make sense to begin graded exercise therapy. At that point, the root cause of CFS symptoms has been dealt with, and the next priority is to deal with muscle deconditioning which is not an insignificant factor in ongoing symptoms.
I absolutely do not condone forcing still-sick patients to exercise if it’s making their symptoms worse. This should be obvious.

Others

The heart rate variability evidence suggests the parasympathetic nervous system (vagus nerve) is under-activated in ME/CFS while the sympathetic nervous system is over-activated.  The SNS activation, in fact, may be due to the PNS’s inability to rein it in.  The increased heart rate at rest, for instance, could be due to be due to the inability of the vagus nerve to slow it down. In your theory, though,  the vagus nerve appears to be activated by the localized infection.  I’m a bit confused.

Is an infection contributing to the autonomic nervous system problems in ME/CFS?

This has to do with the fact that the vagus nerve is a mixed cranial nerve, meaning it has both sensory (afferent, or towards the brain) and motor (efferent, or away from the brain) divisions. Its parasympathetic influence over the body results from efferent activity; its function in detecting peripheral infection and triggering sickness behavior results from afferent activity.
However, terms like over-active and under-active are a bit too simplified – what matters is that the nerve is able to respond and signal appropriately, to be able to create a functional signal-to-noise ratio.
Researchers have been looking for cytokines in ME/CFS for decades. Sometimes they find them, sometimes they don’t. When they do find them sometimes research groups find similar cytokines and sometimes they don’t. The one constant is that they keep looking. You mentioned that lung infections are also not associated with increased cytokine levels in the blood.  Are there many other infections like this?
Well, to be more accurate, it’s not necessarily that lung infections won’t show a cytokine response in the blood. It’s more that we cannot be certain to find a cytokine response from a local infection – that is, any local infection. If a lung infection were severe enough, you might find cytokines in the blood. Cytokine studies are quite prone to false negatives, and it’s a mistake to infer from a negative cytokine blood test that there is no cytokine response happening anywhere in the body.
In studies that look for cytokines in blood, there are 3 relevant questions:

1. Is there any cytokine response in the first place?
2. Did that cytokine response diffuse into peripheral blood?
3. Did the method of detection work?

VE notes the difficulties present in finding a cytokine response in an infectious disease

The question we’re interested in is #1, however it’s a big assumption that the answers to #2 and #3 are “yes” when we infer from a negative blood test that there is no cytokine response.
Those of us who think that CFS is not psychologically-based tend to think there’s an immune dysfunction of some sort. People have been looking for cytokines because they are an obvious potential link between the immune system and CFS symptoms, but a lot of studies have ignored how cytokines work.
If a research group is unfamiliar with the cytokine literature they may have also made some easy mistakes in the cytokine assay – the actual lab methods for looking for these proteins.
For example, cytokines are relatively labile, meaning unstable. If someone who didn’t know any better stored their blood samples in a refrigerator instead of a -80° freezer, you can bet they did not find cytokines. If blood samples went through freeze-thaw cycles, the cytokines will also start to denature (break down). There are definitely a lot of really good researchers who have looked into cytokines, but the literature can get muddied pretty easily by bad studies. And because the symptoms are systemic, most people have been thinking in systemic terms (i.e., not thinking about a localized infection causing CFS).
In general, I’m skeptical of any attempts to find a “cytokine profile” for CFS or any other infectious disease. That doesn’t mean it can’t be done, but it’s difficult. Cytokine responses are very complex, they interact with each other and they change in daily and hourly rhythms. You could study one individual and not find a “cytokine profile” unless you took several samples a day for many days.

Response to the Hypothesis and the Future

This is a really intriguing theory. Kristin Loomis of the HHV-6 Foundation was excited by it.  Have you gotten much response from it? 
I’ve actually been really pleasantly surprised by the response. I’ve had the idea for quite a long time, and spent a lot of time and effort trying to set up a collaboration with a rat lab, to create an animal model. To make a very long and frustrating story short, nothing worked out.

