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Health : The MMR story that wasn't
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Posted by sylvia on Wednesday, July 18, 2007 (08:44:46)
The Guardian
By Ben Goldacre
Whatever you think about Andrew Wakefield, the real villains of the MMR scandal are the media. Just one week before his GMC hearing, yet another factless "MMR causes autism" news story appeared: and even though it ran on the front page of our very own Observer, I am dismantling it on this page. We're all grown-ups around here.
The story made three key points: that new research has found an increase in the prevalence of autism to one in 58; that the lead academic on this study was so concerned he suggested raising the finding with public heath officials; and that two "leading researchers" on the team believe that the rise was due to MMR. Within a week the story had been recycled in several national newspapers, and the news pages of at least one academic journal.
But where did the facts come from? I contacted the Autism Research Centre in Cambridge: the study the Observer reported is not finished, and not published. The data has been collected, but it has not been analysed. Unpublished data is the antithesis of what science is about: transparency, where anyone can appraise the methods, and the results, and draw their own conclusions.
This study is the perfect example of why this is important: it was specifically designed to look at how different methods of assessing prevalence affected the final figure. So it is no surprise that one of the results from an early analysis is high, "one in 58", using techniques which deliberately cast the widest net. But even other figures in the initial analysis were less dramatic, and similar to current estimates, and the Observer admits it was aware of them. It seems it simply cherry picked the single most extreme number and made it a front page splash story.
The Observer is unrepentant: it says it has the "final report", from 2005. I can't get it to show it to me but the Cambridge team suspect the paper has seen the last of the quarterly progress reports to the funders. So how did the Observer manage to crowbar MMR into this story?
First, it claimed that the lead researcher, Professor Simon Baron Cohen, "was so concerned by the one in 58 figure that last year he proposed informing public health officials in the county." Prof Cohen is clear: this is inaccurate and scaremongering.
And the meat? The Observer claims that "two of the academics, leaders in their field, privately believe that the surprisingly high figure [one in 58] may be linked to the use of the controversial MMR vaccine." This point is repeatedly reiterated, with a couple of other scientists disagreeing to create that familiar, illusory equipoise of scientific opinion which has fuelled the MMR scare in the media for almost a decade now.
But in fact, the two "leading experts" who were concerned about MMR, the "experts", the "leaders in their field", were not professors, or fellows, or lecturers: they were research associates. I rang both, and both were very clear that they wouldn't describe themselves as "leading experts". One is Fiona Scott, a psychologist and very competent researcher at Cambridge. She said to me: "I absolutely do not think that the rise in autism is related to MMR." And: "My own daughter is getting vaccinated with the MMR jab on July 17."
She also said, astonishingly, that the Observer never even spoke to her. And in the Observer's "readers' editor" column one whole week later, where the Observer half heartedly addressed some of the criticisms of its piece, the Observer persisted in claiming she believes MMR causes autism: it believes it knows the opinions of this woman better than she knows her own mind. Despite her public protestations. The only voice that Dr Scott could find - bizarrely - was in the online comments underneath the readers' editor piece, where the Observer continued to call her an MMR "dissenter", and where she posted an impassioned and slightly desperate message, protesting her support of MMR, and threatening legal action.
That's one of the leading experts. The other is Carol Stott. She does believe that MMR causes autism (at last). However, she is no longer even a "research associate" at the Autism Research Centre.
Carol Stott works in Dr Andrew Wakefield's private autism clinic in America, which the Observer failed to mention, and she was also an adviser to the legal team which failed in seeking compensation for parents who believed that MMR caused their child's autism, which the Observer failed to mention. She was paid £100,000 of public money for her services. She says her objectivity was not affected by the sum, but even so this seems an astonishing pair of facts for the Observer to leave out.
And were Stott's views private, or secret, or new? Hardly. Stott is so committed to the cause against MMR that when the investigative journalist Brian Deer exposed the legal payouts in 2004, although she had no prior contact with him, she spontaneously fired off a long series of sweary emails titled "game on": "Try me, shit head ... Believe me, you will lose ... so go fuck yourself. Got it yet shit head. Try me ... Twathead ... waiting ... oh yes ... Stick that where it feels good. Shit head ... well, ur a bit slow on the uptake ... Give it time I s'pose. Twat." And so on.
On the phone I genuinely warmed to her, and she regrets that many people have fallen into entrenched positions on MMR on both sides. But she's not a leading expert (as she herself agrees); she's not a sombre Cambridge academic suddenly expressing a fresh concern (her views are very public); and in any case, even she is very clear that this new research reported in the Observer would tell us nothing whatsoever about MMR causing autism.
