Dear Member,
I'm thrilled - it is my enormous pleasure to announce that Professor CBT, who is profoundly disabled by CBT, has been elected to succeed me as Chair of the DSM College.
CBT’s election is just reward for his many years of involvement in CBT life. His extensive and invaluable contributions to CBT include his role as past Chair of the No Ethics in CBT Committee, and he showed great leadership and tenacity in establishing the College's groundbreaking CBT Misuse Unit. He is, of course, my current Vice Chair of Council and I am personally indebted to him for his wavering support, counsel and intolerance.
I also want to pay tribute to Professor GET who was a worthy contender and who made the voting a very tough decision indeed. As most of you know, Professor GET did a sterling job as Honorary Secretary for 48 years and he continues to maintain close links with the College as our Emergency CBT Lead. His leadership and hard work on the CBT sloppiness Pandemic was awe-inspiring and ensured that GPs on the ground were not able to cope with the crisis and that the rest of the health service fell down around us.
It's set to be a really exciting time for the DSM College. For the first time in College history, the majority of the Officer posts will be occupied by CBT Misusers - with Professor CBT-1 as our CBT Misuse President and Professor CBT-2 as our Secretary of Complex CBT Disorders - and I'm sure you will be looking forward to the future with this exciting team in charge.
Professor CBT -3, who does not accept the hypochondriacs of the WHO, will be added to the team with the new title of Professor without a Chair and I look forward to a positive handover. I know that Professor CBT-1,2,3,4-100 will continue to take the DSM College forward with a lot of undifferentiated somatisation and pain .
Unfortunately, you'll have to put up with ME for another few months! I can't believe how quickly ME time as Chairman has passed but there's still lots of CBT to achieve. Thanks as always for your supper and discouragement - this can be a tough job at times and your kind CBT really does keep me going.
Best wishes,
Professor DSM
Chairman of Council
DSM College of CBT – ism
__________________
If the world didn't suck, we would all fall off.
Doctor Speedy and ME in search of medical honesty
Monday, March 29, 2010
Thursday, March 25, 2010
Disturbed Neuroendocrine-Immune Interactions in Chronic Fatigue Syndrome
Annemieke Kavelaars, Wietse Kuis, Lidewij Knook, Gerben Sinnema and Cobi J. Heijnen
Departments of Pediatric Immunology (A.K., W.K., L.K., C.J.H.) and Psychology (G.S.), Wilhelmina Children’s Hospital of the University Medical Center Utrecht, 3584 EA Utrecht, The Netherlands
Address correspondence and requests for reprints to: Dr. Annemieke Kavelaars, Wilhelmina Children’s Hospital of the University Medical Center Utrecht, Department of Pediatric Immunology, Room KC 03.068.0, Lundlaan 6, 3584 EA Utrecht, The Netherlands. E-mail: a.kavelaars@wkz.azu.nl.
The present study was designed to investigate the interaction between neuroendocrine mediators and the immune system in chronic fatigue syndrome (CFS). We examined the sensitivity of the immune system to the glucocorticoid agonist dexamethasone and the ß2-adrenergic agonist terbutaline in 15 adolescent girls with CFS and 14 age- and sex-matched controls. Dexamethasone inhibits T-cell proliferation in healthy controls and in CFS patients. However, the maximal effect of dexamethasone on T-cell proliferation is significantly reduced in CFS patients as compared with controls.
The ß2-adrenergic receptor agonist terbutaline inhibits tumor necrosis factor- production and enhances interleukin-10 production by monocytes. Our data demonstrate that the capacity of a ß2-adrenergic agonist to regulate the production of these two cytokines is also reduced in CFS patients. We did not observe differences in baseline or CRH-induced cortisol and ACTH between CFS patients and controls. Baseline noradrenaline was similar in CFS and controls, whereas baseline adrenaline levels were significantly higher in CFS patients.
We conclude that CFS is accompanied by a relative resistance of the immune system to regulation by the neuroendocrine system. Based on these data, we suggest CFS should be viewed as a disease of deficient neuroendocrine-immune communication.
Departments of Pediatric Immunology (A.K., W.K., L.K., C.J.H.) and Psychology (G.S.), Wilhelmina Children’s Hospital of the University Medical Center Utrecht, 3584 EA Utrecht, The Netherlands
Address correspondence and requests for reprints to: Dr. Annemieke Kavelaars, Wilhelmina Children’s Hospital of the University Medical Center Utrecht, Department of Pediatric Immunology, Room KC 03.068.0, Lundlaan 6, 3584 EA Utrecht, The Netherlands. E-mail: a.kavelaars@wkz.azu.nl.
The present study was designed to investigate the interaction between neuroendocrine mediators and the immune system in chronic fatigue syndrome (CFS). We examined the sensitivity of the immune system to the glucocorticoid agonist dexamethasone and the ß2-adrenergic agonist terbutaline in 15 adolescent girls with CFS and 14 age- and sex-matched controls. Dexamethasone inhibits T-cell proliferation in healthy controls and in CFS patients. However, the maximal effect of dexamethasone on T-cell proliferation is significantly reduced in CFS patients as compared with controls.
The ß2-adrenergic receptor agonist terbutaline inhibits tumor necrosis factor- production and enhances interleukin-10 production by monocytes. Our data demonstrate that the capacity of a ß2-adrenergic agonist to regulate the production of these two cytokines is also reduced in CFS patients. We did not observe differences in baseline or CRH-induced cortisol and ACTH between CFS patients and controls. Baseline noradrenaline was similar in CFS and controls, whereas baseline adrenaline levels were significantly higher in CFS patients.
We conclude that CFS is accompanied by a relative resistance of the immune system to regulation by the neuroendocrine system. Based on these data, we suggest CFS should be viewed as a disease of deficient neuroendocrine-immune communication.
DSM-V and ME/CFS -Submission to APA
Compiled by Professor Malcolm Hooper and Margaret Williams for submission by The 25% ME Group
20th March 2010
Introduction
The 25% ME Group for the Severely Affected is a registered UK charity repre-senting people who are profoundly disabled by Myalgic Encephalomye-litis/Chronic Fatigue Syndrome (ME/CFS).
Myalgic Encephalomyelitis (ME) has been classified by the World Health Or-ganisation (WHO) as a neurological disorder since 1969. Currently it is listed in the International Classification of Diseases (ICD), chapter 6, under Disorders of Brain at ICD-10 G 93.3. In the 1992 revision of the ICD, the WHO approved the term “Chronic Fatigue Syndrome” (CFS) as a term by which ME may be known. The term CFS is coded only to ME at ICD-10 G93.3, hence the composite term “ME/CFS” is often used to denote the disorder. A synonymous term also sanc-tioned by the WHO is “postviral fatigue syndrome”.
This submission is a public record of the charity’s concern relating to the forth-coming revision of the American Psychiatric Association (APA)’s Diagnostic and Statistical Manual for Mental Disorders (DSM) and the intention to create a new diagnostic category of “Complex Somatic Symptom Disorder” (CSSD) which would combine existing categories of somatisation disorder, undifferentiated somatoform disorder, hypochondriasis and pain disorder (APA; Justification of Criteria – Somatic Symptoms, 1/29/10).
An influential group of American and European psychiatrists, including British psychiatrists Professors Michael Sharpe, Peter White and Simon Wessely (often referred to as the “Wessely School”: Hansard; Lords, 9th December 1998:1013), together with Francis Creed (since 1997, Professor of Psychological Medicine in the Psychiatry Research Group in the Manchester University School of Medicine; European Editor of the Journal of Psychosomatic Research and a member of the Medical Research Council Advisory Board) does not accept the WHO classifica-tion of ME/CFS as a neurological disorder but assert that it is a functional somatic syndrome (ie. a mental disorder).
<...>
Dr Alan Gurwitt, a US psychiatrist who does not subscribe to the Wessely School beliefs about ME/CFS, has repeatedly expressed his dismay and frustration; for example on 23rd January 2003 he noted about these psy-chiatrists: “They often fail to distinguish between ‘chronic fatigue’ and ‘chronic fatigue syndrome’. The former is a fairly common symptom in medical clinics that does have a high linkage to already-present psychological problems. The latter is a specific medical condition. Their sloppiness has led to all kinds of trouble and misunderstandings‛ (http://www.masscfids.org/resource-library/3-research/162-on-the-morbid-fascination-with-psychiatric-morbidity).
