Government Propaganda Masqueraded as Science

by Robert Whitaker, psychologytoday.com, March 25, 2011:

Five years ago, Maryland psychologist Ed Pigott read the first published results of the NIMH's large STAR*D study of antidepressants and depression.

However, even as he read that first article, he got the sense that "significant researcher trickery was afoot." Since then he has systematically exposed the trickery, piece by piece.

His latest article on the study, "STAR*D: A Tale and Trail of Bias," has just been published in Ethical Human Psychology and Psychiatry. He is also now blogging about his findings on madinamerica.com, and has posted documents there that he relied upon in his "deconstruction" of the $35 million study.

I. The study was designed to produce an inflated "remission" rate

II. Various statistical manipulations were used to inflate the reported "remission" rate

III. In its press releases, the NIMH further hyped the already inflated results

Read more>>

Sounds very much like the Silly PACE Trial and other CBT research to ME ...

Got a headache take an aspirin, but what do people with retroviruses get currently ?

POSTED BY ABOUT ME_CFS_UNITE:

the bottom line is that we "are testing Positive" and legitimate medical research to help us needs to be done because a retrovirus, no matter how you got it, is a dangerous thing and needs to be treated ASAP. Got a headache take an aspirin, but what do people with retroviruses get currently ?

Nada, unless they choose try some of the old HIV drugs because real current serious research to help us has NO Place to be budgeted for and done. Only HIV and HTLV-1 and 2 seem to be legit. Humm funny.. Wonder why ?

If Trine or Dr. Oz or any other wealthy politician had a new human retrovirus how much you wanna bet that the research money would suddenly show up ? Think they would wait for 25 yrs and for 17 million to get it ? I would not want to wish this illness on anyone, but seriously folks, someone had better start "getting REAL" pretty darn fast ! Read more>>

First study of organ donation by CFS patients who did NOT have CFS reported in Transplantation

by The CFIDS Association of America on Sunday, March 27, 2011:

In the April 15, 2011 issue of the journal Transplantation, Rajeev Desai and James Neuberger of the NHS Blood and Transplant (United Kingdom) report the results of a small retrospective study of 10 deceased solid organ donors who had been diagnosed with CFS (as defined by Fukuda) and the health of the recipients of their organs. In a Letter to the Editor, Desai and Neuberger state that none of the 18 organ recipients had developed CFS in the post-transplant follow-up period (average 38 months, range 15-71 months). The donors had donated a total of 27 organs: 17 kidneys, 6 livers, 2 lungs, 1 heart and 1 pancreas.

They conclude with the suggestion that there is no justification for excluding those with CFS from organ donation, due to the shortage of organs and significant mortality of those awaiting transplants.

The authors acknowledge the conflicting evidence for XMRV infection in CFS and indicate that transmission of viruses by solid-organ transplantation is well-recognized in cases of hepatitis B and C and HIV. There is generally more aggressive disease in the recipient than there was in the donor due to immunosuppression. This study was aimed at whether organ transplants could transmit CFS. In this particular study, the CFS patients who donated organs were deceased, so the impact of transplantation on the donor was not evaluated or addressed.

Safety of Solid-Organ Transplantation from Donors with Chronic Fatigue Syndrome. Desai R, Neuberger J. Transplantation. Vol. 91, No. 7. 2011 Apr 15: e51-52.

A quote from the article: "Because of the retrospective nature of our analysis, the robustness of the diagnosis of CFS could not be established."

Julia said: However, I would say that this study is severely flawed in that ALL Transplant patients are put on Valcyte (except for Liver transplants) for at least 6 months. Of Course there will be no CFS development for at least 12 months. What about HHV-6, CMV and EBV..... what were the before and after titers?

Were any donors or recipients tested for XMRV infection ? NO.

See also: PACE trial results are out: ME is caused by an oncogenic virus or The putative agent of ME/CFS can be transferred to monkeys.

Professor, scientific studies show 99% of men would like to be a tablecloth

By AS: Its the only chance they get of being laid 3 times a day & pulled off last thing at night.

AIDS-like retrovirus threatens koalas with extinction

By John Platt, Scientific American:

Koalas (Phascolarctos cinereus) may be one of the world's cuter critters, but that doesn't mean they have it easy.

