"The Guideline Development Group was
clear that CBT was not about unhelpful advice or dictation of
illness beliefs, but about changes in lifestyle and learning to
achieve improvements with the patient's abilities. The GDG did not
regard CBT or other behavioural treatments as curative or directed
at the underlying disease process. Rather, such treatments can help
some patients cope with the condition and consequently experience an
improved quality of life" (6.3.7 / Deriving Recommendation /
Discussion of the Evidence)."
Noble-sounding words, but this sweet-talking does not stop the UK ME
community from seeing such surreptitious amendment as a case of
"Come into my parlour, said the spider to the fly", especially given
that NHS Plus has not waited for the final NICE Guideline but has
gone ahead and published its 64-page Policy Document referred to
above (Occupational Aspects of the Management of Chronic Fatigue
Syndrome: a National Guideline". Department of Health: 6th October
2006: 273539) that is grounded entirely on the psychosocial model of
ME/CFS and which recommends that patients who are still working
should be advised to stay at work even if they feel "tired".
- Importantly, it stipulates that
no-one with a diagnosis of ME/CFS should be permitted to retire
until they have undergone "rehabilitation" by means of CBT/GET.
- It is noted that the key
players in this document are Professor Trudie Chalder, Professor
Mike Sharpe and Professor Peter White, all of whom are
well-known for their intransigent belief that "CFS/ME" is a
- It is also noted that the
"Guideline Leader" does not work for the NHS but for a private
medical insurance company.
To accompany this Policy Document,
NHS Plus has produced three booklets: one for employers, one for
employees and one for healthcare professionals, all of which contain
misinformation about ME (about which the parent document states:
"The descriptive term CFS is preferable to previously used terms
such as post-viral fatigue syndrome or ME").
The booklet for employers states:
"This leaflet summarises the
evidence-based guidance on how to support individuals back into,
and to remain in, work. CFS is an illness characterised by
severe, disabling tiredness. A feeling of being tired all the
time is very common. ME and post-viral fatigue syndrome are
terms that people with CFS often use (but) most healthcare
professionals prefer the term CFS. (Appropriate treatments) for
CFS (are) CBT, a structured form of psychotherapy (and) GET, a
structured programme designed to increase aerobic activity. If
an individual complains of fatigue, an employer should refer
them to an occupational health professional. Ill-health
retirement should only be considered if appropriate treatments
such as CBT and GET have been explored".
The booklet for employees says much
"It is a good idea to try to
stay at work even though you feel tired. CBT and GET are
treatments that research has shown can increase the chance of
returning to work. Ill-health retirement is not a first choice".
The booklet for healthcare
professionals is even more damaging:
"The perpetuation of CFS may
include deconditioning, inappropriate avoidance of activity as a
coping mechanism, personal conflicts and fears about the
condition itself. Management (is by) a biopsychosocial approach.
There are two interventions supported by good quality evidence
(sic): CBT involves cognitive restructuring to tackle negative
beliefs. (Its) effectiveness may be limited by excessive focus
on bodily symptoms and taking medical retirement or disability
benefit during the treatment. (In) GET, patients 'negotiate' an
aerobic exercise programme. Patients should be advised against
seeking early medical retirement until all rehabilitation
strategies have been explored". The reference to support this
last statement says: "Evidence from expert opinion".
There is no reference
to the research evidence that has demonstrated
serious, multi-system pathology:
healthcare professionals (ie. the decision-makers)
are given no information about the proven
dysfunction of virtually all body systems, including
cardio-vascular, respiratory, gastro-intestinal,
musculo-skeletal, opthalmic, neurological, and most
importantly, the immune system (with the evidence of
Not to do so is, by
any standards, deceptive.
Curiously, Professors Peter
White and Mike Sharpe seem to be somewhat confused: whilst on
the one hand they say that the effectiveness of CBT may be
limited by being in receipt of disability benefit, in the same
document they also say: "being in receipt of sickness benefit at
the start of treatment may be a marker of severity".
