Global Advances in Health and Medicine : Scientific Narratives in Autism Spectrum Disorder (novembre 2013)

jeudi 16 janvier 2014

La revue Global Advances in Health and Medicine a consacré son numéro de novembre 2013 à la question de l’autisme.

1. Baker SM. Scientific narratives in autism spectrum disorder. Global advances in health and medicine : improving healthcare outcomes worldwide. 2013 Nov ;2(6):5.

Autism spectrum disorder (ASD) has increased in prevalence in the United States from one in 10 000 in the 1950s to one in 88 today. And in South Korea, the prevalence is now one in 44.(1) If the current rate of increase in the incidence of ASD continues, it could become the norm in children in 30 years. Scientific research continues to reveal potential connections between ASD and the gut microbiome or cancer gene mutations. It occurs in all socioeconomic and ethnic groups and is almost five times more common in boys than in girls. The costs to families and society is high-Medicaid costs for children with ASD are almost five times higher than for children without a diagnosis of ASD. And these costs do not begin to include those of intensive behavioral intervention.(2) Why is the prevalence of this condition increasing, and can a systems-oriented approach be used to resolve this pressing health challenge ?

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2. Baker SM, Milivojevich A. Gender differences among children with autism spectrum disorder : differential symptom patterns. Global advances in health and medicine : improving healthcare outcomes worldwide. 2013 Nov ;2(6):8-18.

The gender ratio among children in the autism spectrum of more than four boys to every girl is widely recognized. The authors present an analysis of gender differences among 79 482 symptoms and strengths in 1495 boys and 336 girls aged 2 to 18 years from parent-identified autistic children reported to a structurally novel anonymous parent-entered online database, Autism360. The data reveal differences that provide previously undetected clues to gender differences in immune and central nervous system and gastrointestinal functional disturbances. Together with published observations of male/female differences in inflammation, oxidative stress, and detoxication, these findings open doors to research focusing on gender physiology as clues to etiologic factors in autism. This study exemplifies a research method based on a large, detailed, patient-entered, structured data set in which patterns of individual illness and healing may answer collective questions about prevention and treatment.

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3. Kienle GS, Albonico H-U, Baars E, Hamre HJ, Zimmermann P, Kiene H. Anthroposophic Medicine : An Integrative Medical System Originating in Europe. Global Advances in Health and Medicine. 2013 2013/11/01 ;2(6):20-31.

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4. Compart PJ. The Pathophysiology of Autism. Global advances in health and medicine : improving healthcare outcomes worldwide. 2013 Nov ;2(6):32-7.

Autism has been classically defined by its behavioral symptoms. Traditional medical research has focused on genetic or intrinsic brain-based causes of autism. While both of these are important, additional research has focused on the underlying disordered biochemistry seen in many individuals with autism. Many of these biomedical factors are amenable to treatment. This article will review the main pathophysiologic factors seen in individuals with autism spectrum disorders.

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5. Compart PJ. The Pathophysiology of Autism. Global Advances in Health and Medicine. 2013 2013/11/01 ;2(6):32-7.

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6. Baker SM. Learning About Autism. Global advances in health and medicine : improving healthcare outcomes worldwide. 2013 Nov ;2(6):38-46.

A medical essay written in 1923 pointed out the fallacy of blaming a chronic illness on the name of a disease. The focus of treatment should be the individual, not the disease. With a focus on options based on the individuality of each patient, I ask a simple two-part question : Does my patient need to avoid or be rid of substances and/or to be provided with substances that would favor nature’s impulse toward healing ? In my academic training as a physician, I learned that a clinically effective stance favored an optimistic intent combined with the objective application of my skills-refined though the practice of listening, prescribing, and observing outcome. My understanding of autism has rested on a foundation of the individuality of every living thing, the rhythmicity of life, and the balance that characterizes healthy systems. The first autistic child I examined struck me with a nonverbal message : "I am in here ; see me." The recognition of the role of bacterial toxins amplified my notion that a general disorder of the microbiome underlies the loss of immune tolerance that accompanies the global state of sensitivity found in individuals in the autism spectrum. Depletion of organisms that have populated the human gut since before the dawn of our species arises as the most recent elevation of my learning curve.

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7. James SJ. Autism and Folate-dependent One-carbon Metabolism : Serendipity and Critical Branch-point Decisions in Science. Global advances in health and medicine : improving healthcare outcomes worldwide. 2013 Nov ;2(6):48-51.