The response to VE’s hypothesis has been very positive; he is working on putting a study together to test his hypothesis

I’ve been telling anybody who would listed about the hypothesis. It’s not like doors were getting slammed in my face, but most people simply didn’t have a background in the different literatures that the hypothesis ties together.
It wasn’t until recently that I discovered this unique journal, Medical Hypotheses, so I made some time to write up the idea. It gave me a forum to really give people the background they needed to understand the idea, and allows people to check the citations themselves. Based on past experience, I thought I’d have to keep cold-calling researchers to push the hypothesis. But it really took off right away.
I put it up online for free, and it’s been downloaded over 1000 times there; I don’t know how many people have downloaded it from the publisher through a university or hospital subscription. I’ve heard from researchers from 5 continents. Somebody translated the paper into Dutch and put it up online.
The week the paper came out, Anthony Komaroff contacted me, we’ve been in contact since. He finds the hypothesis to be “provocative and plausible” and shares my hope that functional imaging can help to shed some light on it. I’ve been in contact with a lot of other well-known CFS researchers, and I think the idea is at least changing the way that some people think about the problem.

Van Elzakker will be at the IACFSME conference with a poster presentation of his hypothesis

I also know that the paper is already being taught at some universities and medical schools, so hopefully it will at least get young scientists to start thinking about CFS. I hope people start to think about new CFS findings through the lens of this hypothesis because in my experience, it explains a lot of phenomenology.
Even if the hypothesis doesn’t turn out to be accurate, or is only partially accurate, I hope that it gets us closer to effective treatments that are actually attacking the root causes of CFS symptoms and not just helping people cope with them.
Some reports suggest you’re engaged in a pilot study. Can you comment on that?
On the record, I’d just say that I’ve put together a really great team to pursue the VNIH and that Dr. Komaroff is part of it. There are a lot of technical issues but we’re hoping to use functional imaging to gain enough preliminary data that we can pursue it further.

• One Theory to Explain Them All? The Vagus Nerve Infection Hypothesis? 

 

Tags: herpesviruses, vagus nerve, VanElzakker, VNIH

TwitterFacebook

Jeanie

February 14, 2014 at 5:56 pm - Reply

What an encouraging article! Thank you, Dr. Van Elzakker, for taking CFS on! We all sure do need you and researchers like yourself. What a light in the dark you are. And I am so glad Dr. Komaroff if going to be a part of this research. He has been with us forgotten sick people for so long. He is one of my heroes in this, and you are now one, too.

• 

  Cort Johnson

  February 15, 2014 at 4:54 pm - Reply

  I’ve had some concerns about Dr. Komaroff, from time to time, but he jumped on this very quickly! He’s also talking on new advances in ME/CFS at the IACFS/ME conference. I imagine this theory will be a central focus of that talk.

Kathy

February 14, 2014 at 6:50 pm - Reply

I’ve had this awful illness for more than 30 years and for many years now I’ve stayed away from trying anything ‘new’ in treatment because I came to believe that it was useless until someone had a real understanding of just what is going on in ME/CFS. Then I read Dr. VanElzakker’s theory and shouted EUREKA! it was a moment of clarity and certainty and I have absolutely no doubt that this theory will play a major part in the understanding and hopefully treatment in the hopefully not too distant future.
Thank you, Dr. VanElzakker, please keep up the great work!.

• 

  Cort Johnson

  February 15, 2014 at 5:03 pm - Reply

  I think you’re not alone, Kathy…Of course, you never know until the fat lady sings, but hopefully VE will get the study together and it will work. To me it has more going for it than any other theory that I’ve seen.
  • 

    Jeanie

    February 16, 2014 at 3:20 pm - Reply

    Just “hearing” you say that , Cort, give me so much happiness and hope.

Virginia

February 15, 2014 at 3:12 am - Reply

My son developed Vagus nerve issues after a severe case of appendicitis. The fatigue is awful.

• 

  Cort Johnson

  February 15, 2014 at 4:55 pm - Reply

  No kidding. Did the doctors state why they think that happened. Are they able to do anything for him?
  • 

    Virginia

    February 18, 2014 at 5:35 pm - Reply

    The response to Cort and VE re my son. Yes, they are able to treat his symptoms to make him feel better. If you would like a more full report of his treatments please e-mail me and I will send you a few pages worth of his current treatments and medicine list. He has been going through treatment for 4 years now. . Three months ago I took him to an Internist/Integrative Medical doctor that also found he had an underlying infection of Babesia Duncani-tick borne infection. Now he is undergoing 8 months of antibiotics for that as well. Never give up is my motto. My theme song is” Your an Overcomer”. Being a nurse helps but sometimes I feel like I am trying to understand a whole new language.
    • 