Thus in the UK things are far from transparent: the NICE Draft
Guideline says one thing, but the NHS Plus documents have
pre-empted the NICE Guideline (due in April 2007) and say
another thing entirely.
Those in the UK ME community who might be tempted to accept the
NICE Draft Guideline's assurances that CBT is not about
"dictation of illness beliefs" need to remember that the
psychotherapy it recommends will still be delivered in
psychiatric units at the behest of psychiatrists who will still
harbour their ill-founded prejudices against ME patients.
Confusion about CBT in the US
In November 2006 Nancy Klimas, Professor of Medicine at Miami,
and Anthony Komaroff, Professor of Medicine at Harvard (both of
whom are not only clinicians but also long-time researchers into
ME/CFS) attended the launch by the US Centres for Disease
Control (CDC) of its "CFS Toolkit" and its campaign to advance
knowledge of (ME)CFS.
At the launch, Professor Klimas said:
"Historically, the lack of
credibility afforded this illness has been a key obstacle to
understanding it. Today, with solid evidence that CFS has
identifiable biologic underpinnings, and with evidence that
people with CFS experience a level of disability equal to that
of patients with multiple sclerosis, advanced HIV disease and
undergoing chemotherapy, I hope we can begin to put an end to
the stigma surrounding this illness."
Also at the launch, Professor
Komaroff said about the lingering belief that (ME)CFS is
psychological and somehow imagined: "That debate raged for 20 years,
and now it's over".
As reported on 3rd
November 2006 by United Press International, there
are over 3,000 research papers that have established
(ME)CFS as a valid physiological illness, with
evidence of inflammation, reduced blood flow and
impaired cellular function. It was described as a
"brutal" disease which often occurs in conjunction
with other diseases such as lupus and Lyme disease,
and its symptoms can be as severe and painful as
renal failure, AIDS or multiple sclerosis.
Importantly, distinctions were
drawn to the two different types of (ME)CFS: one that occurs
immediately after an infection and one that develops gradually
over time, and to the fact that the two types seem to differ
Many parts of the Toolkit are helpful:
||the CDC points out (and
accepts) that irritable bowel syndrome, multiple
chemical sensitivity, fibromyalgia and Gulf War Syndrome
may be co-morbid conditions;
||that allergies are seen
in many patients and that many (ME)CFS patients are very
sensitive to medications; that alternative therapies
should be considered (and that the practitioner should
remain open-minded about them);
||the need to be alert to
dizziness in patients and the need to refer them a
neurologist and / or a cardiologist before initiating
||that there is
considerable variation in symptom expression and
||that symptoms are
unpredictable; that the disorder can have a profound
impact on daily life, requiring significant lifestyle
changes; that (ME)CFS is an 'invisible illness' in which
patients often do not look sick and that this
contributes to patients being misunderstood and
isolated; that a therapy which works for one patient may
be of little benefit for another;
||that advising patients
to engage in aerobic activity can be detrimental as it
can cause a full-scale relapse that can last for weeks,
||and that patients with
(ME)CFS can lose their jobs, economic security and home.
However, when it comes to treatment,
there seems to be confusion, with Klimas saying at the launch:
"Although there's no
single treatment-no hoped for 'magic bullet'-that fixes the
illness at its core, there are treatments that can improve
symptoms, increase function and allow CFS patients to engage in
activities of daily living. Current best practices for clinical
care include a combination of symptom management, activity
management and exercise therapies."
This seems at variance with her
previous on-the-record views about CBT, for example:
- "I don't take the British view
that CBT is the one thing you can do to effectively treat (ME)CFS.
