WILL PETER WHITE PLEASE STAND UP!
Angry. Why am I angry? Because hundreds of thousands of people have a disease that is allowing doctors to abuse patients, all behind closed doors, for those who speak out to be deemed mentally unstable (of course, that’s an easy answer right?) and for those who are so severely ill being denied any tests or treatment because they cannot in the eyes of the medical profession, possibly be sick.
“What on earth am I talking about”, you may ask? I am talking about the disease that is laughed at every time its name is uttered. I myself cringe whenever doctors say it. I am of course talking about “Chronic Fatigue Syndrome” or to show respect to such a serious illness, Myalgic Encephalomyelitis.
The ‘doctors’ (I use this term loosely – since when is psychiatry an applied science?) in charge of the top M.E/CFS units in London (Barts, Kings, Maudsley) therefore setting the precedent for the rest of the country, do not believe in M.E – despite the same monotonous speech penned from the Department of Health stating that they follow the WHO classification of M.E as a neurological disease (ICD10-G.93).
I understand that these doctors do not believe M.E/CFS exists but they are wrong. So very wrong. I wish it didn’t exist either but it does. I understand that the psychiatric lobby will probably never admit that they are wrong but all I ask of them is one thing, and one thing only; READ THE EVIDENCE. Don’t IGNORE IT.
The evidence of M.E as a neuroimmune disease does not come from nowhere, the research has been conducted by some of the worlds’ most prestigious institutes; Harvard University, Stanford University, Colombia University New York. The man who is working on M.E right now is none other than Professor Ian Lipkin, the worlds’ top virus hunter who discovered the West Nile Virus and the SARS virus. Professor Lipkin is one of the most intelligent men in the world whose opinion cannot be ignored, yet it is and in a manner of gross negligence.
M.E is the illness caused by an infectious pathogen; that much is clear.
Jose Montoya from Stanford has showed that 11% of people came down with CFS following an infection with one of four pathogens and exclaimed that “our patients told us this all along yet a study had to be done to prove that they were right,” and then he turned to another recent study which showed that about 4% of adolescents who come down with infectious mononucleosis have CFS after 2 years. Importantly, he noted studies have suggested that the more severe the initial illness the more likely a person is going to come down with CFS and later suggested that giving short courses of antivirals to people with severe infection was an idea. Ian Lipkin, the most prestigious virus hunter in the world even stated at his recent phone in conference with the United States Centers for Disease Control that M.E is likely to be caused by an “infectious agent”.
Lipkin also spoke about the finding of an Anellovirus – which he stated he does not know the meaning of yet but Judy Mikovits remains convinced of a retroviral footprint in the blood of M.E patients.
This does not fit in with the mass endemic lie of ‘CBT and Exercise’ and ‘most get better in months or years’ No. They don’t. People with fatigue, mostly get better. Not autoimmune disease which has no current treatment protocol on offer. (Ben Dixon).
Below are basic immune assays that have shown abnormalities in patients with M.E/CFS (taken from Redlabs).
PERFORIN EXPRESSION ASSAY
Natural Killer cells (NK) cells are cytotoxic cells that mediate the immune response against certain cancer and virus-infected cells. NK cells are normally found in the peripheral blood, and are classified by their cell surface markers as CD3-/CD56+cells. NK cells activity is altered in several disorders such as multiple sclerosis, lupus, and CFS, and is very sensitive to various environmental pollutants. Since NK cells play a central role in the defense against viruses, decreased NK activity can lead to the development of opportunistic viral infections. NK cells exert their cytotoxic effect by releasing perforin, a protein that will destroy the cytoplasmic membrane of target cells and finally kill them. Expression of perforin mRNA can be measured as a mean to evaluate NK cell activation.
ELASTASE EXPRESSION ASSAY
Elastase is an inflammatory protease expressed in immune cells (monocytes, neutrophils). Elastase contributes to immune defense by inactivating foreign bacteria but at the same time it causes damage to connective tissue, breaks down cytokines, immunoglobulins and immune cells receptors. An excess, chronic production of elastase is therefore detrimental. In CFS patients, elastase is responsible for the cleavage of RNase L. Expression of elastase mRNA can be quantified as a specific marker of inflammation.
CD57+/CD3- ABSOLUTE CELL COUNT
CD57+/CD3- cells are a subset of NK cells. Their exact function, and what differentiates them from CD56+ NK cells, is not well understood. The absolute number of CD57+/CD3- cells is low in patients suffering from chronic Lyme disease (a disease that follows an infection by a bacteria called Borrelia). Patients with very low CD57 have significantly more co-infections and persistent immunologic defects than patients with higher counts. In patients that respond to antibiotic therapy, the number of cells come back to normal, hence this is a useful marker to follow the effect of a therapy.