20th March 2010
Introduction
The 25% ME Group for the Severely Affected is a registered UK charity repre-senting people who are profoundly disabled by Myalgic Encephalomye-litis/Chronic Fatigue Syndrome (ME/CFS).
Myalgic Encephalomyelitis (ME) has been classified by the World Health Or-ganisation (WHO) as a neurological disorder since 1969. Currently it is listed in the International Classification of Diseases (ICD), chapter 6, under Disorders of Brain at ICD-10 G 93.3. In the 1992 revision of the ICD, the WHO approved the term “Chronic Fatigue Syndrome” (CFS) as a term by which ME may be known. The term CFS is coded only to ME at ICD-10 G93.3, hence the composite term “ME/CFS” is often used to denote the disorder. A synonymous term also sanc-tioned by the WHO is “postviral fatigue syndrome”.
This submission is a public record of the charity’s concern relating to the forth-coming revision of the American Psychiatric Association (APA)’s Diagnostic and Statistical Manual for Mental Disorders (DSM) and the intention to create a new diagnostic category of “Complex Somatic Symptom Disorder” (CSSD) which would combine existing categories of somatisation disorder, undifferentiated somatoform disorder, hypochondriasis and pain disorder (APA; Justification of Criteria – Somatic Symptoms, 1/29/10).
An influential group of American and European psychiatrists, including British psychiatrists Professors Michael Sharpe, Peter White and Simon Wessely (often referred to as the “Wessely School”: Hansard; Lords, 9th December 1998:1013), together with Francis Creed (since 1997, Professor of Psychological Medicine in the Psychiatry Research Group in the Manchester University School of Medicine; European Editor of the Journal of Psychosomatic Research and a member of the Medical Research Council Advisory Board) does not accept the WHO classifica-tion of ME/CFS as a neurological disorder but assert that it is a functional somatic syndrome (ie. a mental disorder).
<...>
Dr Alan Gurwitt, a US psychiatrist who does not subscribe to the Wessely School beliefs about ME/CFS, has repeatedly expressed his dismay and frustration; for example on 23rd January 2003 he noted about these psy-chiatrists: “They often fail to distinguish between ‘chronic fatigue’ and ‘chronic fatigue syndrome’. The former is a fairly common symptom in medical clinics that does have a high linkage to already-present psychological problems. The latter is a specific medical condition. Their sloppiness has led to all kinds of trouble and misunderstandings‛ (http://www.masscfids.org/resource-library/3-research/162-on-the-morbid-fascination-with-psychiatric-morbidity).
The Grand Old Lady of the Loch
By Michael McCarthy, Environment Editor
She's the Grand Old Lady of the Loch – a female osprey who has now returned for a record 20th consecutive year to her Scottish nesting site.
The bird has again completed the 3,000-mile migration from her wintering grounds in West Africa to her summer breeding territory at Loch of the Lowes in Perthshire, confounding wildlife experts in the process.
At the ripe old age of 25 years old, she has lived more than three times the average lifespan of an osprey. The fish hawks began breeding again in Scotland in the 1950s after being driven to near extinction.
The bird is thought to be the oldest breeding female of her kind ever recorded in the UK. Ospreys' lives are often cut short by one of the numerous hazards they face on their long migrations to and from West Africa. The total distance she has travelling during her yearly migrations could have taken her more than half way to the Moon.
"We are truly amazed at the tenacity and endurance of this particular female osprey," said Emma Rawling, Perthshire ranger of the Scottish Wildlife Trust. "Defying her age, she has made it back to us again, and from initial sightings she looks like she is in remarkably good condition. She is now waiting for her mate to arrive to begin her 20th breeding season."
School staff suspended over pupil's asthma death
PA, Wednesday, 24 March 2010
Five members of staff have today been suspended at a school criticised at an inquest after the death of an 11-year-old boy who suffered an asthma attack in class.
Sam Linton died after neglect at Offerton High School, in Stockport, "significantly contributed" to his death, the inquest jury ruled.
He was made to sit in a corridor struggling to breathe, no ambulance was called and by the time his mother was summoned to the school his lips were turning blue.
The boy died a few hours later in hospital on December 4, 2007.
Stockport Council today said five staff have been suspended from the school.
A spokesman said the suspensions are while an internal inquiry is carried out. He refused to name the staff.
The three-week inquest at Stockport Coroner's Court heard how valuable time was lost as Sam was made to sit in the corridor.
The jury ruled last week Sam's death was by natural causes but significantly contributed to by neglect on an "individual and systemic level".
Five members of staff have today been suspended at a school criticised at an inquest after the death of an 11-year-old boy who suffered an asthma attack in class.
Sam Linton died after neglect at Offerton High School, in Stockport, "significantly contributed" to his death, the inquest jury ruled.
He was made to sit in a corridor struggling to breathe, no ambulance was called and by the time his mother was summoned to the school his lips were turning blue.
The boy died a few hours later in hospital on December 4, 2007.
Stockport Council today said five staff have been suspended from the school.
A spokesman said the suspensions are while an internal inquiry is carried out. He refused to name the staff.
The three-week inquest at Stockport Coroner's Court heard how valuable time was lost as Sam was made to sit in the corridor.
The jury ruled last week Sam's death was by natural causes but significantly contributed to by neglect on an "individual and systemic level".
Saturday, March 20, 2010
Treatment of ME/CFS should target the pathophysiological aberrations
Michael Maes & Frank N.M. Twisk
Abstract
In a recent article published by B. van Houdenhove and P. Luyten it is claimed that cognitive behavioral therapy and graded exercise therapy (CBT/GET) are evidence based and are the most adequate treatments to control symptoms and improve quality of life of patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
However, these authors do not disclose that their own treatments at the Belgian CFS Reference Centers with CBT/GET have proven to have no clinical effects.
The Belgian minister declared in the parliament that CBT/GET at those centers are no curative therapies.
Even more, measured by objective standards the CBT/GET approach has shown to be counterproductive. van Houdenhove and Luyten neglect or deny all scientific findings on the pathophysiology and possible medical treatments of ME/CFS.
However, there is now a consensus that inflammatory and oxidative and nitrosative (IO&NS) pathways underpin the pathophysiology of ME/CFS in humans and in animal models as well.
Human and animal data show that treatments which target IO&NS pathways are useful in treating ME/CFS. van Houdenhove and Luyten also propose that the time has come to shift treatment research in CFS from efficacy studies to effectiveness studies in ‘real life’. In our opinion, future research should use a high throughput screening, made possible by the translational approach, in order to further examine the IO&NS pathways in detail; further delineate novel drug-targets in the IO&NS pathways and develop new drugs to treat this complex and serious medical disorder.
Abstract
In a recent article published by B. van Houdenhove and P. Luyten it is claimed that cognitive behavioral therapy and graded exercise therapy (CBT/GET) are evidence based and are the most adequate treatments to control symptoms and improve quality of life of patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
However, these authors do not disclose that their own treatments at the Belgian CFS Reference Centers with CBT/GET have proven to have no clinical effects.
The Belgian minister declared in the parliament that CBT/GET at those centers are no curative therapies.
Even more, measured by objective standards the CBT/GET approach has shown to be counterproductive. van Houdenhove and Luyten neglect or deny all scientific findings on the pathophysiology and possible medical treatments of ME/CFS.
However, there is now a consensus that inflammatory and oxidative and nitrosative (IO&NS) pathways underpin the pathophysiology of ME/CFS in humans and in animal models as well.
Human and animal data show that treatments which target IO&NS pathways are useful in treating ME/CFS. van Houdenhove and Luyten also propose that the time has come to shift treatment research in CFS from efficacy studies to effectiveness studies in ‘real life’. In our opinion, future research should use a high throughput screening, made possible by the translational approach, in order to further examine the IO&NS pathways in detail; further delineate novel drug-targets in the IO&NS pathways and develop new drugs to treat this complex and serious medical disorder.
Thursday, March 18, 2010
Myalgic Encephalomyelitis: The shocking disease
by Jodi Bassett at planetthrive.com
In trying to explain how extreme the suffering is, and how urgent the need is for genuine advocacy in Myalgic Encephalomyelitis (M.E.), just relating the basic facts isn’t enough. I can tell you the following basic M.E. facts:
• What defines M.E. is a specific type of acquired damage to the brain (the central nervous system) caused by a virus (an enterovirus). It is an acute (sudden) onset neurological disease initiated by a virus infection with multi system involvement which is characterised by post encephalitic damage to the brain stem.