Nothing has changed, and this scare will never be allowed to die. If we had the right regulatory structures, almost every section of the media would be in the dock, alongside Wakefield.
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Health : Legislation would extend medical coverage to more autism treatments
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Posted by Sylvia on Saturday, January 27, 2007 (17:55:44)
Charlotte Biz Journals
January 2007
Health insurers in New York would be forced to pay for additional medical and other health therapies to treat autistic children under legislation filed Tuesday.
State Assemblyman Peter Rivera, a Bronx Democrat, said insurers continue to be reluctant to cover a wide range of treatments that have shown some promise for autistic children. About 1 in 166 children are now diagnosed with some autism-related health condition.
People with autism do not develop properly emotionally or behaviorally. There is no cure for the condition.
Under Rivera's legislation, a panel of experts from the state departments of mental health and health would compile a list annually of treatment methods and their rates of success. Those that have proven to be successful would be added annually to the state insurance department's list of treatments that would have to be covered in New York.
Wendy Harnisher of the Capital District Biomedical Support Group for Autism Spectrum Disorders said she has found people everywhere who have had to choose between bankruptcy and losing their homes or getting the best available treatment for people with autism.
Pamela Finch of the Employer Alliance for Affordable Health Care said about 100 bills are filed each year in the New York state Legislature adding health insurance coverage mandates in the state. She said that her group is not opposed to providing adequate health care coverage, but she said the overall costs of those mandates have to be better tracked and studied.
The Employer Alliance for Affordable Health Care has been lobbying for years for the establishment of an independent commission to appraise the cost and effectiveness of the health care mandates imposed on insurers and employers in New York state.
Gov. Eliot Spitzer said he wants all uninsured New Yorkers to get coverage, starting with uninsured children, but that state leaders also have to be wary of the unaffordability of health care mandates.
Rivera is chairman of the mental health committee in the Assembly.
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Health : A stress-free pregnancy can deliver a popular child
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Posted by sylvia on Thursday, March 23, 2006 (17:18:48)
Daily Mail
By Tahira Yaqoob
All mothers-to-be wonder what kind of adult their baby will become.
Will their child grow into a sociable creature, for instance, bonding easily with others? Or will he or she struggle to make friends?
Scientists now believe they have discovered the key to ensuring a child's success in forming relationships - their mother must avoid stress while pregnant.
Experts think hormones produced by pregnant women have a direct impact on their children's future ability to socialise, communicate and develop language skills.
Stressed mothers-to-be produce more of the male hormone testosterone, thought to be responsible for poor people and communication skills and even the condition autism.
So the secret to having a more sociable baby is to relax during pregnancy, say researchers.
The impact of stress on babies in the womb from as early as 13 weeks is thought to be so great it can lead to children being slower at picking up language skills, finding it harder to form relationships and being more inclined to develop obsessional traits.
In the extreme, they could show symptoms of autism, a neurological condition characterised by a difficulty in developing relationships and being obsessed with routine.
Foetuses produce testosterone naturally but are also affected by levels of the hormone in the surrounding amniotic fluid which come from the mother.
Professor Simon Baron-Cohen, director of Cambridge University's autism research centre, revealed his findings yesterday at a conference in London examining whether women made better leaders.
His team studied 100 children, from early in the womb to the age of seven, to see how testosterone levels have affected their development.
They found that even 24 hours after being born, boys - who have up to ten times as much testosterone as girls - were showing less interest in people and more interest in mechanical objects than females.
At 12 months, babies with higher levels of the hormone in the womb had poor eye contact with their parents.
And at 18 months, children with high pre-natal testosterone could not talk or had a limited vocabulary while other youngsters spoke up to 600 words.
When they started school, children with higher levels were finding it more difficult to socialise.
Professor Baron-Cohen said while testosterone was partly genetic, it was also present in fluctuating amounts in the amniotic fluid.
He added: "The mother's level of stress is a factor in the testosterone level and makes it go up. We do not know what percentage of that level is genetic.
"What we do know is that the higher the level in the womb, the slower children are at making eye contact and developing language.
"Less testosterone means better human relationships. The differences may become even clearer as the children in our study get older."
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Health : Controversy over vitamin jab for autism
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Posted by sylvia on Saturday, December 17, 2005 (14:01:38)
Sunday Herald October 2005
By Rachelle Money
A Controversial vitamin injection claimed to help autistic children recover is to be promoted in Scotland by its American developer.