CD14 is expressed in monocytes/macrophages and plays a critical role in the recognition of bacterial cell wall components (LPS). The extracellular part of CD14 can be cleaved and released in the plasma, where it will inactivate circulating LPS. Serum soluble CD14 levels are significantly elevated in patients with inflammatory bowel disease, Crohn’s disease, but also in patients suffering from Brucellosis or Lyme disease.
C4a SERUM LEVEL
C4a is an anaphylatoxin generated by cleavage of complement component 4 (C4), upon activation of the complement system. C4a increase causes local inflammatory response and symptoms of hypersensitivity. C4a levels are elevated following exercise in CFS patients. A US study has reported that elevated complement C4a was an early marker for Lyme disease in tick bite patients.
In the absence of laboratory tests to the contrary, chronic illnesses are often misdiagnosed as somatoform disorders caused by stress and other nonorganic factors.(9) Patients with CFS, FMS and GWI usually have cognitive problems, such as short term memory loss, difficulty concentrating and other problems, and physicians who find psychological or psychiatric problems in these patients often decide that these conditions are caused by somatoform disorders, not organic problems.(1) Stress is often mentioned as an important factor or the important factor in these disorders. Indeed, GWI patients are often diagnosed with Post Traumatic Stress Disorder (PTSD) in veterans’ and military hospitals.(10) The evidence that has been offered as proof that stress or PTSD is the source of GWI sickness is the assumption that veterans must have suffered from stress by virtue of the stressful environment in which they found themselves during the Gulf War,(10) but the veterans themselves do not feel that stress-related diagnoses are an accurate portrayal of their illnesses. Most testimony to date refutes the notion that stress is the major factor in GWI,(11) suggesting that stress, albeit important, is not the cause of GWI.(12) But most physicians would agree that stress can exacerbate chronic illnesses and suppress immune systems, suggesting that stress plays a secondary not primary role in chronic illnesses, such as GWI, CFS, and FMS.(1) However, in the absence of physical or laboratory tests that can identify possible origins of FMS, CFS or GWI, many physicians accept that stress is the cause of these chronic illnesses. It has been only recently that other causes were seriously considered, including chronic infections. (http://www.gulfwarvets.com/article24.htm)
A majority of Chronic Fatigue Syndrome (CFS) patients have systemic bacterial and viral infections. In our study of 200 CFS patients we found a high prevalence (52%) of mycoplasmal infections. Using forensic polymerase chain reaction we also examined whether these same CFS patients showed evidence of co-infections with various mycoplasmas, Chlamydia pneumonia and/or Human Herpes Virus-6 (HHV-6). We found that 7.5% of the patients had C. pneumonia and 30.5% had HHV-6 infections. Since the presence of one or more infections may predispose patients to other infections, we examined the prevalence of C. pneumoniae and HHV-6 infections in mycoplasma-positive and –negative patients. Unexpectedly, we found that the incidence of C. pneumoniae or HHV-6 was similar in mycoplasma-positive and –negative patients. Also, the incidence of C. pneumoniae in HHV-6-positive and –negative patients was similar. Control subjects had low rates of mycoplasmal (6%), HHV-6 (9%) or chlamydial (1%) infections, and there were no co-infections in control subjects. Differences in bacterial and/or viral infections in CFS patients compared to control subjects were significant (P<0.001). The results indicate that a very large subset of CFS patients show evidence of bacterial and viral co infections. (Bacterial and Viral Co-Infections in Chronic Fatigue Syndrome (CFS/ME) Patients Garth L. Nicolson,1 PhD, Marwan Y. Nasralla,2 PhD, Kenny De Meirleir,3 MD, PhD and Jeorg Haier,4 MD, PhD)
In his Testimony before the US FDA Scientific Advisory Committee on 18th February 1993, Paul Cheney, Professor of Medicine and Director of the Cheney Clinic, North Carolina and one of the world’s leading experts on ME/CFS, testified as follows:
“I have evaluated over 2,500 cases. At best, it is a prolonged post-viral syndrome with slow recovery. At worst, it is a nightmare of increasing disability with both physical and neuro-cognitive components. The worst cases have both an MS-like and an AIDS-like clinical appearance. We have lost five cases in the last six months. The most difficult thing to treat is the severe pain. Half have abnormal MRI scans. 80% have abnormal SPECT scans. 95% have abnormal cognitive-evoked EEG brain maps. Most have abnormal neurological examination. Most have evidence of T-cell activation. 80% have evidence of an up-regulated 2-5A antiviral pathway. 80% of cases are unable to work or attend school. We admit regularly to hospital with an inability to care for self”.
