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Re: "Biomedical Treatment - Parents' Group "
the following is a brief summary on the biomed approaches mentioned in the autism conference held earlier in august, done by a parent. good for new parents considering biomed to get a quick grasp of the theory and treatments involved.
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Opening the door: Biomedical intervention and recovery from autism
There has been much controversy in recent years over the dramatic increase in the incidence of autism and autism spectrum disorders (ASD). The most controversial claim was the proposed link between the development of autism and the MMR (measles-mumps-rubella) vaccine.1
In the USA, the prevalence of ASD is 1 in 166, increasing 15-fold since 1976.2 Data from the UK indicate a similarly alarming rise. For example, the prevalence of “autistic syndrome” in England and Wales in 1976 was 4-5 per 10,000.2 Thirty years later, the prevalence of childhood autism in the South Thames region was 38.9 per 10,000.3 The phrase “autism epidemic” has been used to describe this trend.4
Despite the apparent surge in ASD, there has been a major change in the response to diagnosis. No longer is ASD considered untreatable and incurable. There is hope of recovery. This was the message of the Asian Autism Conference 2006 held on 12-13 August 2006 at the Hong Kong Academy of Medicine.
The conference was organised by the Autism Parents Network Foundation (APNF) – a Hong Kong based parents support group. APNF emphasises the paramount role of biomedical intervention and therapeutic approaches such as Applied Behaviour Analysis in effecting recovery from ASD.
The conference attracted over 300 participants from Hong Kong and other parts of southeast Asia, including Japan, South Korea, Philippines, India, Singapore, Malaysia, Macau, Taiwan, and The People's Republic of China. One third of the participants were medical practitioners. Parents and professional groups including paramedics, therapists, clinical psychologists, academics and teachers of children with special needs comprised the remainder. The aim of the conference was to improve understanding of the advances in treatment methods, correct misconceptions of the cause and treatment options available, and strengthen frameworks for managing treatment strategies, so that informed decisions can be made.
What is autism?
Autism is a pervasive developmental disorder that is defined by characteristic developmental and behavioural features that occur before the age of 3 years, including: 1) qualitative impairment in social interaction (eg marked impairment in the use of multiple non-verbal behaviours, such as eye-to-eye gaze); 2) qualitative impairments in communication (eg delay in, or total lack of, the development of spoken language); and 3) restricted, repetitive, and stereotyped patterns of behaviour, interests, and activities (eg inflexible adherence to specific, non-functional routines or rituals).5
ASD include Asperger’s syndrome (also known as high-functioning autism), Rett’s disorder, childhood disintegrative disorder and pervasive developmental disorder not otherwise specified (PDD-NOS).5 The disorders vary greatly in their severity and the boundaries between specific diagnoses are often blurred. Many practitioners in this field now consider attention deficit disorder (ADD), attention deficit hyperactivity disorder (ADHD) and other specific language deficits such as dyslexia, among the ASDs (Fig 1). The theories of the causes of autism are too numerous to mention here. ASDs are likely to be caused by a combination of innate genetic and external environmental causes.
What is biomedical intervention?
The fundamental concept driving biomedical interventions for ASD is the profound interaction between the gut and the brain (Fig 2). It has been proposed that damage to the gastrointestinal (GI) lining allows partially digested proteins to enter the bloodstream and cross the blood-brain barrier where they affect the normal development and function of the brain leading to many of the characteristic symptoms of ASD. These peptides, derived from the major wheat and milk proteins gliadin and casein are called gliadomorphins and casomorphins, respectively, for their ability to affect the brain in a way similar to endogenous opioid peptides and the drug morphine. A Cochrane review of combined gluten-free casein-free diets in autistic subjects noted the significant reduction in autistic behaviours whilst on the diet, while other characteristic symptoms (cognitive skills, linguistic ability and motor ability) were not significantly reduced.6 Left uncorrected, it is hypothesised that persistent GI damage results in reduced nutrient/mineral/vitamin absorption and dysbiosis of gut flora, which is manifested as an overgrowth of undesirable bacteria (eg Clostridium spp) and yeasts (eg Candida spp.). Biomedical intervention aims first to address the profound nutritional deficiencies that may be involved in the induction of autistic behaviours.
It is impossible to do justice to the detailed presentations made by the speakers during the conference. However, some highlights illustrate the range of topics covered.