Not only have koala populations become heavily fragmented due to habitat loss, they face numerous threats that they never encountered before: household cats and dogs frequently kill koalas; hundreds die every year after being run over by cars and trucks; and now a deadly virus is spreading to koalas throughout Australia.

The koala retrovirus, which infects and alters the animal's DNA, has been linked to a variety of diseases and medical problems, including leukemia, bone marrow failure, cancer and AIDS-like immune deficiencies. First found in 2000, the retrovirus is already forcing some smaller koala populations into extinction, says Jon Hanger, director of research and ecological services at the Australian Wildlife Hospital. Hanger was the first person to genetically sequence the koala retrovirus after its discovery.

Hanger equates the koala retrovirus with the deadly devil facial tumor disease (DFTD) devastating the world's Tasmanian devils (Sarcophilus harrisii), which many fear may soon drive that species into extinction. He has called for support akin to that given to help protect the devils to stop the spread of the koala retrovirus. "Twenty-two million dollars has been committed by government to manage the contagious cancer afflicting Tasmanian devils. The koala disease epidemic is just as devastating but we know little about it," Hanger recently told Brisbane's Courier–Mail. Read more>>

Severely disabled Abbie Dorn wins the right to spend time with her children

By Maria L. La Ganga, Los Angeles Times, March 26, 2011:

After an acrimonious yearlong legal battle, a Los Angeles County Superior Court judge ruled Friday that a paraplegic woman who communicates largely by blinking has a legal right to see her 4-year-old triplets.

In a 10-page tentative ruling, Los Angeles County Superior Court Judge Frederick C. Shaller said that even though Abbie Dorn, 34, "suffers from a profound brain injury that had led to her near total and complete disability," it would be in the children's best interests to have a relationship with their mother.

"The court finds that even though [Abbie] cannot interact with the children, the children can interact with [Abbie] — and that the interaction is beneficial for the children," Shaller wrote. "They can touch her, see her, bond with her, and can carry those memories with them."

In fact, he wrote, if the children cannot develop a relationship with Dorn, "the court finds that they will likely suffer psychological harm that will negatively affect their development and their relationship with their father." Read more>>

See also: The Diving Bell and the Butterfly, Patients who are conscious but almost entirely paralysed could be aided by French research that reads their brain

A water contamination case in Woburn, the American Camelford ?

From Wikipedia, the free encyclopedia:

This article is about the novel. For the film, see A Civil Action (film).
A Civil Action

Author Jonathan Harr
Country United States
Language English
Genre(s) Non-Fiction
Publisher Vintage
Publication date August 27, 1996
Media type Print (Hardcover and Paperback)
ISBN ISBN 0-679-77267-7
OCLC Number 35587711
LC Classification KF228.A667 H37 1996
Followed by The Lost Painting: The Quest for a Caravaggio Masterpiece
A Civil Action is a 1996 work of non-fiction by Jonathan Harr depicting a water contamination case in Woburn, Massachusetts in the 1980s. The book became a best-seller and won the National Book Critics Circle Award for nonfiction.
The case is Anderson v. Cryovac. The first reported decision in the case is at 96 F.R.D. 431 (denial of defendants' motion to dismiss).
A film by the same name based on the book was produced in 1998, starring John Travolta as Jan Schlichtmann and Robert Duvall as Jerome Facher.
Plot summary

After finding her child is diagnosed with leukemia, Anne Anderson begins to notice a high incidence of leukemia, which should be a relatively rare disease, in her city. Eventually she gathers other families and seeks a lawyer, eventually Jan Schlichtmann, to consider their options.
Though Schlichtmann originally agrees to take the case, the lack of evidence and a clear defendant results in it being ignored. Later picking up the case, Schlichtmann finds evidence suggesting trichloroethylene (TCE) contamination of the town's water supply by Riley Tannery, a subsidiary of Beatrice Foods; a chemical company W.R. Grace; and another company named Unifirst.
In the course of the lawsuit, Schlichtmann gets other attorneys to assist him. He spends lavishly as he had in his prior lawsuits, but the length of the discovery process and trial soon stretch his assets to their limit.
Though Unifirst settles for a little over $1 million, the money is immediately invested in the remaining case against Grace and Beatrice. The plaintiff's case against Grace was far stronger for two reasons: (1) Schlichtmann had personal testimony of a former employee of Grace who had witnessed dumping, and (2) a river between Beatrice's tannery and the contaminated wells made their contribution to the contamination less plausible. The case against Beatrice was dismissed. Though Schlichtmann's firm had anticipated a much higher settlement, the dire state of their finances forced the firm to accept settlement from W.R. Grace for $8 million.
Schlichtmann disbursed the settlement to the families, excluding expenses and attorney's fees. When some of the families thought Schlichtmann had overbilled expenses, he acquiesced and surrendered more of his fee. Schlichtmann would later file for bankruptcy after losing his condo and car and living in his office for a time.