But it's a tool that helps some patients" (The Science and
Research of CFS: CFIDS Chronicle Special Issue, 2005-2006)
- "The question arises whether a
formal CBT or GET program adds anything to what is available in
the ordinary medical setting. A well informed physician empowers
the patient by respecting their experiences, counsels the
patients in coping strategies, and helps them achieve optimal
exercise and activity levels within their limits in a common
sense, non-ideological manner" (ME/CFS: Clinical Working Case
Definition, Diagnostic and Treatment Protocols. Bruce M Carruthers, Nancy G Klimas et al JCFS 2003:11:1:7-115).
How is it that in 2003, Klimas said
that a competent physician would give his patient common sense
counselling in coping strategies, but three years later she now says
the same patient should be handed over for psychotherapy?
Is the answer that CBT has been "redefined" in the US also, so in
the absence of any remotely therapeutic intervention, Klimas might
well recommend CBT to help patients with ME/CFS cope with it
(whereas in the UK Wessely et al have used it to deny the very
existence of ME/CFS)?
Klimas is also on record as saying
at the CDC:
"It's critical for patients and their healthcare
providers to know that there is hope and that we can help".
On the matter of management, some of what the Toolkit says is hardly
controversial, namely that the objective of an effective management
programme is threefold: (1) to help patients develop effective
coping strategies (2) to relieve symptoms and (3) to teach patients
to manage activity levels so as to avoid post-exertional malaise on
the one hand and deconditioning on the other.
However, it also states:
"The goal of CBT is to change perceptions
and behaviours that can contribute to symptom expression" and
"Working with a CBT therapist, (ME)CFS patients can examine their
beliefs and coping behaviours and modify these as necessary to
manage the illness more effectively".
As in the UK, there seem to be a confusing divergence about the
nature of CBT for those with (ME)CFS.
Changes in the UK?
Are things changing in the UK? On the basis of the Wessely School
psychiatrists' chameleon stances (depending on whether their
audience is in the US or the UK), they may currently see advantages
in creating the illusion that the aim of CBT has always been to help
patients cope with overwhelming illness:
if so, are we
witnessing the construction of an escape route made
necessary by the realisation that -- in the light of
such substantial and convincing biomedical evidence
-- they've been wrong ?
For illustrations of the
pliability of Wessely School opinions about the efficacy of CBT
depending on the country in which they were delivered, see
So why is the Wessely School model of CBT/GET not only
unsuitable but potentially dangerous for those with ME/CFS?
The following notes, taken from
Cheney's DVD (a two disc boxed set: for details, send an email to
firstname.lastname@example.org as notified on Co-Cure on 27th October
2006), may provide some answers.
It should be
compulsory viewing for every member of the NICE
Guideline Development Group on "CFS/ME".
Others have already reported on Cheney's seminar, so what
follows is a simplistic summary and makes no attempt to explain
the disrupted metabolic and biochemical pathways that were
demonstrated in detail by Cheney.
Cheney - who has been involved with (ME)CFS since the Lake Tahoe
outbreak in the early 1980s -- began by acknowledging his debt
to the work of Peckerman, who had found that half of the
patients studied had low cardiac output as measured by impedance
cardiography. (Peckerman noted that this could be due to the
heart itself, but that it could also be due to problems in the
peripheral blood vessels).
This fascinated Cheney, who in 2003
underwent a successful heart transplant because of dilated
cardiomyopathy, as a result of which he had observed at first hand
the spiralling effects on differing body systems of low cardiac
Important Clinical Findings
There is an objective database in key medical literature that
includes evidence (sic) of diastolic dysfunction and heart failure
in (ME)CFS. PFO is found in at least 80% of patients with (ME)CFS.
Oxygen should not be transported into a cell that cannot use it
without effective defences against its by-products (oxygen being the
precursor of free radical formation).
Symptoms are usually manifestations of defence responses and reflect
but do not cause the underlying problem.
Symptom-based treatment alone is therefore flawed at best and
dangerous at worst: to treat symptoms without understanding the
underlying disease process can cause death: the third leading cause
of death is treatment by physicians, which kills 250,000 people per
year (the first being heart disease and the second being cancer) --
most drugs are not aimed at the primary cause of disease but at
symptoms and are therefore dangerous (see below for Cheney's view
about the dangers of giving Prozac to those with (ME)CFS).
