For a long time it was thought that chronic
Epstein Barr Virus
(EBV) infection was the sole cause of CFS/ME but this theory has lost support as research
has shown CFS/ME to be a much more complex illness.
Recent studies are still finding a link to EBV however, at least in a subset of
patients. There are studies ongoing into other possible viral causes,
Human Herpes Virus
Six (HHV-6) has often been detected in the blood of CFS/ME patients and has attracted
a lot of attention in the past but some recent studies have failed to find a link.
Most recently two papers from separate researchers were published in the Journal of
Clinical Pathology in September 2007 indicating that CFS/ME is associated with chronic
of the stomach. Researchers believe this may account for many of the gastrointestinal
symptoms experienced by CFS/ME sufferers.
Despite inconclusive research findings with respect to specific viral causes for CFS/ME,
it is still thought by many that a dysfunctional immune response to viruses and chronic
viral infections are at the heart of the condition.
One key piece of evidence for this position comes from the finding that CFS/ME patients
have abnormalities of RNase L. RNase L is an enzyme found in every cell in the body which
is activated within a particular cell when it comes under attack from viruses, and to a
lesser extent bacteria and some toxins. The job of RNase L is to take care of the threat
from invading viruses by destroying their RNA or by signaling an already infected cell to
die, taking the virus with it.
It has been found in numerous studies that CFS/ME patients have fragmented RNase L and
the RNase L system as a whole is
dysfunctional. As a result the patient has compromised
defenses against viral infection. The RNase L abnormalities are seen as the closest thing
to a bio-marker for CFS/ME currently available as the findings are so consistent.
There is substantial evidence for mycoplasma infection playing a role in CFS/ME.
Mycoplasma can be defined as the smallest organisms lacking cell walls that are
capable of self-replication and can cause various diseases in humans. Although
usually associated with respiratory and urinary disease, mycoplasma are thought by a
growing number of medical professionals to be responsible for a number of
unexplained symptoms, especially chronic fatigue states.
has been found in the blood of CFS/ME patients at a much higher rate than in the
In an article entitled Scientific Facts
Versus Fiction About Mycoplasma, Aristo Vojdani, Ph.D., M. T. (30) describes
recent findings about Mycoplasma fermentans:
"Although mycoplasma's are recognized primarily as extra cellular parasites or pathogens
of mucosal surfaces, recent evidence suggests that certain species may invade the host
cells. The molecular and cellular bases for the invasion of M. fermentans from mucosal
cells to the bloodstream and its colonization of blood remain unknown. Also, it
remains unclear whether M. fermentans infection of white blood cells is
transient, intermittent or persistent. It is not clear how these stages influence any
disease progression. The invasion of host blood cells by M. fermentans is due to
inhibition of phagocytosis by a variety of mechanisms, including antiphagocytic proteins
such as protease's, phospholipases and by oxygen radicals produced by mycoplasma's."
CFS/ME has long been considered to be an illness of immune dysfunction and there is
ample evidence that considerable immune dysfunction is present in patients. Immune
activation is a global finding with a range of specific abnormalities present in
significant numbers of patients.
The most common of these include elevated T lymphocyte numbers and elevated
circulating cytokines (immune signaling chemicals). Despite this, immune cell function
of CFS/ME patients is poor, with low natural killer cell cytotoxicity (NKCC), poor
lymphocyte response to
mitogens in culture,
and frequent antibody deficiencies, most often IgG1 and IgG3.
Another finding is that the immune system of CFS/ME patients is unbalanced, with
T-helper (Th) cells of type 2 heavily outnumbering those of type 1. Th1 cells
stimulate immunity directed at organisms which invade cells, such as viruses whereas
Th2 cells stimulate immunity targeted towards invaders found outside of cells such
as bacteria, parasites, toxins and allergens. This finding could certainly explain the
fact that CFS/ME sufferers have a higher occurrence of allergies than the healthy
population. It also provides a reason why CFS/ME patients may have chronic viral
infections as immunity is directed away from protecting against them.