A report from the Environmental Protection Agency later concluded that both companies had contaminated the wells based on new evidence from the sludge that had been removed from the site. Schlichtmann attempted in 1988 to reraise the case against Beatrice. The judge dismissed the case, citing testimony from Beatrice's soil chemist.


Medical Expert Witnesses:

Coffin, Dr. John: (hired by defense) said TCE would not hurt humans

WHAT ABOUT ME? new teaser-trailer

Greg Towers: No Evidence of XMRV or Related Retroviruses in a London HIV-1-Positive Patient Cohort

Eleanor R. Gray1*, Jeremy A. Garson1, Judith Breuer1, Simon Edwards2, Paul Kellam1,3, Deenan Pillay1, Greg J. Towers1:

1 Department of Infection and Immunity, University College London, London, United Kingdom, 2 Mortimer Market Centre, Camden Primary Care Trust, London, United Kingdom, 3 Pathogen Genetics, Wellcome Trust Sanger Institute, Cambridge, United Kingdom

Abstract Top

Background
Several studies have implicated a recently discovered gammaretrovirus, XMRV (Xenotropic murine leukaemia virus-related virus), in chronic fatigue syndrome and prostate cancer, though whether as causative agent or opportunistic infection is unclear. It has also been suggested that the virus can be found circulating amongst the general population. The discovery has been controversial, with conflicting results from attempts to reproduce the original studies.

Methodology/Principal Findings
We extracted peripheral blood DNA from a cohort of 540 HIV-1-positive patients (approximately 20% of whom have never been on anti-retroviral treatment) and determined the presence of XMRV and related viruses using TaqMan PCR. While we were able to amplify as few as 5 copies of positive control DNA, we did not find any positive samples in the patient cohort.

Conclusions/Significance
In view of these negative findings in this highly susceptible group, we conclude that it is unlikely that XMRV or related viruses are circulating at a significant level, if at all, in HIV-1-positive patients in London or in the general population.

Received: November 15, 2010; Accepted: February 21, 2011; Published: March 23, 2011


Funding: This work was undertaken at UCLH/UCL, which received a proportion of funding from the Department of Health's NIHR Biomedical Research Centres funding scheme. Additional funding was provided by a Wellcome Trust Senior Fellowship WT090940 to GJT and the Medical Research Council. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

* E-mail: e.gray@ucl.ac.uk

Full ARTICLE

My Note: typical for Greg Towers: "In view of these negative findings in this highly susceptible group, we conclude that it is unlikely that XMRV or related viruses are circulating at a significant level, if at all, in HIV-1-positive patients in London or in the general population."

"or in the general population": was the general population tested or in any way part of this study? NO, so more denial nonsense ...

PS: again NO culture done ...

PACE trial's Prof Peter White: Exercise causes Immunological damage in Chronic Fatigue Syndrome and is NOT safe

Prof Peter White, Prof A. J. Pinching, et al; JCFS 2004.pdf
The main finding of this pilot study was the elevated median concentration of transforming growth factor beta, which seemed to be related to activity. We also found significantly fewer CD3+ and CD4+ lymphocytes and fewer expressing HLA DR, but there was no difference between groups in response to exercise, but no importance should be attached to this in view of the small numbers of subjects in this study.

Finally, we found that exercise induced a sustained elevation in the concentration of TNF-α, which was still present three days later, and this only occurred in CFS patients.

TGF-β was grossly elevated when compared to controls before exercise, and showed no differential response to exercise, but did show an increase in response to the exercise entailed in getting to the study center.

These data replicate three out of four previous studies finding elevated TGF-β in subjects with CFS (6, 7, 9, 10).

These preliminary findings require replication in a larger single blind case-control study before we can judge their significance, particularly since we were aware of case-control status for some subjects.