Principles that are important in (ME)CFS
Adaptation to chronic disease is generally coded as a phenotype
shift (ie. one still has the same genes but they are expressing
themselves differently). There is an emerging literature that
shows phenotypic adjustments are defining illnesses by which genes
are changing. Why is this going on? Is the gene shift causing the
disease, or is it defending the host? It is mostly the latter, and
this is very important, so we need to treat the underlying cause as,
once changed, the patient can never return to his/her original
phenotype. If genes have changed (and there is evidence that they
have), a patient can be genotypically shifted as well and
phenotypically shifted, and this is a big issue that stands in the
way of a quick fix solution: if chronic disease can never be fixed,
how can people be helped to feel better? The answer lies in
suppressing the defence mechanism, but this is not very good,
because if you fix the defence mechanism, at some deep level you can
A key principle is not to use too much oxygen (because it kills). (ME)CFS
protects against almost certain death by adapting to a low energy
Patients withdraw from activity: they have a dynamic dysfunction
that is more than simply an adaptation - there is something about
the disease that is making them this way.
The (ME)CFS Case Definition
Cheney outlined the case definition, saying that the classic triad
is: no energy, brain dysfunction, and pain. If a patient does not
have pain, s/he does not meet the (ME)CFS case definition: (ME)CFS
is very much a painful disorder.
Cognitive dysfunction occurs in 99% of cases (processing speed;
short-term memory loss; sensory and information overload;
information searching; multi-tasking problems; spatial
disorganisation). "Fatigue features in so many other disorders,
but what makes (ME)CFS special is the brain component".
Mood disturbances occur: depression is rarely severe and is
reactive; anxiety disorders abound, as does mood lability, but 40%
do not have any mood disorder, so (ME)CFS is not a psychiatric
The evolution of (ME)CFS
There are four phases:
1. the onset, or trigger phase
2. the triad phase
3. the dynamic dysfunction phase (although the fatigue and pain
and brain dysfunction are a little better, patients in this
phase can do less than when they were more sick)
4. DNA phenotype adaptation phase (there is a phenotypic
adaptation that locks this in at gene level).
Key scientific articles
Phase 1: (immune activation: fever, swollen glands, sore
throat, malaise: general indications of immune activation)
- Suhadolnick et al (Temple
- Komaroff et al (Harvard, USA)
- Klimas et al (Miami, USA)
Phase 2: (the centre of
gravity of this illness: fatigue, brain problems and pain;
xenobiotic toxicity coming from the gut and the environment)
- McGregor et al (Newcastle
- Pimental (UCLA, USA)
Phase 3: (the brain and heart
- Demitrack et al (NIH, USA)
- Moorkens et al (Antwerp,
- Schwartz et al (Harvard, USA)
- Peckerman et al (NMJ & D, USA)
- Drexler et al (Hanover,
Phase 4: (phenotypic and
genotypic adapatation à oxidative stress)
- Vernon et al (CDC, USA)
- Kerr et al (London, UK)
- Urowitz et al (Berkeley, USA)
- Pall (WSU, USA)
- Kennedy et al (Cheney's
overhead stated "USA", but if he means Kennedy and Spence, it
should be Dundee, Scotland)
Oxidative stress links (ME)CFS to
fibromyalgia, multiple chemical sensitivity and Gulf War Syndrome.
Do people recover from (ME)CFS?