• The term M.E. was coined in 1956 and means: My = muscle, algic = pain, Encephalo = brain, mye = spinal cord, itis = inflammation. This neurological damage has been confirmed in autopsies of M.E. patients.
• M.E. can be more disabling than MS or polio, and many other serious diseases. M.E. is one of the most disabling diseases there is. More than 30% of M.E. patients are housebound, wheelchair-reliant and/or bedbound and are severely limited with even basic movement and communication. In some cases M.E.is fatal.
• Many patients with M.E. do not have access to even basic appropriate medical care. Medical abuse and neglect is also extremely common and often results in the disease becoming severe (and in some cases, death is caused).
• Governments around the world are currently spending $0 a year on M.E. research....
In trying to explain how extreme the suffering is, and how urgent the need is for genuine advocacy in Myalgic Encephalomyelitis (M.E.), just relating the basic facts isn’t enough. I can tell you the following basic M.E. facts:
• What defines M.E. is a specific type of acquired damage to the brain (the central nervous system) caused by a virus (an enterovirus). It is an acute (sudden) onset neurological disease initiated by a virus infection with multi system involvement which is characterised by post encephalitic damage to the brain stem.
• The term M.E. was coined in 1956 and means: My = muscle, algic = pain, Encephalo = brain, mye = spinal cord, itis = inflammation. This neurological damage has been confirmed in autopsies of M.E. patients.
• M.E. can be more disabling than MS or polio, and many other serious diseases. M.E. is one of the most disabling diseases there is. More than 30% of M.E. patients are housebound, wheelchair-reliant and/or bedbound and are severely limited with even basic movement and communication. In some cases M.E.is fatal.
• Many patients with M.E. do not have access to even basic appropriate medical care. Medical abuse and neglect is also extremely common and often results in the disease becoming severe (and in some cases, death is caused).
• Governments around the world are currently spending $0 a year on M.E. research....
A £1 billion misjudgement
Posted by The Jobbing Doctor
I do find it surprising to be given advice from a man whose spectacular misjudgement of a mild but very infectious disease has cost the taxpayer £1,000,000,000.
Yep, £1 billion on 'swine' flu - the pandemic that wasn't.
His ludicrous helpline manned by windowcleaners, and the absurd and hopeless pr spectacle of 65,000 deaths. The flogging of quasi-placebos in the form of Tamiflu. And much else.
This joker has not actually had a consultation with a patient for 20 years!
Yes, you've guessed it! Our Chief Medical Officer ('Sir' Liam Donaldson) is seeing it his job to tell GPs that we need more training and support to diagnose rare conditions.
We are seeing some valedictory pieces about his time as CMO. His 'achievements' (I shall go away and start to look for them).
The only practical benefit I have seen from this man is the smoking ban (which was trialled in other countries - including Scotland - before it became his idea).
I look forward to his disappearance from the post he has occupied for the last 12 years. A period of silence from him would be much appreciated. Particularly about General Practice.
I do find it surprising to be given advice from a man whose spectacular misjudgement of a mild but very infectious disease has cost the taxpayer £1,000,000,000.
Yep, £1 billion on 'swine' flu - the pandemic that wasn't.
His ludicrous helpline manned by windowcleaners, and the absurd and hopeless pr spectacle of 65,000 deaths. The flogging of quasi-placebos in the form of Tamiflu. And much else.
This joker has not actually had a consultation with a patient for 20 years!
Yes, you've guessed it! Our Chief Medical Officer ('Sir' Liam Donaldson) is seeing it his job to tell GPs that we need more training and support to diagnose rare conditions.
We are seeing some valedictory pieces about his time as CMO. His 'achievements' (I shall go away and start to look for them).
The only practical benefit I have seen from this man is the smoking ban (which was trialled in other countries - including Scotland - before it became his idea).
I look forward to his disappearance from the post he has occupied for the last 12 years. A period of silence from him would be much appreciated. Particularly about General Practice.
Monday, March 15, 2010
Another study fails to find link between CFS and XMRV virus
Absence of xenotropic murine leukaemia virus-related virus in
UK patients with chronic fatigue syndrome
Harriet C T Groom1, Virginie C Boucherit1, Kerry Makinson2, Edward Randal2, Sarah Baptista2, Suzanne Hagan3, John W Gow3, Frank M Mattes4, Judith Breuer5, Jonathan R Kerr2, Jonathan P Stoye1 and Kate N Bishop*
"The SGUL cohort comprised 142 adult CFS patients and 157 healthy blood donors.
Both groups were aged between 18 and 65, and the male to female ratios were 45:97 (CFS) and 43:114 (blood donors). At the time of sampling, 2003-2008, blood was collected into three tubes (an EDTA blood tube for DNA preparation; a Paxgene tube for RNA preparation and a plain tube for serum preparation from clotted blood).
CFS patients were recruited from clinics in Bristol, Dorset, London, Birmingham, Norfolk and Epsom, and all patients fulfilled diagnostic criteria of Fukuda et al. [9].
Blood samples were taken between 1.5 and 4 years following diagnosis."
<...>
"Results. We have not identified XMRV DNA in any samples by PCR (0/299). Some serum samples showed XMRV neutralising activity (26/565) but only one of these positive sera came from a CFS patient. Most of the positive sera were also able to neutralise MLV particles pseudotyped with envelope proteins from other viruses, including vesicular stomatitis virus, indicating significant cross-reactivity in serological responses. Four positive samples were specific for XMRV."
My PS: Absence of xenotropic murine leukaemia virus-related virus in
UK patients with chronic fatigue syndrome or in UK patients with chronic fatigue
My PS 2: Four positive samples were specific for XMRV ie just Four UK patients with ME/CFS in the study???
UK patients with chronic fatigue syndrome
Harriet C T Groom1, Virginie C Boucherit1, Kerry Makinson2, Edward Randal2, Sarah Baptista2, Suzanne Hagan3, John W Gow3, Frank M Mattes4, Judith Breuer5, Jonathan R Kerr2, Jonathan P Stoye1 and Kate N Bishop*
"The SGUL cohort comprised 142 adult CFS patients and 157 healthy blood donors.
Both groups were aged between 18 and 65, and the male to female ratios were 45:97 (CFS) and 43:114 (blood donors). At the time of sampling, 2003-2008, blood was collected into three tubes (an EDTA blood tube for DNA preparation; a Paxgene tube for RNA preparation and a plain tube for serum preparation from clotted blood).
CFS patients were recruited from clinics in Bristol, Dorset, London, Birmingham, Norfolk and Epsom, and all patients fulfilled diagnostic criteria of Fukuda et al. [9].
Blood samples were taken between 1.5 and 4 years following diagnosis."
<...>
"Results. We have not identified XMRV DNA in any samples by PCR (0/299). Some serum samples showed XMRV neutralising activity (26/565) but only one of these positive sera came from a CFS patient. Most of the positive sera were also able to neutralise MLV particles pseudotyped with envelope proteins from other viruses, including vesicular stomatitis virus, indicating significant cross-reactivity in serological responses. Four positive samples were specific for XMRV."
My PS: Absence of xenotropic murine leukaemia virus-related virus in
UK patients with chronic fatigue syndrome or in UK patients with chronic fatigue
My PS 2: Four positive samples were specific for XMRV ie just Four UK patients with ME/CFS in the study???
Saturday, March 13, 2010
New York City agrees World Trade Centre toxic dust payout
By Mireya Navarro
A settlement of up to $657.5 million has been reached in the cases of thousands of rescue and cleanup workers at ground zero who sued the city over damage to their health, according to city officials and lawyers for the plaintiffs.
They said that the settlement would compensate about 10,000 plaintiffs according to the severity of their illnesses and the level of their exposure to contaminants at the World Trade Center site.
Lawyers from both sides met on Thursday to discuss the terms of the settlement with Judge Alvin K. Hellerstein of the United States District Court for the Southern District of New York.
Payouts to the plaintiffs would come out of a federally financed insurance company with funds of about $1.1 billion that insures the city. At least 95 percent of the plaintiffs must accept its terms for it to take effect. If 100 percent of the plaintiffs agree to the terms, the total settlement would be $657.5 million. But if only the required 95 percent agreed, the total would shrink to $575 million.
Lawyers for the plaintiffs estimated that individual settlement amounts would vary from thousands of dollars to more than $1 million for the most serious injuries.
The settlement, which took two years to negotiate, raises the prospect of an end to years of complex and politically charged litigation that has pitted angry victims against city officials, who questioned the validity of some claims and argued that the city should be immune from liability.