These preliminary data suggest that “ordinary” activity (i.e., that involved in getting up and traveling some distance) may induce anti-inflammatory cytokine release (TGF-β), whereas more intense exercise may induce pro-inflammatory cytokine release (TNF-α) in patients with CFS (21, 28, 29).

The causal mechanisms involved and the direction of the relationship between these mechanisms remain to be elucidated. Altered cytokine balance, for example, following an infection, may modify the threshold at which cytokine release occurs with exercise or activity, setting up a vicious circle. These processes could contribute to the postexertional
malaise, myalgia and the central fatigue that characterize CFS (1, 2, 4). Future studies should study patients at truly resting baseline levels, over a longer time-course, and should examine gene expression of cytokines, as well as circulating levels (17).

My note: nothing of this sort was done in the BOGUS PACE trial yet this study and the PACE trial were done by Prof White !!
So this study clearly showed that GET is harmful, yet pacing is not !!

Also, why did the PACE trial NOT check any cytokines in their so called CFS patients ? Too many vested interest at stake so it seems ...

WHITE JCFS 2004.pdf
See also: PACE trial results are out: ME is caused by an oncogenic virus or The putative agent of ME/CFS can be transferred to monkeys or Professor of Psychology, Rhona Johnston shows that ME/CFS is NOT a psychological condition (on a UK Government website !!!) … a MUST READ

Symposium: ME-dical malPRACTICE in Belgium's ME/CFS reference centers

Symposium reference centers and CFS policy in Belgium: ME-dical malPRACTICE.

by XMRV Global Action on Friday, March 25, 2011:

Referentiecentra en CVS beleid in België: ME-dische wanPRAKTIJKEN.
Friday May 27, 2011
Antwerp, Belgium

http://www.hetalternatief.org/Symposium%20Antwerpen%202011.pdf

Thanks to cath for the link and to magnetronnie for the translation found here: http://www.mecfsforums.com/index.php/topic,6449.msg75020.html#new

Target audience:
This symposium is intended for politicians, journalists, doctors (insurance physicians, specialists, general practitioners) and patients who want to know about the far-reaching implications of the current (bio) psychosocial policy and the alternative, a medical-oriented approach (research, diagnosis and treatment) that has a much better better chance.

Speakers:
1. The scientific status of ME/CFS.
Maes: biomedical explanation of ME/CFS.
Twisk: CBT/GET as treatment for ME/CFS.

2. The power and impotence of the (bio) psychosocial school.
Hugaerts: theory and practice (RIZIV = institute for social security in Belgium).
Uyttersprot: about opposition by the RIZIV.
Coucke: about the medical practice and opposition
De Bock: about the objectives of the "wake-up call" movement.

3. The effects of malpractice of the current approach.
Maes: about fraud committed by the Belgian government.

NIH's State of the Knowledge conference on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, April 7-8

NIH's State of the Knowledge conference on Myalgic Encephalomyelitis:
Workshop Overview

Chronic fatigue syndrome (CFS), also referred to as myalgic encephalomyelitis (ME), is a poorly-defined, debilitating disease that affects roughly 17 million people worldwide (1 to 4 million in the United States) and it is diagnosed 2 to 4 times more often in women. Research on ME/CFS has been hampered by the lack of a universally accepted case definition, etiological agent, diagnostic criteria, or treatment.

The workshop will bring together subject matter experts who will discuss multiple aspects of ME/CFS, including epidemiology, etiology, pathophysiology, diagnosis and treatment. The workshop panelists will identify gaps in knowledge and opportunities for advancing biomedical research.

Investigators interested in pursuing research on ME/CFS are particularly encouraged to attend. This workshop is open to the public and will be webcast.