Dr James Neubrander, who will discuss the injection at a conference on autism in Edin burgh this week, has a private clinic in New Jersey where he says he has given more than 75,000 shots of methyl cobalamin B12 since May 2002, with, he claims, 94% of children showing improvement.
Methylcobalamin B12 is a type of vitamin B12 produced naturally by bacteria in the colon and then absorbed. Some scientists believe that people with autism are unable to absorb this material.
Neubrander said one injection is given every three days and the effects can be seen within five weeks. “My kids can lose their diagnosis [as autistic] within a year and a half to two and a half years and be in a normal classroom where nobody would know they had autism. When they stop the shots they regress in the same manner a diabetic who stops taking insulin would regress.
“When we first see these kids they can’t talk and now they are totally recovered. This is to the autism world what antibiotics was to the modern world.â€
However, he points out that he is not suggesting his injection is the only treatment.
“I believe in other treatments, like behavioural therapy and speech and language therapy and I tell my patients to continue with them.â€
Some UK doctors are already experimenting with the treatment, which is currently undergoing clinical trials in the US.
Dr Jean Monro, medical director of Breakspear Hospital in Hemel Hempstead in Hertfordshire, said the private hospital has been using the injections on autistic children for several months. She said: “I saw one boy in his early teens who, from having been a chap who couldn’t even sit down, can now co-operate with people. We’ve also not found any side-effects yet.â€
But other medics are sceptical. Dr Iain McClure, a consultant child and adolescent psychiatrist with NHS Argyll and Clyde, is scathing of Neubrander’s claims.
“Dr Neubrander’s website claims his study provides ‘scientific validation for use of methyl B12’ in autism. I feel this cannot be scientifically justified,†he said.
Neubrander’s paper, published last year, reports findings from a study which compared 20 autistic children to 33 healthy children .
But McClure said: “Crucially, the study does not demonstrate any scientific evidence of clinical improvement in the autistic profile of children following these injections.â€
However, a Hampshire mother whose seven-year-old son Alex has been having the injections – bought from a doctor in Chicago – since last November, claimed to have seen improvements. Christina Wood said: “We started to see more language, that’s been the biggest thing. He’d stutter at the start of a sentence but not anymore.â€
A spokesman for the National Autistic Society (NAS) said many interventions for the complex condition had been developed, with various claims of success. “An intervention that may help one individual may not be effective for another . It would not be appropriate for the NAS to recommend any one practice or therapy.â€
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Health : Psychopharmacology of Autism Spectrum Disorders
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Posted by sylvia on Saturday, August 06, 2005 (12:18:59)
Psychiatric Times
By Mark H. Lewis, Ph.D., and Martin Lazoritz, M.D.
Autism is a pervasive neurodevelopmental disorder characterized by difficulties in social interaction and language and communication, as well as the expression of restricted, repetitive behavior. Prevalence rates of autism have increased significantly, with some estimates in the range of one in 500 individuals affected. Although autism is highly heritable (as high as 90% concordance rate for monozygotic twins), the phenotype is quite variable. Moreover, a large number of potential genetic (e.g., chromosome 7) and environmental (e.g., toxins, viruses, food constituents) factors may be involved suggesting multiple, varying etiologies.
Thus, autism is an enormously heterogeneous disorder with a wide range of symptom expression across individuals as well as across disorders on the autism spectrum (high-functioning autism, Asperger's syndrome, pervasive developmental disorder not otherwise specified). In addition, up to 75% of individuals with autism function within the mental retardation range of intellectual development, whereas individuals with high-functioning autism or Asperger's syndrome can be highly intelligent. There is also significant comorbidity in this population, with affective and attention disorders commonly observed. All of these factors make effective pharmacological treatment a challenging proposition.
To add to the challenge, no medication is available that effectively treats the core social and communication deficits that define autism. As we shall illustrate in the following sections, that is not the case for restricted, repetitive behaviors. Nonetheless, current drug therapies have been termed palliative treatments (Gerlai and Gerlai, 2004), and behavioral interventions remain the mainstay of treatment. Thus, it is critical to focus on target symptoms or behaviors commonly associated with autism (e.g., aggression, anxiety) when discussing use of psychotropic agents.
As neither genetic nor environmental causes of autism have been identified, it has been difficult to firmly establish molecular mechanisms that would serve as potential targets for pharmacological intervention. Thus, medications that have been tested for efficacy in individuals with autism have been selected on the basis of their effectiveness in relevant disorders (e.g., obsessive-compulsive disorder, anxiety) or target symptoms (aggression, hyperactivity). These efficacy tests can be characterized by the paucity of well-controlled studies of pharmacological agents for specific symptoms or target behaviors. We will highlight some of these findings by drug class, with emphasis on the few available double-blind, placebo-controlled trials.