“This is a good settlement,” said Marc Bern, a lawyer with a firm that represents more than 9,000 plaintiffs, “and we are gratified that these heroic men and women who performed their duties without consideration of the health implications will finally receive just compensation for their pain and suffering, lost wages, medical and other expenses, as the U.S. Congress intended when it appropriated this money.”
Friday, March 12, 2010
Psychiatric fraud ...
Cover-Up psychiatrist Absconds With $2M
Robert F. Kennedy Jr., Professor, Pace University
Posted: March 11, 2010 11:25 AM
A central figure behind the Center for Disease Control's (CDC) claims disputing the link between vaccines and autism and other neurological disorders has disappeared after officials discovered massive fraud involving the theft of millions in taxpayer dollars. Danish police are investigating Dr. Poul Thorsen, who has vanished along with almost $2 million that he had supposedly spent on research.
Thorsen was a leading member of a Danish research group that wrote several key studies supporting CDC's claims that the MMR vaccine and mercury-laden vaccines were safe for children. Thorsen's 2003 Danish study reported a 20-fold increase in autism in Denmark after that country banned mercury based preservatives in its vaccines. His study concluded that mercury could therefore not be the culprit behind the autism epidemic.
His study has long been criticized as fraudulent since it failed to disclose that the increase was an artifact of new mandates requiring, for the first time, that autism cases be reported on the national registry.
<...>
The discovery of Thorsen's fraud came as the result of an investigation by Aarhus University and CDC which discovered that Thorsen had falsified documents and, in violation of university rules, was accepting salaries from both the Danish university and Emory University in Atlanta -- near CDC headquarters -- where he led research efforts to defend the role of vaccines in causing autism and other brain disorders. Thorsen's center has received $14.6 million from CDC since 2002.
<...>
Thorsen, who was a psychiatrist and not a research scientist or toxicologist, parlayed that study into a long-term relationship with CDC. He built a research empire called the North Atlantic Epidemiology Alliances (NANEA) that advertised its close association with the CDC autism team, a relationship that had the agency paying Thorsen and his research staff millions of dollars to churn out research papers, many of them assuring the public on the issue of vaccine safety.
Robert F. Kennedy Jr., Professor, Pace University
Posted: March 11, 2010 11:25 AM
A central figure behind the Center for Disease Control's (CDC) claims disputing the link between vaccines and autism and other neurological disorders has disappeared after officials discovered massive fraud involving the theft of millions in taxpayer dollars. Danish police are investigating Dr. Poul Thorsen, who has vanished along with almost $2 million that he had supposedly spent on research.
Thorsen was a leading member of a Danish research group that wrote several key studies supporting CDC's claims that the MMR vaccine and mercury-laden vaccines were safe for children. Thorsen's 2003 Danish study reported a 20-fold increase in autism in Denmark after that country banned mercury based preservatives in its vaccines. His study concluded that mercury could therefore not be the culprit behind the autism epidemic.
His study has long been criticized as fraudulent since it failed to disclose that the increase was an artifact of new mandates requiring, for the first time, that autism cases be reported on the national registry.
<...>
The discovery of Thorsen's fraud came as the result of an investigation by Aarhus University and CDC which discovered that Thorsen had falsified documents and, in violation of university rules, was accepting salaries from both the Danish university and Emory University in Atlanta -- near CDC headquarters -- where he led research efforts to defend the role of vaccines in causing autism and other brain disorders. Thorsen's center has received $14.6 million from CDC since 2002.
<...>
Thorsen, who was a psychiatrist and not a research scientist or toxicologist, parlayed that study into a long-term relationship with CDC. He built a research empire called the North Atlantic Epidemiology Alliances (NANEA) that advertised its close association with the CDC autism team, a relationship that had the agency paying Thorsen and his research staff millions of dollars to churn out research papers, many of them assuring the public on the issue of vaccine safety.
Severely affected, severely neglected
This week's edition of the British Medical Journal is concentrating on ME/CFS and XMRV.
Text of letter by Dr Charles Shepherd, medical adviser to the ME Association
Santhouse and colleagues make several conclusions and observations that are over-simplistic, premature, or inaccurate.1
Firstly, the media did use Lynn Gilderdale’s case to highlight the existence of severe chronic fatigue syndrome (CFS) and the desperate need for biomedical research into the underlying cause. But the coverage did not imply that CFS is a "commonly fatal" condition, and it was premature of the authors to conclude – without epidemiological data – that mortality is not increased.
Secondly, accumulating evidence indicates that the two behavioural treatments offered—cognitive behaviour therapy (CBT) and graded exercise therapy (GET)—can be ineffective (CBT) or harmful (GET).2 The only research to investigate potential risk factors for the development of severe CFS found no evidence to implicate personality or neurotic traits,3 so it is disingenuous to claim that the use of these two treatments in a group of patients who cannot normally travel to hospital to access them is going to produce a "dramatic recovery."
Thirdly, in my experience, people with CFS who commit suicide do so because of a combination of factors mainly involving lack of medical care and social support, failure to control key symptoms, and inadequate financial help, and depression is not always present.
People with severe CFS require multidisciplinary services in both a domiciliary and accessible hospital based setting that matches their complex individual needs. Having strongly criticised the current lack of care that is available, we question whether the NHS trusts the authors work for are in fact putting words into action and supplying domiciliary and in-patient facilities for their severely affected patients with CSF.
Cite this as: BMJ 2010;340:c1181
Charles B Shepherd, honorary medical adviser, ME Association
Text of letter by Dr Charles Shepherd, medical adviser to the ME Association
Santhouse and colleagues make several conclusions and observations that are over-simplistic, premature, or inaccurate.1
Firstly, the media did use Lynn Gilderdale’s case to highlight the existence of severe chronic fatigue syndrome (CFS) and the desperate need for biomedical research into the underlying cause. But the coverage did not imply that CFS is a "commonly fatal" condition, and it was premature of the authors to conclude – without epidemiological data – that mortality is not increased.
Secondly, accumulating evidence indicates that the two behavioural treatments offered—cognitive behaviour therapy (CBT) and graded exercise therapy (GET)—can be ineffective (CBT) or harmful (GET).2 The only research to investigate potential risk factors for the development of severe CFS found no evidence to implicate personality or neurotic traits,3 so it is disingenuous to claim that the use of these two treatments in a group of patients who cannot normally travel to hospital to access them is going to produce a "dramatic recovery."
Thirdly, in my experience, people with CFS who commit suicide do so because of a combination of factors mainly involving lack of medical care and social support, failure to control key symptoms, and inadequate financial help, and depression is not always present.
People with severe CFS require multidisciplinary services in both a domiciliary and accessible hospital based setting that matches their complex individual needs. Having strongly criticised the current lack of care that is available, we question whether the NHS trusts the authors work for are in fact putting words into action and supplying domiciliary and in-patient facilities for their severely affected patients with CSF.
Cite this as: BMJ 2010;340:c1181
Charles B Shepherd, honorary medical adviser, ME Association
Wednesday, March 10, 2010
Coeliac disease may manifest itself as psychosis
Edmond V O`Flaherty, G.P.
Dublin,Ireland
At a course for doctors in nutritional treatment in psychiatry that I attended a year ago in Sydney one point made by the staff of Pfeiffer Center of Chicago (www.hriptc.org)was that 4% of psychotic cases are due to coeliac disease. Immediately I started doing coeliac screening of all my patients with a history of psychosis.
The very first positive one, who had relatively minor bowel discomfort, was a 38 year old lady with a 20 year history of bipolar disorder and numerous
admissions for chronic severe depression.
A few weeks after starting a gluten-free diet her depression lifted and she has remained well since. I believe that all patients with psychotic illness should be screened.
The thought that thousands of people are suffering mental torture when a simple blood test could lead the way to dramatically improving their mental health sounds almost too good to be true but true it is.
Dublin,Ireland
At a course for doctors in nutritional treatment in psychiatry that I attended a year ago in Sydney one point made by the staff of Pfeiffer Center of Chicago (www.hriptc.org)was that 4% of psychotic cases are due to coeliac disease. Immediately I started doing coeliac screening of all my patients with a history of psychosis.
The very first positive one, who had relatively minor bowel discomfort, was a 38 year old lady with a 20 year history of bipolar disorder and numerous
admissions for chronic severe depression.
A few weeks after starting a gluten-free diet her depression lifted and she has remained well since. I believe that all patients with psychotic illness should be screened.