Functional recovery is seen: one's ability to do things can improve,
but it can go the other way, or there may be no change over time. In
functional improvement, do patients really get better, or do they
just adapt? The longer things go on, the more difficult it is to see
functional recovery. Komaroff's data from Harvard is that after 10
years of illness, there is only a 30% chance of any functional
The Physical Examination
In phase 1: (immune activation), one sees
- Lymphyodynia (seen in 80-90%)
- Crimson crescents bilaterally
on soft palate (seen in 80%)
- Sub-normal temperature
In phase 2: one sees
- Evidence of subcortical brain
- Vestibular dysfunction (seen in
- Hyper-reflexia, especially of
the knees and ankles (seen in 70%)
In phases 3 and 4: the most
interesting are the metabolic disturbances:
- There is shortened
breath-holding capacity (seen in 60%)
- There is very poor oxygen
transport (seen in 90%): pulse oximetry readings measuring
saturation of haemoglobin show a significant inhibition to
- There is finger-print
destruction (seen in 50%): cross-hatching occurs, with
degradation of the ridges; punch biopsies found perivascular
lymphoid infiltrates ie. an inflammatory cuffing exactly as seen
in lupus, which signifies a non-specific immune activation issue
(so the finger-print changes could be reflecting much more than
just loss of finger-prints and may represent a vasculopathy)
- There is sub-normal temperature
(seen in 80%)
- There is low systolic blood
pressure (in 50% of patients it is less than 100)
- There is orthostatic B/P or
pulse changes (seen in 70%)
- Hypertension is very rare
These findings portend significant
physiological issues, chief of which is that oxygen is being
prevented from getting into the cell, and if there's no oxygen,
there's no energy.
Magnetic Resonance Spectroscopy
- 70% of patients show elevated
lactate levels in the ventricular system (the lactate elevation
is not normal and indicates a defect in energy in the brain: (ME)CFS
patients have significantly elevated lactate levels and the
fatigue correlated significantly with the level of lactate)
- 10% have evidence of neuronal
destruction and elevated choline peaks, typically in the
Magnetic Resonance Imaging
- 78% of patients have punctate
lesions which are most consistent with small strokes and there
is evidence to support this (ie. they are not caused by a virus
or by inflammation).
Mixed venous blood gas picture
- PvO2 is 25 (it should be 40)
- PvCO2 is 55 (it should be 45)
This is a differential hypoxia with
hypercarbia. There are only two diseases where this is seen: one is
pulmonary hypertension; the other is (ME)CFS.
The arterial side is normal.
Where does the oxygen go? It's being transported somewhere, but not
to the mitochondria. (ME)CFS patients have been shown to have
increased pooling of extra-cellular fluid in the belly, pelvis and
legs which might contain this dissolved oxygen, but it is more
likely being consumed by the oxidative pathway to create superoxide
in massive amounts. Superoxide is the progenitor of all free
radicals. The consequences are increased intra-cellular oxdidative
If you intervene and give Prozac, you up-regulate superoxide, which
is why serotinergic drugs kill neurons.
Intervening with drugs
in situations not fully understood breeds chaos and
(ME)CFS as cellular metabolic dysfunction
There are problems at cell level in energy production, and
because of this degraded energy problem, patients suffer a
defect in the ability to detoxify toxins, especially in the
portal circulation (giving rise to gut toxicity as seen in phase
2). Gene alterations (seen in phase 4) generate a massive
disturbance in the development of energy at the cell level. If
you lose energy, you lose glutathione, but the more glutathione
you give, the more you just create oxidised glutathione, which
generates loss of citrate, causing a left shift on
oxyhaemoglobin desaturation. Citrate also binds to magnesium, so
over time the patient will develop a severe magnesium depletion
syndrome. When that happens, you've had your last good night's
sleep: when you lose magnesium, you can't sleep any more.
How and why would a low energy state lead to an inability to
transfer oxygen? Cheney concludes that it's part of a bigger
picture that uses low oxygen transport to stablise the system.
In (ME)CFS, these serious issues are a big problem, especially
in the brain, the heart and in muscle. (ME)CFS is a compensatory
response to down-regulate energy production and oxygen transport
in order to reduce tissue damage.
Attempts to push beyond
energy limits will cause injury.