Antipsychotics
Historically, dopamine antagonists, particularly haloperidol (Haldol), were the mainstay of pharmacological treatment for individuals with autism (Campbell et al., 1978). Although haloperidol was reported to improve some symptoms of autism, including motor stereotypies, withdrawal and hyperactivity, its adverse effects limited its usefulness.
More recently, the atypical antipsychotics, particularly risperidone (Risperdal), have been widely used. The best evidence for the efficacy of risperidone in autism was the Research Units in Pediatric Psychopharmacology network study that involved a multisite trial of over 100 patients (McCracken et al., 2002). In this eight-week, double-blind, placebo-controlled study, 69% of patients were rated as much or very much improved versus 11% for placebo on the Clinical Global Impression-Improvement (CGI-I) scale at week 8. For the children with autism, there was a 57% decrease in Irritability subscale scores of the Aberrant Behavior Checklist (Aman et al., 1995) versus 14% for placebo. There was also improvement on the Stereotypy and Hyperactivity subscales but not on the Social Withdrawal or Inappropriate Speech subscales. Not surprisingly, weight gain was the most frequent side effect.
These results are consistent with an earlier report by McDougle et al. (1998) who demonstrated decreased aggression, repetitive behavior, irritability, anxiety and depression with risperidone under double-blind, placebo conditions.
Open-label studies and case reports of risperidone have also suggested improvements in aggression, self-injury, irritability and anxiety, as well as repetitive behaviors. Little, if any, evidence exists for improved social interaction or language and communication following treatment with risperidone or with any atypical antipsychotic. There are no double-blind, placebo-controlled trials of other atypical antipsychotics in autism, although open-label studies suggest the efficacy of olanzapine (Zyprexa) (Malone et al., 2001; Potenza et al., 1999).
Antidepressants
It is not surprising that serotonin reuptake inhibitors (SRIs) have been tested for their efficacy in autism, given the purported role of serotonin in this disorder. Indeed, antidepressants have been the most widely prescribed psychotropic for individuals with autism (Langworthy-Lam et al., 2002). In a double-blind, placebo-controlled trial of clomipramine (Anafranil), Gordon et al. (1993) found that this medication not only reduced compulsive behavior, but also reduced stereotypies, aggression and self-injury. In a test of the selective serotonin reuptake inhibitor fluvoxamine (Luvox), McDougle et al. (1996) reported that eight of 15 adults with autism were responders, showing decreased repetitive behavior, aggression and inappropriate repetitive language. Zero of 15 in the placebo group were responders. Similar results were not found, however, when studying children with autism (McDougle et al., 2000). Only one of 18 children improved, whereas 14 showed adverse effects. It is important to note, however, that no randomized, controlled trials have been published on children with autism. The lack of empirical support for the efficacy of SSRIs in children with autism is compounded by the recent U.S. Food and Drug Administration finding of increased suicidality in children and the FDA directive for drug manufacturers to add a "black-box" warning to labeling of antidepressant medication.
Mood Stabilizers
The comorbidity of epilepsy with autism is well documented, and prevalence findings suggest that 13% of individuals with autism will be treated with anticonvulsants, many of which will stabilize mood (Aman et al., 1995). Survey data, however, suggest that only a small percent of individuals with autism are treated with mood stabilizers, independent of treatment for seizure disorder (Langworthy-Lam et al., 2002). Moreover, there have been few systematic studies on the effects of this class of drugs. In a small open trial, Hollander et al. (2001) found a favorable response to divalproex (Depakote), with improvement in affective stability, impulsivity and aggression. Clinically, there may be a place for drugs such as divalproex as adjunctive treatment for irritability or as a supplement to the atypical antipsychotics.
Stimulants
Hyperactive behavior is often associated with children diagnosed with autism spectrum disorder (ASD), and stimulants are frequently prescribed for this population. Aman and Langworthy (2000) reported that in only 10 of 41 studies were patients prescribed stimulants. However, in clinical practice, it is likely that many more higher-functioning patients received stimulants during treatment. There are few controlled data supporting efficacy of stimulants in ASD, however. Early reports by Campbell et al. (1972) noted little effect on hyperactivity with dextroamphetamine (Adderall) but a worsening of stereotypies and irritability. Two controlled trials of methylphenidate (Ritalin, Concerta, Metadate) both showed improvement in symptoms of hyperactivity, but social withdrawal and irritability were noted as side effects (Handen et al., 2000; Quintana et al., 1995). A multisite, double-blind, placebo-controlled trial of the dopamine agonist amantadine (Symmetrel) was conducted with children with autism and high levels of hyperactivity and irritability (King et al., 2001). Clinician ratings indicated a positive effect for the medication, but this effect was not reflected in parent ratings. Thus, stimulants appear to be only weakly effective and poorly tolerated. Clinically, trials of methylphenidate may prove effective in higher-functioning patients with ASD whose symptoms may represent a true comorbidity with attention-deficit/hyperactivity disorder.