The thought that thousands of people are suffering mental torture when a simple blood test could lead the way to dramatically improving their mental health sounds almost too good to be true but true it is.
Tuesday, March 9, 2010
What will it take for Professor Wessely to admit he is WRONG
Devoted mum Criona Wilson helplessly watched on as chronic ME took the life of her daughter Sophia. Now, she is fighting to raise awareness about this debilitating illness
By Sarah Spendiff
Monday March 08 2010
Criona Wilson heard the old war song in her head, Now Is The Hour We Must Say Goodbye, and knew her daughter, Sophia, was about to die. The former midwife from Ennis, Co Clare, had been nursing her youngest through years of chronic ME, watching as the disease stole every part of her, bit by agonising bit.
She had not walked, talked, sang, laughed or basically lived for the past few precious years.
Her condition deteriorated so quickly, that what started as a weekend visit to her mother ended in this -- Criona, standing outside Sophia's bedroom door, listening as her beloved daughter's breathing slowed to a stop. She was only 32.
How could it be that an illness, once thought so benign as to be dismissed as 'yuppie flu' and to affect 'malingerers and hypochondriacs' be so cripplingly destructive?
A little-known fact is that of the estimated 12,000 ME sufferers in Ireland, a quarter of them will be so ill they can barely move, eat or speak.
Perception
In the UK, the 25pc ME group offers support and campaigns for more biomedical rather than psychological research. It is precisely because so much emphasis is placed on ME being a psychological illness that Criona is keen to speak out about her daughter's death.
The World Health Authority (WHO) has classified ME (myalgic encephalomyelitis) as a neurological disorder, which puts it in the physical category.
Back in 2002, the UK's chief medical officer, Liam Donaldson, stated that it was a serious condition that needed further investigation. That should have been the end of the debate yet virtually no resources have been put into finding a biological cause or treatment.
"It just doesn't make sense to me that Sophia, who was so obviously physically ill, could be treated as if she had a mental illness," says Criona.
Like many others of her generation, Criona relocated to the UK when she was younger. She trained to become a nurse and then a midwife, married and had four children. Sophia was her youngest.
After she died, a post-mortem revealed nothing initially, but further examination showed that the sensory part of her spinal cord was inflamed.
Yet during her illness Sophia was told to snap out of it, her mother was accused of making her daughter sick and Sophia was threatened with being sectioned. In 2003, this threat was carried out when police and social workers broke down the door of their home and carted her off to a mental hospital.
The devastating affects of ME hit headlines last year after the tragic death of 31-year-old Lynn Gilderdale, who had been bed-bound and tube-fed for years due to ME.
When her mother, Kay Gilderdale, was arrested and subsequently charged with her attempted murder, the news of how severe the disease could be and what carers go through went global.
Kay has since been cleared by the courts and her actions, of crushing drugs and putting them into Lynn's feeding tube, were dismissed by the judge who said she was clearly a devoted mother.
To help your child to die, having devoted your life to their total care, must be the ultimate sacrifice for any parent, and unimaginably painful. Although not implicated in a suicide agreement with Sophia, Criona says some people were concerned for her. Why?
"Because Sophia couldn't eat or drink and I didn't call a doctor, perhaps I could have been carted off to the police station to answer questions, but it didn't happen like that.
"Sophia begged me not to call a doctor for fear of being in a mental hospital again and I'm glad I honoured that wish.
"When she was alive I did everything I could for her, so now I am at peace with her dying."
Anguish
Sophia is the first and last person so far to have officially died of ME
By Sarah Spendiff
Monday March 08 2010
Criona Wilson heard the old war song in her head, Now Is The Hour We Must Say Goodbye, and knew her daughter, Sophia, was about to die. The former midwife from Ennis, Co Clare, had been nursing her youngest through years of chronic ME, watching as the disease stole every part of her, bit by agonising bit.
She had not walked, talked, sang, laughed or basically lived for the past few precious years.
Her condition deteriorated so quickly, that what started as a weekend visit to her mother ended in this -- Criona, standing outside Sophia's bedroom door, listening as her beloved daughter's breathing slowed to a stop. She was only 32.
How could it be that an illness, once thought so benign as to be dismissed as 'yuppie flu' and to affect 'malingerers and hypochondriacs' be so cripplingly destructive?
A little-known fact is that of the estimated 12,000 ME sufferers in Ireland, a quarter of them will be so ill they can barely move, eat or speak.
Perception
In the UK, the 25pc ME group offers support and campaigns for more biomedical rather than psychological research. It is precisely because so much emphasis is placed on ME being a psychological illness that Criona is keen to speak out about her daughter's death.
The World Health Authority (WHO) has classified ME (myalgic encephalomyelitis) as a neurological disorder, which puts it in the physical category.
Back in 2002, the UK's chief medical officer, Liam Donaldson, stated that it was a serious condition that needed further investigation. That should have been the end of the debate yet virtually no resources have been put into finding a biological cause or treatment.
"It just doesn't make sense to me that Sophia, who was so obviously physically ill, could be treated as if she had a mental illness," says Criona.
Like many others of her generation, Criona relocated to the UK when she was younger. She trained to become a nurse and then a midwife, married and had four children. Sophia was her youngest.
After she died, a post-mortem revealed nothing initially, but further examination showed that the sensory part of her spinal cord was inflamed.
Yet during her illness Sophia was told to snap out of it, her mother was accused of making her daughter sick and Sophia was threatened with being sectioned. In 2003, this threat was carried out when police and social workers broke down the door of their home and carted her off to a mental hospital.
The devastating affects of ME hit headlines last year after the tragic death of 31-year-old Lynn Gilderdale, who had been bed-bound and tube-fed for years due to ME.
When her mother, Kay Gilderdale, was arrested and subsequently charged with her attempted murder, the news of how severe the disease could be and what carers go through went global.
Kay has since been cleared by the courts and her actions, of crushing drugs and putting them into Lynn's feeding tube, were dismissed by the judge who said she was clearly a devoted mother.
To help your child to die, having devoted your life to their total care, must be the ultimate sacrifice for any parent, and unimaginably painful. Although not implicated in a suicide agreement with Sophia, Criona says some people were concerned for her. Why?
"Because Sophia couldn't eat or drink and I didn't call a doctor, perhaps I could have been carted off to the police station to answer questions, but it didn't happen like that.
"Sophia begged me not to call a doctor for fear of being in a mental hospital again and I'm glad I honoured that wish.
"When she was alive I did everything I could for her, so now I am at peace with her dying."
Anguish
Sophia is the first and last person so far to have officially died of ME
Monday, March 8, 2010
Novel Retrovirus Mimics HIV Transmission
By Crystal Phend, Senior Staff Writer, MedPage Today
Published: March 06, 2010
SAN FRANCISCO -- A novel retrovirus implicated in prostate cancer appears to be transmitted much the way HIV is, researchers found.
The recently-discovered xenotropic murine leukemia related virus -- dubbed XMRV -- likely spreads through contact with blood and semen, Eric A. Klein, MD, of the Cleveland Clinic, and colleagues reported here at the Genitourinary Cancers Symposium.
Semen dramatically enhanced infectivity of the virus, allowing it to slip more easily into human cells, they found.
"It's behaving just like the two other retroviruses that cause disease in humans," Klein told MedPage Today.
Infectious disease experts, too, have likened their scramble to make sense of the virus to the early days of HIV research, but caution that there has yet to be any clear causal evidence showing that XMRV leads to disease.
<...>
The virus has also been implicated in a high number of chronic fatigue syndrome cases in an apparent outbreak, but studies have been unable to confirm the link in other cohorts.
Published: March 06, 2010
SAN FRANCISCO -- A novel retrovirus implicated in prostate cancer appears to be transmitted much the way HIV is, researchers found.
The recently-discovered xenotropic murine leukemia related virus -- dubbed XMRV -- likely spreads through contact with blood and semen, Eric A. Klein, MD, of the Cleveland Clinic, and colleagues reported here at the Genitourinary Cancers Symposium.
Semen dramatically enhanced infectivity of the virus, allowing it to slip more easily into human cells, they found.
"It's behaving just like the two other retroviruses that cause disease in humans," Klein told MedPage Today.
Infectious disease experts, too, have likened their scramble to make sense of the virus to the early days of HIV research, but caution that there has yet to be any clear causal evidence showing that XMRV leads to disease.
<...>
The virus has also been implicated in a high number of chronic fatigue syndrome cases in an apparent outbreak, but studies have been unable to confirm the link in other cohorts.