Prolonged energy deficits can
cause semi-permanent DNA phenotype adaptations and complications
can occur, especially within energy-sensitive systems such as
the heart, the brain and the muscles.
The most likely cause (not trigger) of (ME)CFS is a disruption
in handling the toxic by-products of oxygen utilisation.
In (ME)CFS, catalase is deficient in the heart, lungs and liver
(catalase is the most protective enzyme in the body against the
ravages of superoxide), and Cheney noted that electromagnetic
fields [EMFs] "screw up" superoxide dismutase (SOD), which is a
major anti-oxidant scavenger.
Is there an (ME)CFS-associated cardiomyopathy?
(ME)CFS patients have a high heart rate but a low cardiac
output. In (ME)CFS there is a cardiac dimension that is
independent of (but not excluding) autonomic function or blood
82% of patients have abnormal cardiac impedence.
It's hard to talk about a low cardiac output without talking
about the involvement of the brain and the adrenal glands.
A mismatch between metabolic demand and cardiac output, even
very briefly, will kill.
If the cardiac output goes down, in order not to die, there is a
rise in noradrenergic tone (also involving the adrenal glands)
to bring the output back up. In (ME)CFS, this is a serious
problem, because when the adrenals are exhausted, there will be
low cardiac output.
There is no such thing as an (ME)CFS patient who is NOT
hypothyroid: this has nothing to do with thyroid failure, but
everything to do with matching metabolic demand and cardiac
Order of sacrifice in cases of declining microcirculation.
First is the skin; second is the muscles and joints; third is
the liver and gut (patients can usually only tolerate a few
foods); fourth is the brain; fifth is the heart; sixth is the
lung and lastly is the kidney (for a more detailed discussion of
this order of sacrifice, see
Among the major causes of death in (ME)CFS is heart failure:
Jason et al (August 2006) found that 20% die of heart failure.
There are two types of heart failure: systolic (which is a
failure to eject) and diastolic (which is not a failure to
eject, but a failure to fill properly).
There are two types of diastolic heart failure: primary
relaxation deficit giving rise to decreased cellular energy as
seen in (ME)CFS and secondary relaxation deficit as seen in
hypertension, diabetes and the elderly over age 75.
Primary relaxation deficit is a disorder that seems to have gone
right under the radar of most cardiologists (who focus on the
secondary relaxation deficit).
Diastolic heart failure was first described in the 1980s but
there was no significant literature until the 1990s, and no
significant way to measure it until 2001.
In July 2006 The New England Journal of Medicine carried a
significant paper on more than 4,500 patients studied with
diastolic heart failure (which is higher than those with
systolic heart failure). This is unexplained, but is
accelerating (is it in fact an explosion of (ME)CFS?).
One is just as likely to die of diastolic heart failure as from
systolic heart failure.
Doppler mitral in-flow velocities show diastolic dysfunction.
Concluding the first disc, Cheney stated there is (quote) "a
whopping percentage of (ME)CFS people with diastolic
In the second DVD, Cheney expounds on PFO in relation to (ME)CFS.
He says that at least half of patients exhibit atrial cavitation,
and that when these patients stood up, in 80% the filling volume
collapsed. He tested this with magnesium and the results were
significant: magnesium restored 12% of energy in one minute.
Magnesium affects the intracellular energetics, proving that
patients have a "tremendous" energy problem that is very
sensitive to magnesium. (The reason magnesium is so important is
that without it, ATP cannot be converted to ADP for the
production of energy).
(ME)CFS patients "squeeze the hell" out of their left ventricle,
resulting in a "whopping" 70% increase in left ventricular wall
motion thickness. The reason why patients are squeezing so hard
is because they do not have enough energy to fill the chambers
of the heart properly so they are trying to compensate by
squeezing a lot harder (ie. the way patients are compensating
for this loss of cardiac output is by squeezing the left
ventricle much harder).