The α2-adrenergic agonists are often used as an adjunct in the treatment of ADHD. Clonidine (Catapres) has been shown to reduce irritability, hyperactivity and impulsivity in two double-blind trials (Fankhauser et al., 1992; Jaselskis et al., 1992). Gradual development of tolerance was noted in these studies. In addition, side effects such as hypotension, rebound hypertension and over-sedation may cause clinical problems. Guanfacine (Tenex) may be less sedating and causes less rebound. In a retrospective, open-label study, Posey et al. (2004) found a CGI response rate of 23.8%, with improvements in insomnia, tics, hyperactivity and inattention.
Anxiolytics
Survey data suggest a small percentage of individuals are being treated with this class of drugs (Langworthy-Lam et al., 2002). Buspirone (BuSpar) has been shown to reduce aggressive symptoms and anxiety in a small group of adults with mental retardation (Ratey et al., 1991). Realmuto and colleagues (1989) found some improvement in hyperactivity in their small trial study. These few studies suggest that there may be some improvement with these medications, but there are no controlled trials to suggest that buspirone or benzodiazepines have much utility, except for short-term adjunctive treatment of specific periods of high anxiety.
Other Pharmacological Agents
Autism is a disorder associated with many unsubstantiated claims of effective treatment and considerable use of alternative medicine. For example, dimethylglycine has been advanced as a useful treatment of ASD, largely based on anecdotal reports from parents. Little empirical evidence is available to support such claims of efficacy, and at least one small placebo-controlled trial failed to show a drug effect (Bolman and Richmond, 1999). Secretin, initially proffered as a new treatment for ASD, has failed to show efficacy (Sandler et al., 1999). Levy and Hyman (2003), in a review of complementary and alternative treatments for ASD, highlighted the need for scientific scrutiny of new treatments and assessment of the risks and benefits to families. Testimonials concerning the effectiveness of untested treatments may well be due to the high placebo response rate in this population.
Summary
There are a number of psychotropic medications being routinely prescribed for individuals with autism with inadequate evidence of efficacy. Indeed, almost half of individuals with autism were receiving psychotropic medication, not including anticonvulsants (Langworthy-Lam et al., 2002). Antidepressants were the most widely prescribed class of psychotropic drugs. Currently, no psychotropic agents are FDA-approved for the treatment of autism, and no medications have been proven to be efficacious in the treatment of the core social or communication impairment seen in this disorder. Open-label and controlled studies conducted with both children and adults have demonstrated the efficacy of various medications in treating repetitive behavior, as well as the associated symptoms of autism (i.e., hyperactivity, inattention, aggression and self-injury).
In addition to atypical antipsychotics, SRIs may be useful in adults with autism but may not be indicated for children and adolescents. Controlled studies of methylphenidate and clonidine suggest the utility of these medications in the treatment of hyperactivity in individuals with high-functioning autism. Little information is available regarding mood stabilizers and anxiolytics. Pharmacotherapy for autism should target associated symptoms of autism (e.g., aggression, anxiety), as well as repetitive behavior that have been demonstrated to respond to medication in controlled treatment studies.
Our review, although admittedly selective, points out the need for well-controlled trials with larger sample sizes. Given the important role of behavioral interventions, there also needs to be systematic examination of the integration of pharmacological and behavioral therapies (Campbell et al., 1978). The need for controlled trials is underscored by the widespread use of alternative therapies, which have not been systematically examined.
As neither genetic nor environmental causes of autism have been identified, it has been difficult to firmly establish molecular mechanisms that would serve as potential targets for pharmacological intervention. Nevertheless, progress is being made in this area including development of relevant animal models. Clearly, a great deal more work in such areas as proteomics and bioinformatics needs to be done before drug targets can be identified with confidence.
NOTE: Dr. Lewis is professor and associate chair for research in the department of psychiatry at the University of Florida. He has conducted research in developmental disorders, including autism, for over 20 years.
NOTE: Dr. Lazoritz is associate chair for clinical operations and medical director for the department of psychiatry and Vista Medical Center.
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