      Witherwings

      February 19, 2014 at 1:09 pm - Reply

      That’s very interesting, Virginia. I’m curious to know his treatment plan, but I don’t think I’m able to contact you about it. Interestingly enough, I also had a positive test on a tick-borne infection, namely lyme disease and rickettsia. But me and my docs are still doubting to try AB because of my severe GI-issues and because we are still not entirely sure how big a role these possible infections play in my case (the test I’ve done (an LTT) also isn’t recognised by every doctor and my antibodies don’t come out positive). My doctor also spoke about the coxsackie virus because of my symptoms and if this would be an issue, the treatment plan would be a lot different. I wish you and your son the very best!
• 

  Kathy

  February 15, 2014 at 5:02 pm - Reply

  I had ‘chronic appendicitis’ at age 17, it took months of sickness before a doctor correctly diagnosed it just as it was becoming acute and I had surgery to remove it. That at age 17 and severe mono at age 14 that put me in the hospital for a week in isolation are a combination that I believe led to my developing CFS later.
  • 

    Cort Johnson

    February 15, 2014 at 5:06 pm - Reply

    I know of several people who developed ME/CFS after gastrointestinal infections. and, of course, Dr. Chia thinks they play a huge role. I think any serious infection might do, though. In VE’s theory, as I understand, a gut infection could lead to viruses establishing in the ganglia associated with the gut.
    Pridgen believes the same thing in FM; in about a month we should have the results of his first trial – and he’s checking gut tissues for bugs. It’ll be interesting!
    • 

      Witherwings

      February 18, 2014 at 2:28 pm - Reply

      Very interesting to see these cases of appendicitis over here. I also have developed a serious condition after I had an appendicitis (with peritonitis and sepsis as a result – I was REALLY ill) as a teenager – for a few years now I’m bedridden because of this – doctors still haven’t any clue what has exactly happened back then that has made me this ill. Sure, I got diagnosed with CFS/ME, but what does that actually mean? I’m very eager to find out what is exactly wrong with me and I find this study very promising! I also have dysautonomia (POTS) and serious stomach issues so this whole hypothesis really makes sense to me. Thank you very much for publishing this and I’m looking forward to the results of their research.

Kirsten

February 15, 2014 at 4:54 am - Reply

Thankyou so much to Michael and Cort for this interview. The hypothesis has intrigued me from the first time I read about it and I’ve become a bit obsessed with trying to understand it ever since (and frustrated that my brain doesn’t seem to have the knowledge or function to compute the complexities).
In reading some of the forum comments about this I was quite saddened and embarrassed by the way in which Michael’s work was being received by many in the ME/CFS community. While I very much understand (and I am so glad to read that Michael does too) how loaded some words and concepts are for us given the history, I also despair when it seems people can’t look a bit deeper and actually make sure there really is some sinister intent before jumping to conclusions.
All to say that I very much appreciate both this interview and the time and effort Michael has put both into the hypothesis and into communicating with the community in various ways since it was released. I wish him only the best as he follows this lead and hope that it might turn out to be the game-changer we so desperately need.

• 

  Cort Johnson

  February 15, 2014 at 5:00 pm - Reply

  Thanks Kristin, I’m kind of flabbergasted to hear that. I imagine it has to do with the comments on CBT. Focusing on those and ignoring the rest, reminds me of the princess and the pea story or someone dying of thirst in the desert complaining there’s no ice in the drink you’re rescuer’s gave you. If VE is right the theory opens up huge vistas for chronic fatigue syndrome.
  I’m sorry they’re missing the huge promise in this theory.

Kirsten

February 15, 2014 at 4:57 am - Reply

PS – I started seeing an oesteopath after I began looking into the vagus nerve theory. I have tried osteopathy before to no avail (with the same practitioner, which keeps the variables at a minimum here!). So far I’ve had two appointments, specifically working on vagus nerve impingments, and have felt some subtle but certain changes. I’m going to be very interested to see what happens as we progress with the treatment.

Lilly

February 15, 2014 at 2:53 pm - Reply

Where is he located now and does he need patients to test?

• 

  Cort Johnson

  February 15, 2014 at 5:01 pm - Reply

  I hope to learn more about the parameters of the study which is hopefully getting underway at the IACFS/ME conference.
  • 

    Carol Larsen

    February 22, 2014 at 9:38 pm - Reply

    PS If participants are needed for this study, please let me know.