There are significant consequences of this. One consequence is
that (ME)CFS patients become asynchronised (ie the heart can be
filling and ejecting at the same time).
If out of synchrony, the ventricle cannot cope, so cardiac
output is severely degraded.
A second consequence is that patients develop a strain pattern,
which is an indication of ischaemia. Cheney has seen ischaemic
changes in the inner ventricular wall because of the increased
PFO is a hole in the heart producing a right to left shunt of
unoxygenated blood full of carbon dioxide as well as products of
liver metabolism - the liver is literally draining into the
right heart and that blood is being shot straight to the brain
(this was demonstrated on the DVD by means of Trans Cranial
The assumed cause of the PFO is the same as in the foetus - to
protect the body from oxygen: in (ME)CFS patients are shifted
left to right, not because they have an immature way (as in the
foetus) of handling oxygen, but because they have a defective
way of handling oxygen.
In (ME)CFS patients, there is increased left ventricular strain,
with increased R-L shunting, and cardiac ischaemia develops, and
because of too much squeezing, the PFO (that closed at birth) is
opened up, resulting in significant oxygen toxicity, with
ischaemic reperfusion-type changes.
The diastolic dysfunction that causes dilatation of the left
atrium can actually break the seal of the sealed Foramen Ovale (ie.
the increased pressure blows through a previously sealed PFO).
It is increasingly clear that in (ME)CFS, a diminished threshold
for oxygen toxicity exists, and that each patient will have a
These findings have a significant negative effect on Emergency
Room (A&E) and operating theatre uses of oxygen during surgery -
a patient with (ME)CFS could be given too much oxygen and be
killed on the operating table.
Hyperbaric oxygen could have a very negative impact on some (ME)CFS
The ultimate consequence of this is low cardiac output, arising
from a problem of energy production.
The complications of PFO include:
- Cerebral aneurysm
- Multiple mini-strokes
- Cerebral hypoperfusion
produces pressure headaches; migraine, cognitive impairment and
a lower seizure threshold
- Venous hypoxia complications
are fundamentally linked to intracellular acidosis which
depletes electron buffers
- Depleted acid buffers leads to
increased sensitivity to diet, drugs and the environment.
PFOs cause significant instability.
There is a difference between diastolic dysfunction and diastolic
failure: in diastolic dysfunction there is a filling problem but the
body is compensating for it and achieving enough cardiac output to
match metabolic demand. Diastolic failure begins when the body can
no longer compensate and there is a reduction in cardiac output.
Cheney repeated that this is seen in 80% of (ME)CFS patients.
If patients draw down their lifestyle to live within the means of
the reduced cardiac output, then progression into congestive cardiac
failure (CCF) is slowed down, but if things continue to progress, a
point will be reached where there is no adequate cardiac output, and
dyspnoea will develop, with ankle oedema and other signs of
congestive cardiac failure.
The message from Cheney is clear: in order to stay relatively
stable, it is essential for the (ME)CFS patient not to create
metabolic demand that the low cardiac output cannot match.
The message for NICE
The message for NICE is that (ME)CFS patients instinctively know
that they simply cannot cope with aerobic exercise (as in graded
exercise therapy), and that their instincts have been proved correct
by Cheney's ground-breaking research.
Many (ME)CFS patients are formerly high achievers who do not need to
be patronised by psychiatrists with their behavioural management
regimes about how not to exceed their own limits: they know their
limits and live within them daily in order to survive.
has been pointed out to NICE, what such patients
need is not multi-million pounds to be given to
psychiatrists to try to prove that (ME)CFS patients
will recover with aerobic exercise:
what is needed is biomedical research to find the
cause, without which there can be no hope of
effective treatment or a cure.
In the meantime, as NICE has
also been informed, patients urgently need practical support
services, including help with personal care, shopping,
housework, cooking, adaptations in the home (such as a
chairlift) ie. basic support for the very ill.
But NICE has already indicated that it is not listening.
To read the IiME response to
the NICE guidelines
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