Other infections that have been found are:
IgA/IgM intestinal bacteria (leaky gut) Detection of IgA/IgM directed against Klebsiella pneumoniae, Proteus mirabilis, Pseudo- monas aeruginosa, Citrobacter koseri, Psds. putida, Morganella morganii, Hafnia alvei
Now chronic infection is only one part of the story. The research by Fluge and Meller (you can read more about that here…. http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0026358) indicates that M.E is an autoimmune disease.
Now reading all of the above, one would logically conclude that this disease is a BIOLOGICAL one, a treatable one and most definitely NOT a psychological one. This is where it becomes baffling as a group of doctors have decided to reinvent a completely NEW disease and do what the hell they like with patients suffering from the original disease. In short: the patients eventually die, like Sophia Mirza, Emily Collingridge, Lynne Gilderdale and many many more.
Professor Peter White of the infamous ‘PACE’ trial sits quite comfortably on the new UK M.E/CFS research collaborative and I think people need to be crystal clear on who and what they are dealing with.
The below is part of a medical textbook that is used to teach medical students about M.E/CFS.
I thank those on Phoenix Rising for pointing this out to me.
As CFS would normally not be diagnosed within this timeframe, that means basically most of us have a psychiatric reason for our symptoms (according to them).
This section (and the index entry on CFS) then directs then reader to the CFS piece in Section 22 (Psychological Medicine), where CFS/ME is listed under “Functional or Psychosomatic Disorders: Medically Unexplained Symptoms”.
Anyway this is the text below and the details of the book.
Kumar and Clark – Clinical Medicine
By Parveen Kumar, CBE, BSc, MD, FRCP, FRCP (Edin), Professor of
Clinical Medical Education, Barts and The London, Queen Mary’s School
of Medicine and Dentistry, University of London, and Honorary
Consultant Physician and Gastroenterologist, Barts and The London NHS
Trust, London, UK; and Michael Clark, MD, FRCP, Honorary Senior
Lecturer, Barts and The London, Queen Mary’s School of Medicine and
Denistry, University of London, UK
ISBN 0702027634 Paperback 1528 Pages 1283 Illustrations
Saunders Published August 2005
Anthony W Clare MD FRCPI FRCP FRCPsych MPhil
Professor of Clinical Psychiatry
Trinity College, Dublin;
St Patrick’s Hospital, Dublin, Ireland
Peter D White MD FRCP FRCPsych
Senior Lecturer in Psychological Medicine, Honorary Consultant in
Barts and The London, Queen Mary’s School of Medicine and Dentistry,
University of London, UK
We all have illness behaviour when we choose what to do about a
symptom. Going to see a doctor is generally more likely with more
severe and more numerous symptoms and greater distress. It is also
more likely in introspective individuals who focus on their health.
Abnormal illness behaviour occurs when there is a discrepancy between
the objective somatic pathology present and the patient’s response to
it, in spite of adequate medical investigation arid explanation.
FUNCTIONAL OR PSYCHOSOMATIC DISORDERS: MEDICALLY UNEXPLAINED SYMPTOMS
`Functional’ disorders are illnesses in which there is no obvious
pathology or anatomical change in an organ (thus in contrast
to `organic and there is a presumed dysfunction in an organ or
system. The word psycho-somatic has had several meanings, including
psychogenic, `all in the mind’; imaginary and malingering. The modern
meaning is that psychosomatic disorders are syndromes of unknown
aetiology in which both physical and psychological factors are likely
to be causative,the psychiatric classification of these disorders
would be somatoform disorders, but they do not fit easily within
either medical or psychiatric classification systems, since they
occupy the hinterland between them. Medically unexplained symptoms
and syndromes are very common in both primary care and the general
hospital (over half the outpatients in gastroenterology and neurology
clinics have these syndromes). Because orthodox medicine has not been
particularly effective in treating or understanding these disorders,
many patients perceive their doctors as unsympathetic and seek out
complementary treatments of uncertain efficacy. Examples of
functional disorders are shown in Table 22.4.
Because epidemiological studies suggest that having one of these
syndromes significantly increases the risk of having another, some
doctors believe that these syndromes represent different
manifestations in time of `one functional syndrome’, which is
indicative of a somatization process. Functional disorders also have
a significant association with psychiatric disorders, especially
depressive and panic disorders as well as phobias. Against this view
is the evidence that the majority of primary care patients with most
of these disorders do not have either a psychiatric disorder or other
Functional or psychosomatic syndromes (medically unexplained symptoms)
Atypical facial pain
Atypical chest pain
Other chronic pain syndromes
Chronic or post-viral fatigue syndrome
Multiple chemical sensitivity
Irritable or functional bowel syndrome
Irritable bladder syndrome
It also seems that it requires a major stress or a psychiatric
disorder in order for such sufferers to attend their doctor for help,
which might explain why doctors are so impressed with the
associations with stress and psychiatric disorders. Doctors have
historically tended to diagnose `stress’ or `psychosomatic disorders’
in patients with symptoms that they cannot explain. History is full
of such disorders being reclassified as research clarifies the
pathology. A recent example is writer’s cramp (p. 1233) which most
neurologists now agree is a dystonia rather than a neurosis.