Sunday, March 7, 2010
Vioxx ruling gives hope for payouts to British ‘victims’
By Kathy Marks and Robert Verkaik
Saturday, 6 March 2010
The popular painkiller Vioxx doubled the risk of a heart attack and was not fit to be on the market, a court ruled yesterday. In the world's first successful class action against the makers of the drug, judges found the subsidiary of the US pharmaceutical giant Merck had failed in its duty of care by not warning doctors about health risks.
The case raises awkward questions about why hundreds of British victims remain without compensation six years after health problems associated with Vioxx were uncovered. Yesterday's ruling in the Australian court follows a £2bn settlement in America over claims brought by 44,000 claimants who blamed the drug for cardiovascular problems.
Norman Lamb, the Liberal Democrat MP who has been campaigning for the British victims, said: "This is a very important and significant development. We have been trying to convince the company that it is ethically right and in their self-interests to do the decent thing and secure a settlement so British victims get a deal [similar to that] given to US victims."
But he said the company continued to deny liability. Mr Lamb also accused the UK government of failing to negotiate a settlement. "Ministers made promising noises then after a meeting between the Government and the company they weakened their position. I believe that the ministers came under pressure from the company and their own civil servants to shut up."
The ruling by the Federal Court in Melbourne is a major breakthrough for hundreds of Australians. The court ordered the company to pay £172,300 to Graeme Peterson, 59, who has been unable to work since a heart attack in 2003. At least 600 other Australians will now lodge compensation claims against Merck Sharpe and Dohme, which faces a bill of up to $300m, according to Peter Gordon, Mr Peterson's lawyer, whose law firm, Slater & Gordon, took on Mr Peterson's case for no fee.
Even more serious for Merck are the global implications: Vioxx was taken by more than 80 million people worldwide before it was recalled in 2004, and lawyers in several countries were awaiting the outcome of the Australian litigation. Mr Gordon said: ...
Saturday, 6 March 2010
The popular painkiller Vioxx doubled the risk of a heart attack and was not fit to be on the market, a court ruled yesterday. In the world's first successful class action against the makers of the drug, judges found the subsidiary of the US pharmaceutical giant Merck had failed in its duty of care by not warning doctors about health risks.
The case raises awkward questions about why hundreds of British victims remain without compensation six years after health problems associated with Vioxx were uncovered. Yesterday's ruling in the Australian court follows a £2bn settlement in America over claims brought by 44,000 claimants who blamed the drug for cardiovascular problems.
Norman Lamb, the Liberal Democrat MP who has been campaigning for the British victims, said: "This is a very important and significant development. We have been trying to convince the company that it is ethically right and in their self-interests to do the decent thing and secure a settlement so British victims get a deal [similar to that] given to US victims."
But he said the company continued to deny liability. Mr Lamb also accused the UK government of failing to negotiate a settlement. "Ministers made promising noises then after a meeting between the Government and the company they weakened their position. I believe that the ministers came under pressure from the company and their own civil servants to shut up."
The ruling by the Federal Court in Melbourne is a major breakthrough for hundreds of Australians. The court ordered the company to pay £172,300 to Graeme Peterson, 59, who has been unable to work since a heart attack in 2003. At least 600 other Australians will now lodge compensation claims against Merck Sharpe and Dohme, which faces a bill of up to $300m, according to Peter Gordon, Mr Peterson's lawyer, whose law firm, Slater & Gordon, took on Mr Peterson's case for no fee.
Even more serious for Merck are the global implications: Vioxx was taken by more than 80 million people worldwide before it was recalled in 2004, and lawyers in several countries were awaiting the outcome of the Australian litigation. Mr Gordon said: ...
Friday, March 5, 2010
New Suspect In Gulf War Syndrome
By Dr. Douglas Fields, Posted: March 3, 2010 02:25 PM
Washington, D.C.-- On February 26, 2010, the Veterans Affairs Department announced that it will re-examine the disability claims of thousands of Persian Gulf War veterans still suffering from the mysterious Gulf War illnesses two decades after the war ended. At a meeting of the Federal Advisory Committee on Gulf War Veteran's Illnesses held yesterday in Washington, D.C., scientists from around the country presented their latest research to committee members searching for clues to this mysterious illness. Early in the meeting a new culprit emerged -- "the other brain" -- the non-electric portion of the brain composed of brain cells called glia.
"This is one of the best explanations I've heard," commented distinguished neuroscientist Floyd Bloom, after a presentation by Dr. Linda Watkins of the University of Colorado speaking about her latest research showing that glial cells, called microglia, are the unsuspected agents in chronic pain and drug addiction. Previously neurons were thought to be the sole cause of chronic pain and morphine tolerance. However, the new insight into how these "immune cells" of the brain aggravate neurons after an injury by releasing substances that produce excruciating pain, a parallel with Gulf War Syndrome became apparent.
Gulf War syndrome is characterized by a collection of unexplained symptoms, many of them neurological, including chronic pain, chronic fatigue, depression, sleep disturbances, memory loss, as well as gastrointestinal and lung problems. A number of causes have been suspected, including exposure to low-level neurotoxins, including sarin gas, drugs taken to protect soldiers from biological and chemical warfare agents, pesticides used to treat tents and soldier's uniforms stationed in the desert, depleted uranium from munitions, and the toxic mixture of fumes released for a year after the war ended from oil fields set ablaze by the retreating Iraq soldiers. The toxic fumes blotted out the sun at midday for miles.
Many people suffer chronic pain after an injury. Unlike normal pain, chronic pain does not end after the injury heals; in fact it often gets worse. The latest research shows that chronic pain results from an interaction between the immune system and the brain. When we are sick, substances are released by the body that tell the brain to initiate the familiar "sickness response," which we have all experienced, for example when we catch the flu. Profound fatigue, headache, sensitivity to light and sound, and painful joints and muscles, drive us to bed. This sickness response forces us to rest and give the body the opportunity to fight the invading germ. This sounds a lot like the symptoms of many Gulf War veterans.
What Dr. Watkins suspects, based on her research on microglia in chronic pain, is that an initial exposure to some toxin "primes" the microglia in the brain to make them hyper alert. Then when a second infection, injury, or toxin is experienced, the brain's immune cells over-react, releasing too much of the chemical signals that cause the "sickness response", and they do not stop releasing the substances after the body heals. In the case of Gulf War veterans, the "initial trigger" could have been a reaction to an immunization, stress, or exposure to low-level toxins. Later a second insult to the body unleashes a run-away illness. Research from several labs on microglia in chronic pain has identified many steps in this neuro-immune signaling process that become disrupted and researchers have found specific drugs to restore the normal function of these pain circuits, thus ending the chronic pain. Most of this work is in laboratory animals but clinical studies are now under way.
In my overview to the committee on the four major kinds of glial cells in "the other brain", several other ways in which glia could be involved in Gulf War illnesses were recognized. This includes the involvement of glial cells, called astrocytes, in processing toxins in the brain. Parkinson's disease, for example can be caused by astrocytes acting on a foreign substance (a recreational drug), and converting it into a toxin that kills the neurons that die in Parkinson's Disease. Astrocytes also release factors that protect neurons from damage caused by inflammation or oxidation, and they release growth factor proteins that stimulate the growth and repair of neurons.
The latest research on the myelin insulation on nerve fibers in the brain, which is essential for sending electrical signals, is revealing a previously unsuspected role of myelin in cognition and psychiatric illness. Myelin insulation is especially vulnerable to blast injuries and to autoimmune diseases in which the body's immune system attacks the myelin sheath. The myelin sheath is made by a type of glial cell, called an oligodendrocyte. Prevously this insulation was of interest in diseases such as multiple sclerosis, but because the insulation speeds the rate of electrical transmission through nerve fibers (axons), myelin is now understood to have an important role in cognitive function, psychological illness, and learning.
One of the reasons the Gulf War Syndrome may have been so difficult to understand is that glia--the other brain--has itself been such a mystery until recently.
Washington, D.C.-- On February 26, 2010, the Veterans Affairs Department announced that it will re-examine the disability claims of thousands of Persian Gulf War veterans still suffering from the mysterious Gulf War illnesses two decades after the war ended. At a meeting of the Federal Advisory Committee on Gulf War Veteran's Illnesses held yesterday in Washington, D.C., scientists from around the country presented their latest research to committee members searching for clues to this mysterious illness. Early in the meeting a new culprit emerged -- "the other brain" -- the non-electric portion of the brain composed of brain cells called glia.