Much research has centered around the endocrine system of CFS/ME patients. Particular
interest has been paid to the
hypothalamic-pituitary-adrenal (HPA) axis which is responsible for the stress
response. A number of abnormalities have been observed in CFS/ME patients with regards to
this including low cortisol and DHEA sulphate levels as well as altered melatonin
Cortisol and DHEA-S work in synergy to control how the body reacts to stress. Low
levels affect your ability to deal with stress and can cause fatigue, low blood
pressure, hypoglycemia, poor brain function and a number of other problems common to
CFS/ME sufferers. Melatonin
is a hormone whose main action appears to be to induce sleep. During the day the pineal
gland, stimulated by light signals the body to produce serotonin and other chemicals to
wake the body up. When light levels fall the pineal gland signals the production of
melatonin in place of serotonin, preparing the body for sleep. If melatonin production
is disturbed as it has been seen to be in CFS/ME then this can cause disruption to sleep
as is commonly seen in CFS/ME patients. Adding weight to this hypothesis is the fact that
low doses of hydrocortisone (cortisol) have been shown to improve symptoms in a number
of studies. Many physicians also prescribe DHEA and melatonin in low doses for their
patients and many find that they are of great benefit.
Autonomic Nervous System Dysfunction
One common problem in CFS/ME that is often overlooked is a feeling of dizziness, weakness
and feeling lightheaded upon standing. Studies have confirmed that a majority of
CFS/ME patients have what is known as neutrally mediated hypotension (NMH). This means
that when CFS/ME patients stand up or exert themselves (especially walking up hills
or climbing stairs) their blood pressure can drop dramatically.
When a healthy person carries out these activities the autonomic nervous system
automatically increases output of adrenal hormones (corticosteroids, adrenalin etc) which
in turn cause the heart to pump harder and blood pressure to increase. In CFS/ME this
often doesn't happen correctly so there is a lack of blood flow to the head and the
symptoms described above result. Researchers and doctors are now trying to treat NMH in
CFS/ME patients where it is identified. Research has centered around administering small
doses of corticosteroids to provide the body with the amount it should be producing by
itself. Results so far have not been favorable but research in this area is ongoing.
Despite the failure of these studies to see an improvement using low dose corticosteroids
a number of doctors specializing in CFS/ME are adamant that this treatment benefits a
subset of their patients where definite NMH is present. Many doctors treating CFS/ME
also recommend dramatically increasing salt and water intake to help increase blood
pressure and reduce NMH related symptoms.
Both CFS/ME and FM patients suffer from strange cognitive difficulties. Often
feeling overwhelmed by sounds, smells and other sensory information, especially when in
busy public places such as a mall or office. Skin often feels very sensitive to the touch
as well. Dr. Jay Goldstein believes these and the other symptoms of CFS/ME can be
explained by neurological dysfunction.
When the brain receives sensory information such as this, the prefrontal cortex decides
on the importance of the information before passing it on to the rest of the brain
for processing. In CFS/ME sensory information that should be classified as low importance
is given high importance. As a result, the brain is overwhelmed by all this
"important" information all at once and the patient feels overwhelmed and exhausted.
At the root of this information processing problem may be deficiency of
certain neurotransmitters, most importantly glutamate, norepinephrine and dopamine.
Researchers have found evidence that CFS/ME may involve distinct neurological
abnormalities. MRI and SPECT scans show abnormalities within the brain. Studies have
shown that CFS/ME patients have abnormalities in blood flow to the brain possibly
indicative of viral cause and similar but not identical compared to patients with
A number of studies have shown that CFS/ME patients have abnormal levels of
neurotransmitters including increased serotonin (the opposite of what is found in
primary depression). Reduced brain serotonin receptor sensitivity or number, and high
auto antibodies to serotonin have also been found. Recent studies found altered
gene expression in the brain's serotonin and sympathetic nervous system pathways,
with altered responses of the HPA axis to serotonin.