Folate-dependent one-carbon metabolism is present in every cell of the body. It represents a central systems biology hub that reverberates into countless other pathways with more specialized roles in specialized cell types throughout the body. I have spent 25 years of research on this core biochemical pathway with several unanticipated iterations that led me from Down syndrome to congenital heart defects to leukemia and finally to autism about 12 years ago. Figure 1 provides an overview of the three interdependent pathways involved in folate-dependent methionine "transmethylation" and "transsulfuration." Methionine is necessary for the synthesis of S-adenosylmethionine (SAM), the major methyl donor for all cellular methylation reactions. It is also the major precursor for cysteine, the rate-limiting amino acid for glutathione synthesis linking transmethylation and transsulfuration pathways. Methionine levels can be negatively affected by genetic and environmental factors that reduce folate availability and/or oxidative inhibition of the methionine synthase enzyme. Because these three metabolic pathways are mutually interdependent, genetic or environmental perturbation of folate or methionine metabolism will indirectly impact glutathione synthesis, and conversely, alterations in glutathione synthesis will alter flux through pathways of folate and methionine metabolism. This interdependency translates into broader impact on essential cellular functions.

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8. Macfabe D. Autism : metabolism, mitochondria, and the microbiome. Global advances in health and medicine : improving healthcare outcomes worldwide. 2013 Nov ;2(6):52-66.

New approaches are needed to examine the diverse symptoms and comorbidities of the growing family of neurodevelopmental disorders known as autism spectrum disorder (ASD). ASD originally was thought to be a static, inheritable neurodevelopmental disorder, and our understanding of it is undergoing a major shift. It is emerging as a dynamic system of metabolic and immune anomalies involving many organ systems, including the brain, and environmental exposure. The initial detailed observation and inquiry of patients with ASD and related conditions and the histories of their caregivers and families have been invaluable. How gastrointestinal (GI) factors are related to ASD is not yet clear. Nevertheless, many patients with ASD have a history of previous antibiotic exposure or hospitalization, GI symptoms, abnormal food cravings, and unique intestinal bacterial populations, which have been proposed to relate to variable symptom severity. In addition to traditional scientific inquiry, detailed clinical observation and recording of exacerbations, remissions, and comorbidities are needed. This article reviews the role that enteric short-chain fatty acids, particularly propionic (also called propanoic) acid, produced from ASD-associated GI bacteria, may play in the etiology of some forms of ASD. Human populations that are partial metabolizers of propionic acid are more common than previously thought. The results from pre-clinical laboratory studies show that propionic acid-treated rats display ASD-like repetitive, perseverative, and antisocial behaviors and seizure. Neurochemical changes, consistent and predictive with findings in ASD patients, including neuroinflammation, increased oxidative stress, mitochondrial dysfunction, glutathione depletion, and altered phospholipid/acylcarnitine profiles, have been observed. Propionic acid has bioactive effects on (1) neurotransmitter systems, (2) intracellular acidification and calcium release, (3) fatty acid metabolism, (4) gap junction gating, (5) immune function, and (6) alteration of gene expression that warrant further exploration. Traditional scientific experimentation is needed to verify the hypothesis that enteric short-chain fatty acids may be a potential environmental trigger in some forms of ASD. Novel collaborative developments in systems biology, particularly examining the role of the microbiome and its effects on host metabolism, immune and mitochondrial function, and gene expression, hold great promise in ASD.

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9. MacFabe D. Autism : Metabolism, Mitochondria, and the Microbiome. Global Advances in Health and Medicine. 2013 2013/11/01 ;2(6):52-66.

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10. Deth RC. Autism : a redox/methylation disorder. Global advances in health and medicine : improving healthcare outcomes worldwide. 2013 Nov ;2(6):68-73.

While autism is still a mysterious developmental disorder, expansion of research efforts over the past 10 to 15 years has yielded a number of important clues implicating both genetic and environmental factors. We can now assert with a measure of confidence that contemporary autism reflects the combined impact of multiple environmental factors on the processes that regulate development in genetically vulnerable individuals. Since epigenetic regulation of gene expression is acknowledged as the most critical factor in development and DNA methylation (the addition of a carbon atom at discrete locations) is the fundamental event for epigenetic regulation, dysfunctional methylation can be considered as a likely cause of autism. Since methylation activity is highly sensitive to oxidative stress (an abnormal redox state) and many environmental factors promote oxidative stress, we have proposed a redox/methylation hypothesis for autism causation. The narrative herein describes the evolution of this hypothesis, which is essentially a series of linked discoveries about how the brain uniquely relies on oxidation and methylation to guide its development and to carry out its cognitive functions.

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11. Rossignol DA. My Experience Learning About Autism. Global Advances in Health and Medicine. 2013 2013/11/01 ;2(6):74-7.

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12. Adams CM. Patient Report : Autism Spectrum Disorder Treated With Camel Milk. Global Advances in Health and Medicine. 2013 2013/11/01 ;2(6):78-80.

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