"This is one of the best explanations I've heard," commented distinguished neuroscientist Floyd Bloom, after a presentation by Dr. Linda Watkins of the University of Colorado speaking about her latest research showing that glial cells, called microglia, are the unsuspected agents in chronic pain and drug addiction. Previously neurons were thought to be the sole cause of chronic pain and morphine tolerance. However, the new insight into how these "immune cells" of the brain aggravate neurons after an injury by releasing substances that produce excruciating pain, a parallel with Gulf War Syndrome became apparent.
Gulf War syndrome is characterized by a collection of unexplained symptoms, many of them neurological, including chronic pain, chronic fatigue, depression, sleep disturbances, memory loss, as well as gastrointestinal and lung problems. A number of causes have been suspected, including exposure to low-level neurotoxins, including sarin gas, drugs taken to protect soldiers from biological and chemical warfare agents, pesticides used to treat tents and soldier's uniforms stationed in the desert, depleted uranium from munitions, and the toxic mixture of fumes released for a year after the war ended from oil fields set ablaze by the retreating Iraq soldiers. The toxic fumes blotted out the sun at midday for miles.
Many people suffer chronic pain after an injury. Unlike normal pain, chronic pain does not end after the injury heals; in fact it often gets worse. The latest research shows that chronic pain results from an interaction between the immune system and the brain. When we are sick, substances are released by the body that tell the brain to initiate the familiar "sickness response," which we have all experienced, for example when we catch the flu. Profound fatigue, headache, sensitivity to light and sound, and painful joints and muscles, drive us to bed. This sickness response forces us to rest and give the body the opportunity to fight the invading germ. This sounds a lot like the symptoms of many Gulf War veterans.
What Dr. Watkins suspects, based on her research on microglia in chronic pain, is that an initial exposure to some toxin "primes" the microglia in the brain to make them hyper alert. Then when a second infection, injury, or toxin is experienced, the brain's immune cells over-react, releasing too much of the chemical signals that cause the "sickness response", and they do not stop releasing the substances after the body heals. In the case of Gulf War veterans, the "initial trigger" could have been a reaction to an immunization, stress, or exposure to low-level toxins. Later a second insult to the body unleashes a run-away illness. Research from several labs on microglia in chronic pain has identified many steps in this neuro-immune signaling process that become disrupted and researchers have found specific drugs to restore the normal function of these pain circuits, thus ending the chronic pain. Most of this work is in laboratory animals but clinical studies are now under way.
In my overview to the committee on the four major kinds of glial cells in "the other brain", several other ways in which glia could be involved in Gulf War illnesses were recognized. This includes the involvement of glial cells, called astrocytes, in processing toxins in the brain. Parkinson's disease, for example can be caused by astrocytes acting on a foreign substance (a recreational drug), and converting it into a toxin that kills the neurons that die in Parkinson's Disease. Astrocytes also release factors that protect neurons from damage caused by inflammation or oxidation, and they release growth factor proteins that stimulate the growth and repair of neurons.
The latest research on the myelin insulation on nerve fibers in the brain, which is essential for sending electrical signals, is revealing a previously unsuspected role of myelin in cognition and psychiatric illness. Myelin insulation is especially vulnerable to blast injuries and to autoimmune diseases in which the body's immune system attacks the myelin sheath. The myelin sheath is made by a type of glial cell, called an oligodendrocyte. Prevously this insulation was of interest in diseases such as multiple sclerosis, but because the insulation speeds the rate of electrical transmission through nerve fibers (axons), myelin is now understood to have an important role in cognitive function, psychological illness, and learning.
One of the reasons the Gulf War Syndrome may have been so difficult to understand is that glia--the other brain--has itself been such a mystery until recently.
Thursday, March 4, 2010
Another £164,000 wasted on silly psycho therapy
2nd March 2010
Media Release
£164,000 awarded for new research into the treatment of a chronic childhood condition
A research study looking into interventions and treatment options for a chronic childhood condition has been awarded funding of £164,000 by the Linbury Trust and the Ashden Trust.
The funding has been awarded to a research team led by Dr Esther Crawley, Consultant Paediatrician at the Royal National Hospital for Rheumatic Diseases NHS Foundation Trust, also known as the Min, and Senior Lecturer at the University of Bristol.
Esther and her team will carry out a pilot project to investigate whether it is possible to look at two different approaches to the intervention and treatment of Chronic Fatigue Syndrome/ME (CFS/ME) in Children.
<...>
The team will carry out a pilot project to investigate how to recruit to a randomised controlled trial looking at the Phil Parker Lightning Process® and specialist medical care.
Media Release
£164,000 awarded for new research into the treatment of a chronic childhood condition
A research study looking into interventions and treatment options for a chronic childhood condition has been awarded funding of £164,000 by the Linbury Trust and the Ashden Trust.
The funding has been awarded to a research team led by Dr Esther Crawley, Consultant Paediatrician at the Royal National Hospital for Rheumatic Diseases NHS Foundation Trust, also known as the Min, and Senior Lecturer at the University of Bristol.
Esther and her team will carry out a pilot project to investigate whether it is possible to look at two different approaches to the intervention and treatment of Chronic Fatigue Syndrome/ME (CFS/ME) in Children.
<...>
The team will carry out a pilot project to investigate how to recruit to a randomised controlled trial looking at the Phil Parker Lightning Process® and specialist medical care.
Wednesday, March 3, 2010
XMRV, 'CFS' and M.E. part 2
Anonymous said:
"I am disappointed in Sarah Shenk. It is discouraging to read rubbish like this from a respected charity like Hummingbird Foundation. It appears Shenk has gone out of her way to remain UN-informed about the Nevada cohort and other patients in the WPI study. The effect of her prejudice against the study is to jeer and denigrate the patients themselves. Shenk is colluding in 'us and them' defamation typical of abusive people anywhere. This offensive essay is beneath the dignity of the respected Hummingbird Foundation and does tarnish their good name and reputation.
The Incline Village outbreak was an ME outbreak - even minimal knowledge of the controversial history and events of that period, and the CDC's mishandling of the outbreak, shows that doctors well-informed about ME, Dr. Hyde and colleagues, had diagnosed the patients as having ME - and walked out of the experts' meeting at the CDC in disgust at CDC manipulation of events and plans to derisively name the outbreak as 'CFS' instead of ME. The result of CDC manipulation was that no patients in the US and few in Canada have been diagnosed with ME since that time - North American doctors simply do no use that diagnosis, and instead follow the directives of the malicious CDC and diagnose ME patients with 'CFS'.
However, it slanders and betrays patients all over North America to pretend that very sick patients don't have ME just because their dianosis is called 'CFS' instead. It's not the patients' fault that the CDC travesty of misnaming this disease in North America has persisted for so long.
Moreover, the WPI study cohort included patients from many countries - when the study results were unblinded in December (see video of Mikovits lecture in January for her report of this data), Mikovits found that there were patients from all over North America as well as Australia, UK, Ireland, Germany and elsewhere in their published Science study. These were patients who had travelled across their country or across the world to see the handful of ME-CFS doctors in North America who are experts in this disease (the real disease, not the 'Oxford' definition travesty), and have been treating patients for years. Anyone claiming to represent a respected ME charity should have done their homework and known this.
Or does Shenk suppose that no ME patients exist in North America? Or that no patients have developed ME since the late 1980s when the CDC took it's fateful turn into 'CFS' politics? Does Shenk suppose ME exists only in Commonwealth countries that she and her mates approve of, those that still have doctors who use the ME diagnosis?
This essay is appalling. Shame on Shenk and the once-noble Hummingbird Foundation for releasing it."
"I am disappointed in Sarah Shenk. It is discouraging to read rubbish like this from a respected charity like Hummingbird Foundation. It appears Shenk has gone out of her way to remain UN-informed about the Nevada cohort and other patients in the WPI study. The effect of her prejudice against the study is to jeer and denigrate the patients themselves. Shenk is colluding in 'us and them' defamation typical of abusive people anywhere. This offensive essay is beneath the dignity of the respected Hummingbird Foundation and does tarnish their good name and reputation.
The Incline Village outbreak was an ME outbreak - even minimal knowledge of the controversial history and events of that period, and the CDC's mishandling of the outbreak, shows that doctors well-informed about ME, Dr. Hyde and colleagues, had diagnosed the patients as having ME - and walked out of the experts' meeting at the CDC in disgust at CDC manipulation of events and plans to derisively name the outbreak as 'CFS' instead of ME. The result of CDC manipulation was that no patients in the US and few in Canada have been diagnosed with ME since that time - North American doctors simply do no use that diagnosis, and instead follow the directives of the malicious CDC and diagnose ME patients with 'CFS'.