Dr Jacquelyn McCandless gave several presentations over the course of the conference focusing on the diagnosis and biomedical treatment of ASD. McCandless outlined an 8-point biomedical treatment plan for ASD (Table 1) emphasising dietary restriction (gluten-free, casein-free, soy-free) to reduce the amount of partially digested and antigenic dietary proteins released into the bloodstream; nutrient therapy (supplementation of minerals, especially zinc and magnesium and vitamins A, C, D and E); and gut pathogen treatment (systemic anti-fungals and antibiotics and supplementation with probiotics such as Lactobacillus acidophilus and Bifidobacterium bifidus. Once the gut is healed, a process that may take several months, measures can be taken to correct other components of the metabolism that may be dysfunctional. These may include supplementing the metabolic methylation pathways, removing heavy metal contamination with chelating agents or enhancing the immune system.
Dr Kenneth A Bock (Rhinebeck Health Center and Center for Progressive Medicine, NY, USA) emphasised the importance of individualising treatment when planning a biomedical intervention programme for children affected by ASD. Bock reviewed the potential damage to the neurological and immune systems from environmental toxins. A key finding was the fact that small amounts of compounds, below the concentrations considered individually toxic, may act synergistically with profound adverse effects on physiological function.7 Coupled with an exposure to a cocktail of environmental toxins, the body’s ability to detoxify these substances is often impaired in persons with ASD. This leads to an overload of toxins in the body, which may result in oxidative stress and chronic inflammatory conditions, such as colitis, atopic dermatitis and asthma. Neuroinflammation has been found in autistic patients.8 Reducing neuroinflammation by enhancing the body’s natural detoxification pathways may improve the clinical course of ASD. To achieve this, Bock uses the “therapeutic quintet” of methylcobalamin (the metabolically active form of vitamin B12 in the central nervous system), folinic acid (a metabolically active form of folic acid), trimethyglycine and thiamine tetrahydrofurfuryl disulfide (methyl and sulfate donors, respectively, in detoxification reactions) and glutathione (an antioxidant and free radical scavenger). Bock underscored the importance of including behavioural and educational therapies as components in any recovery programme.
Dr Jill James (Director, Biochemical Genetics Laboratory, Arkansas Children's Hospital Research Institute, Little Rock, AR, USA) is an expert on gene-nutrient interactions that increase susceptibility to autism. She introduced the basic biochemistry and interdependence of folate-methionine-glutathione metabolism. The importance of glutathione as a key regulator of oxidative stress was developed. Interestingly, the vaccine preservative thimerosal has been shown to deplete glutathione in vitro – supporting the biomedical use of glutathione supplements in ASD. In detailed studies on the metabolic profiles of children with ASD, James documented abnormal methylation and oxidative stress that correlated to the presence of specific genetic lesions and single nucleotide polymorphisms in genes related to methionine metabolism (transcobalamin II), antioxidant capacity (glutathione-S-transferase) and methylation (catechol-O-methyltransferase).9 However, no single polymorphism can predict increased risk for ASD, because, by definition, polymorphisms are highly prevalent in unaffected people as well. Specific combinations of these polymorphisms may interact to affect metabolic pathways that are important in the pathogenesis of ASD. James noted that the abnormal metabolic profile in children with ASD strengthens the hypothesis that an inability to control oxidative stress may be central to the development of the neurologic, immunologic and GI dysfunction that occurs in ASD.
Dr Timothy Buie (Harvard Medical School, MA, USA) is a gastroenterologist. He is known for his expertise in diagnosing children with GI complications of autism. Buie demonstrated the difficulties in diagnosing medical issues in autism. The presentation incorporated actual video film of three patients with what appeared to be classical symptoms of autism. These patients all had non-obvious GI conditions that when identified and treated appropriately resulted in a marked improvement in their “autistic” behaviour. GI issues have been a marked feature of autistic symptomology since the earliest studies. Indeed, the seminal paper on autism by Leo Kanner in 1943, noted that six of the 11 subjects investigated had “feeding or dietary” issues.10 These, however, were attributed to autistic behavioural issues rather than to a co-existing or potentially causative medical condition. A recent study evaluated 50 children with ASD and two control groups matched for age, sex and ethnicity. The control groups comprised 50 children with typical development and 50 with developmental disorders other than ASD. GI symptoms were reported in 70% of children with ASD, 28% of children with typical development and 42% of children with other developmental disorders.11 Buie also highlighted some of the pitfalls of GI/autism research. A large number of the reported studies indicating a link between GI problems and ASD are anecdotal. There is lack of population-based data with some studies suffering from referral and selection bias. Many of the current claims are uncorroborated by other researchers. Another limitation is that much of the current work tries to offer GI issues as a cause of autism. A more promising approach might be to see GI issues as a contribution of autistic behaviour. However, there is clear evidence that medical issues, including GI disorders, exacerbate ASD. Recognition and treatment of these medical conditions will improve functional outcomes and the quality of life of people with ASD.