Ann

February 16, 2014 at 1:52 am - Reply

This is exciting research. I’m also interested in when the FDA approves Ibudilast. That drug sounds promising too.

est_sunshine

February 16, 2014 at 4:12 am - Reply

Dr. Van Elzakker’s hypothesis resonates with me, I have POTS, Dysautonomia, CFS, IBS. Histamine issues. I had gut infections as a child and never really recovered. I notice my vegas nerve is very sensitive and can give me electric shock like jolts after eating. If certainly feels like it could be infected. I have unbalanced gut flora according to a bioscreen test, with high Streptococcus and almost no E-Coli. It all makes for an interesting jigsaw puzzle! Good luck with the next stage of the research.

PALLINE

February 16, 2014 at 4:55 am - Reply

This would fit well with the hypothesis that a subset of CFS is actually Post Polio Syndrome, because it seems that polio survivors have damage in the area of the brain that control the vagus nerve according to Dr Richard Bruno’s writings. I am of the right age and have many symptoms of both, some of which were finally elucidated by the vagus nerve theory.

• 

  Carol Larsen

  February 22, 2014 at 9:48 pm - Reply

  Yes! I’ve been interested in the Post-Polio Syndrome connection. I was conceived when my Dad had polio. The symptoms are similar

Bev Bentley

February 16, 2014 at 5:21 am - Reply

Thank you for this research. People with MS have CCSVI and have treatment to open blocked veins. The vagus nerve is often involved. Would you comment on this please. My son has such terrible lower back pain and all over his body at times due to his MS. Thank you.

Bl Br

February 17, 2014 at 10:13 pm - Reply

Cort Johnson, I am extremely interested in conversing with fellow researchers with this disease who also make great efforts to read all of the latest studies on it. May I have a link to your website and any other groups you are in such as Facebook, Meetup.com, etc.?

• 

  Cort Johnson

  February 18, 2014 at 4:54 am - Reply

  Hi Bl Br I post here on Simmaron Rising and on my own website at cortjohnson.org – hope to see you over there.

Caron Ryalls

February 19, 2014 at 1:04 am - Reply

Some patients with ME or CFS became ill after a vaccination, My daughter was diagnosed with ME/CFS and later POTS after her HPV vaccination at the age of 13, three years ago. How does this theory account for ME/CFS after vaccination, as Many vaccines (including HPV vaccine) do not contain live viruses. How then would the Vagus nerve become infected?

JCB

February 20, 2014 at 4:31 am - Reply

This is very encouraging! I’ve had this condition for well over 30 years, and this is the first concept comprehensive enough to capture most presentations. I also just recently found that I have Lyme, a very old case. Neurological Lyme is microbes within the CNS. I assume it is just as likely that microbes enter the vagus. Would love to hear his thoughts on that sometime. Thanks for the good news!

Carol Larsen

February 22, 2014 at 9:34 pm - Reply

Thank you so much, Cort, on your very helpful interview & views on MS?CFS! I’ve had this illness for 22 years beginning with a Mono infection. Other medical issues have come about since then. It is exciting to read this study and realize that it is carrying on. I’d love to be kept informed about all of this, though it might take reading it a few times-over (with brain fog & non-medical background). Thank you for the interview & Michael’s research! GOOD LUCK!

Joan Zeiber

February 28, 2014 at 9:03 pm - Reply

Pretty interesting stuff. I have been ill for nearly 30 years with CFIDS/Fibro and 7 years ago had a benign meningioma removed. I am pretty curious as to whether CFIDS/Fibro played a role in the development of this brain tumor. Perhaps this research will shed some new light on the never-ending battle.

reven

March 5, 2014 at 10:02 pm - Reply

a study in the Netherlands
The vagus nerve as a regulator of immune tolerance in the intestinal mucosa
http://www.zonmw.nl/nl/projecten/project-detail/the-vagus-nerve-as-a-regulator-of-immune-tolerance-in-the-intestinal-mucosa/samenvatting/

• 

  Cort Johnson

  March 10, 2014 at 8:53 pm - Reply

  Cool – thanks Reven

Stefie

March 25, 2014 at 3:58 am - Reply

Thanks Cort for this article! Not sure how this all fits together but I will be interested in following this. I have severe gastroparesis and damage to the vagus nerve is sited as one of the reasons for this.

Anonnie

July 21, 2014 at 8:52 pm - Reply

Mr. VanElzakker had given a presentation at Quincy Medical Center in Quincy, MA on Sun 4/27/14.
I believe the presentation was audio recorded.
I’ve been searching the web and cannot locate the recording.
Would you kindly advise where I could find it.
Thank you.

• 

  Cort Johnson

  July 31, 2014 at 4:45 pm - Reply

  I will look – thanks for the update.