Sponsored by
The Office of Research on Women's Health,
National Institutes of Health (NIH)
In collaboration with
The Trans-NIH ME/CFS Research Working Group
If you have any questions, call (703) 925-9455 ext. 0 or e-mail icg@infinityconferences.com

Preliminary Agenda



Day 1 – Thursday, April 7

8:00 – 8:05
Welcoming

8:05 – 8:15
Opening

8:15 – 9:15
Plenary talks

9:15 – 10:45
Infectious diseases

10:45 – 11:00
Morning break

11:00 – 12:15
Systems biology

12:15 – 1:00
Lunch (on your own)

1:00 – 2:00
Immunology

2:00 – 3:15
Neurology

3:15 – 3:30
Afternoon break

3:30 – 5:00
Exercise physiology and energy metabolism



Day 2 – Friday, April 8

8:00 – 8:15
Reconvene

8:15 – 10:20
Diagnosis and biomarkers

10:20 – 10:35
Morning break

10:35 – 12:30
Treatment

12:30 – 1:30
Lunch (on your own)

1:30 – 2:30
Communication outreach

2:30 – 2:45
Afternoon break

2:45 – 4:45
Summary and conclusions

4:45 – 5:00
Closing
Thanks to Frank Twisk: hetalternatief.org

Budget boost for clinical trials

Ben Goldacre, The Guardian, Saturday 26 March 2011:

Very occasionally, a government will do something awesomely good. The budget contains plans for a unified Health Research Regulatory Agency to streamline the regulations on clinical trials, and so make them cheaper and easier to run.

It's motivated, disappointingly, by a desire to make the UK a more attractive location for commercial trials. But this is the first time a government has shown signs of seriously addressing one of the most serious ethical problems in medicine: the harm done to patients by ethics committees and regulators.

There is a bizarre paradox in medicine. When there is no evidence on which treatment is best, out of two available options, then you can choose one randomly and be subject to no special safeguards.

If, however, you decide to randomise and so generate new knowledge to improve treatments, then a world of administrative obstruction opens up.

This is not an abstract problem. Here is one example. For years in A&E, patients with serious head injuries were often treated with steroids, in the reasonable belief this would reduce swelling, and so reduce crushing damage to the brain.

But researchers wanted to randomise unconscious patients receiving steroids, or no steroids. to find out which was most effective. This was called the CRASH trial, a famously hard-fought battle with ethics committees, even though both treatments – steroids and no steroids – were in routine use. When approval was granted, it turned out steroids were killing patients.

Only a trial could give us this information. Head injury is common. Patients died unnecessarily while we waited for this trial to be approved.

But it wasn't just the delay to getting the trial approved. Read more>>

Is autism a disease of synaptic function?

By Shari Roan, Los Angeles Times, March 25, 2011:

The synapses are areas in the brain that permit messages to travel from cell to cell through chemicals called neurotransmitters. A study published this week suggests that autism may caused by faulty synapses.

The new study was launched with the knowledge that some genes seem to contribute to autism, including a gene called shank3 that is found in the synapses. Researchers led by Guoping Feng, a professor of brain and cognitive sciences at the McGovern Institute for Brain Research at MIT, decided to test the concept that autism may be caused by dysfunctional synapses. By mutating just the shank3 gene, they were able to produce mice that possessed two key autism traits: compulsive, repetitive behavior and avoidance of social interaction.

"They're just not interested in interacting with other mice," Feng said in a news release.

Developing an autistic mouse is an important step in research because doctors can now study the specific neural circuits that seem to be involved in the behaviors. Moreover, the mouse model allows for testing drugs before trying them on human patients.

Not every person with autism has a shank3 mutation, the study's authors noted. However, it's possible that other gene mutations found in people with autism impair synaptic function. If future studies verify that autism is a problem of faulty synapses, then medications that restore synaptic function may help resolve some symptoms.

HIV Integration requires use of a Host DNA-Repair pathway

ScienceDaily (Mar. 24, 2011): — The human immunodeficiency virus (HIV), the cause of AIDS, makes use of the base excision repair pathway when inserting its DNA into the host-cell genome, according to a new study led by researchers at the Ohio State University Comprehensive Cancer Center -- Arthur G. James Cancer Hospital and Richard J. Solove Research Institute.

Crippling the repair pathway prevents the virus from completing this critical step in the retrovirus's life cycle.

The findings offer potential new targets for novel anti-HIV drugs that may not lead as quickly to viral resistance as current drugs, the researchers say.


"HIV continues to develop resistance to current therapies," says first author Kristine Yoder, assistant professor of molecular virology, immunology and medical genetics.

"But the proteins we talk about in this paper are made by the cell, so drugs that target them might not lead to resistance as quickly as drugs that target viral proteins. And while targeting host proteins does have the potential for side effects, studies of mice suggest that targeting some of these genes may not lead to significant side effects." Read more>>