Other neurotramsmitters have been found affected including glutamate, sensitivity
to acetylcholine associated with vasoconstriction, and autoantibodies to
cholinergic receptors, associated with central pain. Beta-endorphin, a natural pain
killer, has been found to be low in CFS/ME patients, the opposite of what is found in
There is a large proportion of CFS/ME patients who complain of everyday amounts of
volatile chemicals triggering or worsening symptoms, i.e. multiple chemical sensitivity
(MCS). This has led some researchers to look down this path for answers to the CFS/ME
One study quotes the rate of severe chemical sensitivity amongst CFS/ME patients at
20%-47%. The same study provides compelling evidence that the limbic system (the
emotional centre of the brain) of susceptible individuals can become sensitized by
chemical, biological and psychological mechanisms and that subsequent exposure to stimuli
can cause disregulation of multiple body systems including behavioral, autonomic,
endocrine, and immune system functions. Animal models have shown that sensitization can
occur as a result of chronic exposure to everyday amounts of volatile organic
In addition to these findings there is also strong evidence of abnormalities of
detoxification in CFS/ME. Glutathione, the body's most powerful antioxidant, is
consistently found to be low. Glutathione may become depleted due to chronic exposure to
high levels of toxins. This could potentially be as a result of exposure to toxins in
the air or from chemicals of gut origin in the presence of gut
Over activation of the immune system also depletes glutathione so this may come as a
knock on effect from immune system abnormalities. What is certain is that low
glutathione leads to fatigue and muscle weakness and pain due to its role in
energy metabolism. Low glutathione also results in oxidative stress, meaning that
highly reactive oxygen molecules are not neutralized and are thus free to roam the
body damaging cells and interfering with potentially any body system.
Genetics can be said to be a factor of varying importance in the development of any
illness. Consistent with this statement, a number of possible areas of genetic
susceptibility have been identified for CFS/ME in various studies. One such study
involving twins with CFS/ME and healthy control twins found that the CFS/ME group had
much slower reaction times on all speed related cognitive tests. The researchers
postulated that this indicated a central information processing deficit in the brain.
This finding illustrates one theory about the pathogenesis of CFS/ME best described by
Dr. J. Goldstein. Dr. Goldstein has treated thousands of CFS/ME patients based on his
theory that their brains process sensory information abnormally as a result of
certain neurochemical deficiencies. Other research, also centered around brain function,
found that CFS/ME patients have differences in genes responsible for serotonin
production which leads to lower reservoirs of serotonin, the chemical responsible
for maintaining positive moods and also healthy sleep cycles, amongst other
functions. Finally, a study again using twins, found evidence of immune dysfunction
indicating a possible genetic susceptibility.
There have been two genetic studies recently that have been hailed as major advances
in understanding chronic fatigue syndrome:
The first hit the headlines in July 2005. It suggests that gene expression, the pattern
in which genes are switched on and off is significantly different for certain genes in
those with CFS/ME. Researchers at Imperial College, London, looked at the way genes
are activated in immune cells of 25 CFS/ME patients and 25 healthy controls. They
initially found 35 genes that showed differences while more precise examination revealed
16 that showed definite and significant abnormalities.
The lead researcher, Dr Jonathon
Kerr suggests that the results support the theory that the illness is often triggered by
a virus, namely those discussed previously on this page. Many of the genes that
were identified affect the functioning of the mitochondria, the energy generating
plants within cells. As such, the abnormal gene expression could account for symptoms
of fatigue and lack of energy. The energy producing mitochondria within patients cells
may literally be not producing enough energy. The team behind the research hopes to run
a much larger study of 1000 patients in the future and it is hoped the research will
lead to reliable diagnostic tests for CFS/ME and to new treatment approaches.