Pam

July 24, 2014 at 5:06 am - Reply

Anyone with gastroparesis should rule out lyme and coinfections.

Betty

August 6, 2014 at 1:56 am - Reply

It was a nurse…not my new doctor…that suggested to me that the terrible fatigue and then all over not feeling good symptoms which hit me about a 1/2 hr after a bowel movement…could be vagus nerve problems…My blood and urine tests/xrats come out fine. I am just getting SO discouraged. Some days I have GOOD days for which I am so thankful… These are NOT strenuous BMs I speak of… I will try some yoga and deep breathing exercises. I am 77 years old, but that doesn’t mean I can’t give it a good effort!
I am grateful for this site. It makes me feel people ‘understand.’
Betty

Sara

November 15, 2014 at 6:16 am - Reply

The Open Medicine Foundation is raising money to start the End ME/CFS Project. They have top notch scientist and two Nobel Prize winners including James Watson ( as in Watson and Crick). You can find more information here http://www.openmedicinefoundation.org/
https://www.facebook.com/OpenMedicineFoundation

Leslie

November 17, 2014 at 2:45 am - Reply

Misalignment of the atlas bone at the top of the spine may place pressure on the vagus nerve, leading to autonomic nervous system issues. Proper alignment through Atlas Orthogonal treatment (search youtube) may relieve pressure on the nerve. This helped my son immensely.
I am also curious if vagus nerve problems might be playing a role in the lack of hunger or thirst in Landon Jones, an Iowa boy making headlines recently

- See more at: http://simmaronresearch.com/2014/02/michael-vanelzakker-ph-d-talks-vagus-nerve-infection-hypothesis-chronic-fatigue-syndrome-mecfs/#sthash.9CB54rYi.dpuf

Re previous post - or is it the other way round - now my head hurts, I'm confused