Dr Martha Herbert (Massachusetts General Hospital and Harvard Medical School, MA, USA) asked the question, “Is autism a brain disorder or a disorder that affects the brain?” She discussed the growing body of research suggesting that biomedical problems like inflammation and oxidative stress indicate that the brain may not be the prime target but rather caught in the crossfire of system-wide abnormalities whose treatment can lead to improved brain function. Herbert explained that a strongly genetic, brain-based modular model of behaviour (ie gene expression affects brain structure/chemistry, which in turn affects behaviour) is inadequate when trying to understand ASD for several reasons (Fig 3). First, numerous genetic studies for ASD-related genes have produced highly variable and inconsistent results. In addition, the gross brain abnormalities that have been observed in some ASD subjects are not compatible with the rather precise nature of the modular model. Co-existing autistic features such as sleep disturbance, epilepsy and sensory issues likewise cannot be explained by the model. Furthermore, autistic symptoms frequently extend beyond the brain – often involving, for example, the gut and immune system. Finally, altered gene expression alone cannot account for the dramatic increase in ASD cases seen in the autism epidemic.
Rather than a genetically predetermined and irreversible defect in the brain, ASD could equally be viewed as a problem with neuronal network connectivity resulting from a physically sick brain. As noted earlier, neuroinflammation has been documented in ASD.8 Oxidative stress and inflammation can affect an array of cellular brain functions influencing energy production, the maintenance of cellular lipid membranes, neurotransmitter production and specificity and neuronal glial cell support activities, any of which may ultimately affect behaviour.
In summary, Herbert revised the model for the causation of ASD. Environmental triggers and genetic influences affect both the brain and body resulting in a range of metabolic, physiological and biochemical abnormalities. These abnormalities are treatable and recovery from autism has been documented. Indeed, one of the 11 cases of autism recorded in 1943 recovered following treatment for an immune disorder.
Nutrition and behaviour were among the topics discussed by Dr Lillian YY Ko (Chairman, Hong Kong Society for Child Health and Development). She presented an overview of ASD in Hong Kong and China. In 1985, a government-run child assessment centre identified 48 cases of ASD. In 2004, 388 cases were reported. Ko focused on the link between behaviour and heavy metal accumulation and toxicity. Mercury and lead are known to affect mental health and behaviour. The greatest source of mercury in Hong Kong is contaminated fish and seafood. Given China’s rapid economic growth and concomitant environmental pollution, the problem of heavy metal toxicity in children in mainland China looks set to increase. Based on an incidence of 5 per 10,000, there could be 200,000 cases of ASD among China’s 380 million children. Ko favours heavy metal detoxification using chelation therapy.
Heavy metal detoxification was the theme of the presentation given by Dr Anju Usman (Medical Director, True Health Medical Center, IL, USA). She reiterated the view that many ASD subjects have environmentally-induced toxicity that is preventable, treatable and reversible. Heavy metal toxicity, particularly from mercury and lead, is believed to be a prime candidate for triggering ASD. Mercury is a potent neurotoxin, exposure is common and the classic symptoms of mercury poisoning are strikingly similar to autism.12 Conjugation of heavy metals to glutathione is the primary mechanism of excretion and autistics have been shown to have low glutathione levels.13 After challenge with oral chelating agent (dimercaptosuccinic acid, DMSA), autistics excreted 5.8-fold more mercury than controls.14 Other useful chelating agents include ethylenediaminetetraacetic acid (EDTA) and dimercpatopropanesulfonic acid (DMPS).
Dr. Tim Trodd (a private practitioner in Hong Kong) concluded the conference with a presentation on the practical aspects of treating ASD based on data gathered from some of the patients under his care. Among the wide range of topics covered in his talk, Trodd described the use of DMSA as a heavy metal chelating agent in children with ASD. Local children with ASD were found to have high concentrations of mercury (mean 12.4 |
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Carson's birthday in January 2000.
發表於 06-9-15 22:02
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