However, it slanders and betrays patients all over North America to pretend that very sick patients don't have ME just because their dianosis is called 'CFS' instead. It's not the patients' fault that the CDC travesty of misnaming this disease in North America has persisted for so long.
Moreover, the WPI study cohort included patients from many countries - when the study results were unblinded in December (see video of Mikovits lecture in January for her report of this data), Mikovits found that there were patients from all over North America as well as Australia, UK, Ireland, Germany and elsewhere in their published Science study. These were patients who had travelled across their country or across the world to see the handful of ME-CFS doctors in North America who are experts in this disease (the real disease, not the 'Oxford' definition travesty), and have been treating patients for years. Anyone claiming to represent a respected ME charity should have done their homework and known this.
Or does Shenk suppose that no ME patients exist in North America? Or that no patients have developed ME since the late 1980s when the CDC took it's fateful turn into 'CFS' politics? Does Shenk suppose ME exists only in Commonwealth countries that she and her mates approve of, those that still have doctors who use the ME diagnosis?
This essay is appalling. Shame on Shenk and the once-noble Hummingbird Foundation for releasing it."
Tuesday, March 2, 2010
XMRV, 'CFS' and M.E.
Copyright © Sarah Shenk Febraury 2010. From www.hfme.org
There has been much media publicity lately over a small research study that claims to have made a connection between “CFS,” or "ME/CFS", and a retrovirus. While many are touting this as a huge medical breakthrough, there is a large group of doctors, scientists, patients and advocates who look at this information with tempered enthusiasm.
Why? These people are well-versed on the topic, and realize that before moving forward with great jubilation, more information is required. We realize that this research in and of itself, means precious little, so we have not only adopted a more "wait and see" attitude, but are of the opinion that this research is most likely relatively unimportant in the scheme of things and would not place it anywhere near the top of the list in the arena of much needed new M.E. research. We also worry that this research, and the sensationalism with which it is being reported, will detract from the need for genuine M.E. research.
The following comments from M.E. researchers, patients and advocates may help you understand better the "wait and see" attitude these folks have, and why it is so appropriate.
Additionally, as you consider the following insightful comments, please keep in mind what the Whittemore Peterson Institute itself says about the blood samples used in their recent retrovirus study:
"Dr. Peterson has a repository of samples from the original out break in Incline Village, Nevada which also includes longitudinal samples taken from patients from the 1980's through 2005. None of these samples were used in the XMRV study."
Reference link: WPI website
Thus we actually have no way of knowing if any M.E. patients were involved in the study at all, and that makes the results suspect to those of us who do have M.E. Knowing what we know about the wastebasket label "CFS", it makes us feel that the results of this study may not ever come to have any real value at all for M.E. patients, nor for many of those given a ‘CFS’ misdiagnosis. Perhaps the following comments, taken from an informal group discussion, will shed some light on a few of the reasons we need to consider this research with a healthy dose of skepticism.
There has been much media publicity lately over a small research study that claims to have made a connection between “CFS,” or "ME/CFS", and a retrovirus. While many are touting this as a huge medical breakthrough, there is a large group of doctors, scientists, patients and advocates who look at this information with tempered enthusiasm.
Why? These people are well-versed on the topic, and realize that before moving forward with great jubilation, more information is required. We realize that this research in and of itself, means precious little, so we have not only adopted a more "wait and see" attitude, but are of the opinion that this research is most likely relatively unimportant in the scheme of things and would not place it anywhere near the top of the list in the arena of much needed new M.E. research. We also worry that this research, and the sensationalism with which it is being reported, will detract from the need for genuine M.E. research.
The following comments from M.E. researchers, patients and advocates may help you understand better the "wait and see" attitude these folks have, and why it is so appropriate.
Additionally, as you consider the following insightful comments, please keep in mind what the Whittemore Peterson Institute itself says about the blood samples used in their recent retrovirus study:
"Dr. Peterson has a repository of samples from the original out break in Incline Village, Nevada which also includes longitudinal samples taken from patients from the 1980's through 2005. None of these samples were used in the XMRV study."
Reference link: WPI website
Thus we actually have no way of knowing if any M.E. patients were involved in the study at all, and that makes the results suspect to those of us who do have M.E. Knowing what we know about the wastebasket label "CFS", it makes us feel that the results of this study may not ever come to have any real value at all for M.E. patients, nor for many of those given a ‘CFS’ misdiagnosis. Perhaps the following comments, taken from an informal group discussion, will shed some light on a few of the reasons we need to consider this research with a healthy dose of skepticism.
Monday, March 1, 2010
Doctors do not know how to treat pain
By Jane Dreaper
Health correspondent, BBC News, Monday, 1 March 2010
Chronic pain needs to be recognised as a disease in its own right, experts say.
The hospital doctors and academics argue this would lead to more momentum for official strategies and funding to help patients.
Nearly 8m people in the UK are suffering ongoing problems with pain.
But only 2% of them end up seeing specialists - and a quarter believe their doctors do not know how to treat their pain, research shows.
Prescriptions worth a total of £584m are written every year for painkillers.
And pain - including back problems - is the second most common reason cited by incapacity benefit claimants for not working.
Dr Beverly Collett, a consultant in pain medicine from University Hospitals of Leicester and chairman of the Chronic Pain Policy Coalition campaign group , said: "This problem has huge ramifications for society as a whole. Pain is difficult to treat.
"Many patients are seeking reasons for what is behind the pain - but in the vast majority of cases, you can't find one.
"We are trying to get it taken more seriously - and there's a push, particularly in Europe, to say it is a disease in its own right."
Researchers are examining the idea that changes in the spinal cord and brain have the effect of maintaining pain in sufferers, making it an ongoing problem that can lead to depression or anxiety.
Experts believe more training would help GPs in assessing the severity of patients' pain.
Non-medical interventions such as physiotherapy and encouraging patients to stay active can also play a role, with some work showing that distraction can help patients avoid feeling pain.
Professor Steve McMahon, from the Wolfson Centre of Age Related Diseases at King's College London, said the number of new drugs developed to treat pain in the past decade was "very small".
But he said there was interest in the latest trials of a drug called Tanezumab, which might help treat knee and hip pain resulting from osteoarthritis.
Another expert, Irene Tracey, Nuffield professor of anaesthetic science at Oxford University, said: "There is a cultural problem where it's thought that there is a benefit from suffering.
"We have to get over this. It's not acceptable for people to suffer significant pain in the 21st century."
Health correspondent, BBC News, Monday, 1 March 2010
Chronic pain needs to be recognised as a disease in its own right, experts say.
The hospital doctors and academics argue this would lead to more momentum for official strategies and funding to help patients.
Nearly 8m people in the UK are suffering ongoing problems with pain.
But only 2% of them end up seeing specialists - and a quarter believe their doctors do not know how to treat their pain, research shows.
Prescriptions worth a total of £584m are written every year for painkillers.
And pain - including back problems - is the second most common reason cited by incapacity benefit claimants for not working.
Dr Beverly Collett, a consultant in pain medicine from University Hospitals of Leicester and chairman of the Chronic Pain Policy Coalition campaign group , said: "This problem has huge ramifications for society as a whole. Pain is difficult to treat.
"Many patients are seeking reasons for what is behind the pain - but in the vast majority of cases, you can't find one.
"We are trying to get it taken more seriously - and there's a push, particularly in Europe, to say it is a disease in its own right."
Researchers are examining the idea that changes in the spinal cord and brain have the effect of maintaining pain in sufferers, making it an ongoing problem that can lead to depression or anxiety.
Experts believe more training would help GPs in assessing the severity of patients' pain.
Non-medical interventions such as physiotherapy and encouraging patients to stay active can also play a role, with some work showing that distraction can help patients avoid feeling pain.
Professor Steve McMahon, from the Wolfson Centre of Age Related Diseases at King's College London, said the number of new drugs developed to treat pain in the past decade was "very small".
But he said there was interest in the latest trials of a drug called Tanezumab, which might help treat knee and hip pain resulting from osteoarthritis.
Another expert, Irene Tracey, Nuffield professor of anaesthetic science at Oxford University, said: "There is a cultural problem where it's thought that there is a benefit from suffering.
"We have to get over this. It's not acceptable for people to suffer significant pain in the 21st century."
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