The second study, the largest ever to focus on CFS/ME, was completed in 2006 and provided
the results that the CFS/ME community has been waiting for. Dr. Julie Gerberding,
director of the Centers for Disease Control (CDC) said at a press briefing:
"It really is the first credible evidence of a biological basis for chronic
The study involved 227 CFS/ME patients and was conducted in Wichita, Kansas at a cost
of $2 million. The study volunteers spent two days in hospital undergoing detailed
clinical evaluations including sleep studies, cognitive functioning measurements,
autonomic nervous system evaluations, extensive blood work and genetic testing. The
activity levels of 20,000 genes were assessed and it is here where the really
groundbreaking findings were discovered.
At the press briefing, Dr. Reeves, the lead CFS/ME researcher at the CDC, stated:
"For the first time ever, we have documented that people with CFS/ME have certain
genes that are related to those parts of brain activity that mediate the stress response.
And that they have different gene activity levels, that are related to their body's
ability to adapt to challenges and stresses that occur throughout life, such as
infections, injury, trauma or various adverse events."
What this means is that people with chronic fatigue syndrome generally have a lower
tolerance to these various stressors. The result of this is that in people predisposed
to CFS/ME, their bodies can become overwhelmed by events that other people would be able
to shrug off, and this is where dysfunction in various body systems such as the
nervous, endocrine and immune systems sets in. The researchers at the CDC went on to say
that they identified a number of different subgroups within the patients tested,
verifying what many had suspected, that CFS/ME isn't a single easily identifiable disease
with a single cause and diagnostic marker, but rather the result of a complex disease
process. They also stated that this research proves once and for all that CFS/ME is a
very real biological disease and hope that it will lead to better diagnosis and treatment
in the near future.
Around 30 years ago a handful of physicians, most notably Dr's Crook, Truss and
Trowbridge described a syndrome characterized by a wide range of symptoms very similar
to those of CFS/ME which they suggested was caused by overgrowth of the normal
intestinal yeast such as Candida albicans which proliferated due to antibiotic usage and
other factors. They treated their patients with anti fungal drugs with reportedly good
results. A small amount of subsequent research seems to validate their theories with
it becoming clear that antibiotic drugs adversely affect intestinal flora and allow
Candida sp. to become prevalent.
There are studies that appear to show successful treatment of intestinal candidiasis
with anti fungal drugs as well. Strangely, although Dr. Crook in particular
connected intestinal yeast overgrowth with CFS/ME decades ago there has been little
material published regarding this since, apart from a few papers again suggesting the
link due to the observed similarities between supposed yeast related illness and CFS/ME.
The most likely reason for this is the still pervasive view that there are no definitive
tests for intestinal yeast overgrowth. Testing of urine or blood for tartaric acid
would appear to offer just this definitive test however. Tartaric acid is a product
solely of yeast and is not produced as part of human metabolism, therefore any detected
in blood or urine must have originated from the yeast that inhabit the intestinal
tract. Studies could, and should, be undertaken to compare tartaric acid levels
between healthy controls and patients with CFS/ME. Patients of all the illnesses on this
site as well as other unexplained chronic illnesses should also be tested to establish
the role of yeast overgrowth in these conditions.
An important study recently published has shown the link between antibiotic alteration
of gut flora, candida proliferation and the initiation of allergic illness. Since
allergies are prevalent amongst CFS/ME sufferers this research is further evidence that
the link between CFS/ME and intestinal yeast should be investigated. Despite the lack
of published research, all the major diagnostic labs that serve
functional/integrative medicine physicians consistently report a correlation between
yeast markers such as tartaric acid, elevated blood ethanol and Candida antibodies in
samples from CFS/ME patients. A large number of physicians specializing in the treatment
of CFS/ME and related illnesses include anti-fungal agents as a major part of their
treatment protocols. A search of online forums, chat rooms and blogs also reveals a
large number of CFS/ME patients who have had success self-treating with an
anti-fungal protocol. Further research in this area is long overdue.