Chronic fatigue syndrome (CFS)
There has probably been more controversy over the existence and
aetiology of CFS than any other functional syndrome in recent years.
This is reflected in its uncertain classification as neurasthenia in
the psychiatric classification and myalgic encephalomyelitis (ME)
under neurological disorders. There is good evidence for this
syndrome, although the diagnosis is made clinically and by exclusion
of other fatiguing disorders. Its prevalence is 0.5% in the UK,
although abnormal fatigue as a symptom occurs in 10-20%. It occurs
most commonly in women between the ages of 20 and 50 years old, The
cardinal symptom is chronic fatigue made worse by minimal exertion.
The fatigue is usually both physical and mental, with associated poor
concentration, impaired registration of memory, irritability,
alteration in sleep pattern (either insomnia or hypersomnia), and
muscular pain. The name myalgic encephalomyelitis (ME) is
decreasingly used within medicine because it implies a pathology for
which there is no evidence.
Functional disorders often have aetiological factors in common with
each other (see Table 22.5), as well as more specific aetiologies.
For instance, CFS can be triggered by certain infections, such as
infectious mononucleosis and viral hepatitis. About 10% of patients
with infectious mononucleosis have CFS 6 months after the infectious
onset, yet there is no evidence of persistent infection in these
patients. Those fatigue states which clearly do follow on a viral
infection can be classified as post-viral fatigue syndromes. Other
aetiological factors include physical inactivity arid sleep
difficulties. immune and endocrine abnormalities noted in CFS may be
secondary to the inactivity or sleep disturbance commonly seen in
patients. Mood disorders are present in a large minority of patients,
and can cause problems in diagnosis because of the large overlap in
symptoms. These mood disorders may be secondary, independent (co-
morbid), or primary with a misdiagnosis of CFS. The role of stress is
uncertain, with some indication that the influence of stress is
mediated through consequent psychiatric disorders exacerbating
fatigue, rather than any direct effect.
The general principles of the management of functional disorders are
given in Box 22.7. Specific management of CFS should include a
mutually agreed and supervised programme of gradual increasing
activity However, few patients regard themselves as cured after
treatment. It is sometimes difficult to persuade a patient to accept
what are inappropriately perceived as psychological therapies’ for
such a physically manifested condition. Antidepressants do not work
in the absence of a mood disorder or insomnia.
This is poor without treatment, with less than 10% of hospital
attenders recovered after 1 year Outcome is worse with increasing
age. co-morbid mood disorder, and the conviction that the illness is
Table 22.5 Aetiological factors commonly seen in functional disorders
Perfectionist obsessional and introspective personality
Childhood traumas (physical and sexual abuse)
Similar illnesses in first-degree relatives
Chronic fatigue syndrome (CFS)
irritable bowel syndrome (IBS)
Psychologically traumatic events (especially accidents)
Physical Injuries (‘fibromyalgia and other chronic pain syndromes)
Life events that precipitate changed behaviours (e.g. going off sick)
Incidents where the patient believes others are responsible
Perpetuating ( maintaining)
Inactivity with consequent physiological adaptation (CFS
Avoidant behaviours multiple chemical sensitivities (MCS) CFS
Maladaptive illness beliefs (that maintain maladaptive behaviours)
Excessive dietary restrictions (`food allergies’)
Unresolved anger or guilt
Box 22.7 Management of functional disorders
The first principles is the identification and treatment of
maintaining factors (e.g. dysfunctional beliefs and behaviours mood
and sleep disorders)
Explanation of ill-health, including diagnosis and causes
Education about management (including self-help leaflets) .
Stopping drugs (e. g. caffeine causing insomnia, analgesics causing
Cognitive behaviour therapy (to challenge unhelpful beliefs and
change coping strategies)
Supervised and graded exercise therapy for approximately 3 months (to
reduce inactivity and improve fitness)
Specific antidepressants for mood disorders, analgesia and sleep
Symptomatic medicines (e.g. appropriate analgesia, taken only when
This was taken off a Twitter Feed about Peter White and BARTS Treatment protocols – see picture. It’s a public disgrace.
Rumour also has it that Peter White is also involved in the Karina Hansen case – a severely ill Danish girl removed from her home and sectioned against her will, where her health and life are at risk. You can find out more at the Karina facebook page https://www.facebook.com/JusticeForKarinaHansen
In a culture where a disease is refused to be recognise; patients are getting sicker, there is only one thing left to do: BLAME THE PATIENT!!!
We need to stop this right now – we need to challenge these doctors, these clinics, these beliefs and stamp them out.