THE MODERN PROTOCOL FOR EPSTEIN BARR VIRUS

By Michael Biamonte, C.C.N.
EBV is considered an opportunistic infection. An opportunistic infection is one that awaits a failure in your immune system to take hold and make you ill. The “failure” is not a temporary one but one more chronic, lasting weeks or months. This type of “failure” is caused mostly by a combination of drugs, poor diet, stress, damp climate or other viral or bacterial disease. These can also cause the illness to come back if you recover. EBV is a member of the Herpes family, although it does not cause the sores, as would the more well known forms of Herpes. 90% of adults have come in contact with EBV. EBV causes “mono” once called the “kissing disease”. It lives in the salivary glands and in the B-Lymphocytes, which are a type of white blood cell. The virus causes the cells that produce antibodies to attack tissue cells that results in autoimmune disease; autoimmune means to attack oneself.
Swollen lymph nodes, fevers, chills, weakness, fatigue, shortness of breath, sore throats, influenza, pneumonia, chronic candidiasis are all possible symptoms of EBV. EBV is the virus largely credited with causing chronic fatigue. Everyone with EBV has chronic fatigue; not everyone with chronic fatigue has EBV. Chronic fatigue can be caused by low thyroid or adrenal function, copper toxicity, other viral conditions, hypoglycemia, parasites, nutrient deficiency etc.
The common course goes like this. Someone had mono many years ago. They had swollen glands, sore throats, swelling or enlargement in the liver or spleen, flu?like symptoms etc. The mono reduced, they recovered and went on with life. Years later, due to any of the previously mentioned circumstances, the EBV that caused the mono reactivates. The person then begins to experience some or all of the mono symptoms again to a greater or lesser degree. These symptoms now appear in cycles, every few weeks or months. Eventually hypoglycemia begins, memory and concentration become poor. Fatigue is obvious. Allergies may then begin as the immune system weakens. Chronic Candida in any form may begin. The weakening in the immune system will allow Candida to overgrow and spread. This is a case of EBV causing Candida. Thyroid hormone may start to decrease, anemia may appear and the immune system may start to really fail. At this point, allergy skin tests may fail to respond to the inability of the body to produce any real immunoglobulin production; blood cortisol levels may decrease showing adrenal exhaustion. (Cortisol is an adrenal hormone.) This is now full-blown EBV. Encephalitis, myocarditis, pneumonitis, pancreatitis, diabetes, hypothyroidism, transverse myelitis may occur. These “itis” illnesses are examples of the inflammation EBV can produce in the body. The end stage of EBV is associated cancers, originally associated with EBV’s discovery. This cycle can take many years and is not predictable.
EBV growth is within the soft lining of the throat and transmitted by saliva. It can be found in 100% of those who are immuno-suppressed, but even if exposed to the virus, a healthy person has a harder time getting it.
To correctly treat EBV or any opportunistic infection, we must first use non?toxic germicides to eliminate or reduce the virus. Many times the approach first used is to stimulate T?cells, white blood cells and interferon. This is unwise as these cells are diseased and are carriers of the infection. Stimulating these cells can cause a rampant spread of the infection. In the case of the opportunistic infection, we must bypass the body’s own immune system because it has already failed. Stimulating can cause a spreading of the infection as mentioned. So we must reduce or eliminate the infection using the modern protocol. The modern protocol consists of around 30 remedies. Some would be familiar to you, others would not be. They are non?toxic so they can be taken for long periods of time to eliminate large amounts of the infection without altering the natural flora or causing damage (side effects) to glands or organs.
In “Phase I” we want the pH of the body alkaline as it inhibits opportunistic infections. The remedies from the protocol that we choose based on the person’s history, health complaints and lab results must be rotated to be effective. After 7 days of taking any remedy, it will lose effectiveness as the environment within the body adjusts to it. The infection also adjusts. Therefore, we take each remedy 4 days, then move to the next one. When we have used them all, we repeat them again. When this phase is complete, we then go to Phase II.
Here, we cleanse the bowel, rebalance the bacteria, tone the digestion and repair the intestinal tract from damage the infections may have caused. The infection creates more toxins, so to cleanse before the infection is gone will not produce lasting or complete results. Specific for EBV on this Phase, we must support the liver as it can be attacked by the virus.
By now the person will have experienced great improvements but can still relapse unless he completes the last 2 phases. On Phase III we test the person for vitamin, mineral and overall nutrition imbalances. With digestion improved, he can now get full benefit from taking supplements rather than having them not absorbed. Here is normally when the energy systems of the body can be rebalanced. Adrenal, thyroid, pituitary and reproductive functions can be addressed. In the EBV case, a return of energy is very much noticed in this phase. Since the nervous system also stimulates the immune system, Phase III gives the EBV sufferer the balance needed for immune stimulation to work well.
Now Phase IV, the last phase, is begun. At this point it is now safe to stimulate the immune system since the virus has been eliminated or greatly reduced. Substances ranging from sunlight which stimulate interferon response, to T and B cell support formulas which help regulate T and B cells, are now used. As many as 25 substances can be used to enhance immune function on this phase. At this point, the body’s own defenses are able to handle the EBV on its own from this time forward. If EBV is found with other infections, the four phases may take longer to run through.
It is important that when the person reaches Phase IV that he continue to take his supplements and diet so the body can heal. The purpose of the program is to get to Phase IV so that energy and nutrients that can repair, rebuild and heal the body can be utilized. The first, second and third phase are setups for the last.
The fatigue and other symptoms caused by EBV are amongst the most horrible I’ve ever heard. Mainstream medicine offers no hope. Most holistic practitioners can offer as high as 30% improvement, in some cases higher. With this protocol as high as 80% of EBV cases can be handled in an average of 24?30 weeks. The key is the proper sequence of treatment.
Avoidance of viral activators or inducers is also important. Nickel, hydrocortisone, hydrogen peroxide and some traditional Chinese herbs have been reported to activate EBV. Factors that increase calcium retention which include Vitamin D, copper, estrogen, insulin and para?thyroid hormone have also been indicated as potentially vital inducing and activating agents. Avoidance of these would be important during the program.
References:

1. Holistic Protocol for the Immune System, by Scott J. Gregory, M.D.
2. Chronic Fatigue Syndrome, by Jesse A. Stroll, M.D. and Charles R. Pellegrine, Ph.D.
3. Clinical Management of EBV, by Rodrigo Rodriguez. M.D., Robert Bradford. D.Sc., Robert Tapia, M.D. and Henry W. Alien
4. David Watts, Ph.D.

Michael Biamonte holds a Doctorate of Nutripathy, and is a New York State certified Clinical Nutritionist. He is a professional member of the International and American Association of Clinical Nutritionists,The American College of Nutrition and is a member of the Scientific Advisory Board for the Clinical Nutrition Certification Board. He is listed in “The Directory of Distinguished Americans” for his research in Nutrition and Physiology.
For an appointment, contact our office.
©1997 – Current Year: MTB Management, Inc.