With more published research behind it is the idea that small bowel bacterial
overgrowth (SBBO) might play a role in Fibromyalgia (FM). This is something that has
been extensively connected with Irritable Bowel Syndrome (IBS) in recent years and as
CFS/ME and IBS are commonly diagnosed in the same individual, it offers another avenue
of potential treatment. SBBO can be treated with targeted antibiotic drugs or with
Leaky gut syndrome is thought to be a result of gut dysbiosis and food allergies,
amongst other things, and could contribute to the disease process in CFS/ME and a
number of other chronic illnesses.
Heavy Metal Sensitivity
A surprising amount of published research indicates a role for heavy metals as
causative agents in CFS/ME. One study using CFS/ME patients and healthy controls
found that the CFS/ME group had significantly higher serum levels of aluminum at the
expense of iron. The researchers correlate this low iron level with low DHEA which has
we have previously mentioned as a common finding and possible contributor to symptoms
in CFS/ME patients. Another research group found an increased incidence of nickel allergy
in CFS/ME patients compared to control subjects. They suggest that immune activation by
nickel or cross-reacting metals could be an etiological factor in CFS/ME. Mercury
amalgam dental fillings are often cited as a possible cause of chronic illnesses and
there is published evidence that this may well be the case, although specific research
with CFS/ME patients appears to be lacking.
There is some overlap in symptoms between depression and CFS/ME, and sometimes cases of
CFS/ME are mistakenly attributed to clinical depression. There are, however, many
clinical differences between the two.
Clinical depression often responds well to physical exercise, whereas CFS/ME is
characterized by exercise intolerance but with a willingness to be active.
Co-morbid depression occurs in 10-15% of CFS patients and should be treated as usual,
except that the patient's energy level, cognitive dysfunction and drug sensitivity must
be taken into account. Co-morbid depression may be the result of living with CFS or
a pre-existing condition. Low dosages of antidepressants are sometimes prescribed to
help a CFS/ME patient sleep better.
It has been suggested that a significantly high proportion of CFS/ME patients have a
"Type A" personality. This means they are highly driven people who put a lot of pressure
on themselves and need to be the best and first at everything and hate to make any
mistakes, basically they are perfectionists. This has led a lot of people to speculate
that stress and its effects on the functioning of the brain are at the root of the
illness. This theory is strengthened by the evidence discussed above regarding dysfunction
of the HPA axis and stress response in CFS/ME sufferers. Stress also has deleterious
effects on the immune system so it may be that people with a stress prone personality
are more at risk from opportunistic infection or other disease causing factors.
In 2009, researchers from the Whittemore Peterson Institute (WPI) published a study in the
journal Science that suggested a link between XMRV, a newly discovered retrovirus, and
CFS/ME. They found XMRV in about 67% of blood samples from CFS/ME patients. They also
detected it in 3% of healthy controls.
On September 22, 2011, Science published online a
nine-lab study widely seen as the final
blow to the theory, championed by Mikovits and colleagues in an
October 2009 Science paper, that a recently detected
mouse retrovirus might play a causal role in chronic fatigue syndrome (CFS). A letter in
the same issue of Science from one of the contributing labs to the 2009 report revealed
that a contamination had marred its contribution-PCR detection and sequencing of the mouse
virus, dubbed XMRV. Mikovits and colleagues defended the validity of the rest of the
study, known as Lombardi et al., which detected the virus by several other methods, so
issued a rare partial retraction of the
original paper. Mikovits was fired from Whittemore Peterson Institute on
September 29, 2011.
It is clear that there are a large number of abnormalities in multiple body systems in
CFS/ME patients. These abnormalities center around the nervous, endocrine and immune
systems and the way these interact with each other.
Although these abnormalities have
been identified it is still unclear which are causes and which are effects. New research
will hopefully shed more light on this but until then doctors who are seeing the best
results with patients seem to be those who take a multi factorial approach and try to
correct as many of the abnormalities discussed as they possibly can, using currently
As there is significant crossover between CFS/ME and FM,
possible causes of FM may well apply to CFS/ME as well. Take a look at our
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