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Clinically proven
to reduce oxidative stress.
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Oxidative Stress and Autism
Autism is a neurologic disorder characterized by severe social, communication, and behavioral problems. During childhood, autistic children may fall behind their same-aged peers in the areas of communication, social skills, and cognition. There are many forms of this disorder and include: Asperger Syndrome, Fragile X Syndrome, Landau-Kleffner Syndrome, Rett Syndrome, and Williams Syndrome. Although there is no known unique cause of autism, there is growing evidence that autism can be caused by a variety of problems. There is some indication of a genetic influence in autism. For example, there is a greater likelihood that two monozygotic twins (i.e., identical twins) will have autism than two dizygotic twins (i.e., fraternal twins). A dysfunctional immune system has also been associated with autism. Lipid peroxidation markers are elevated, indicating that oxidative stress is increased in this disease. It is thought that autism could result from an interaction between genetic and environmental factors with oxidative stress as a potential mechanism linking the two.
About Autism
- A neurological disorder that affects the normal functioning of the brain
- The fastest growing developmental disability – 10 – 17% annual growth
- $90 Billion annual cost
- 1 in every 166 births
- Four times more prevalent in boys than in girls.
Risk Factors
- No known single cause. Researchers are investigating genetics, problems during pregnancy, as well as environmental factors such as viral infections, metabolic imbalances, and exposure to environmental chemicals.
- Recent studies show greater oxidative stress in children with autism.
Risk Reducers
- Recent studies show that antioxidants can improve autistic symptoms.
The Studies
Altered Vascular Phenotype in autism: Correlation with Oxidative Stress.
Yao Y, Walsh WJ, McGinnis WR, Pratico D. Author Affiliations: Department of Pharmacology, University of Pennsylvania, School of Medicine, Philadelphia.
BACKGROUND: Autism is a neurologic disorder characterized by impaired communication and social interaction. Results of previous studies showed biochemical evidence for abnormal platelet reactivity and altered blood flow in children with autism. OBJECTIVE: To evaluate the vascular phenotype in children with autism.Design and MAIN OUTCOME MEASURES: Urinary levels of isoprostane F(2alpha)-VI, a marker of lipid peroxidation; 2,3-dinor-thromboxane B(2), which reflects platelet activation; and 6-keto-prostaglandin F(1alpha), a marker of endothelium activation, were measured by means of gas chromatography-mass spectrometry in subjects with autism and healthy control subjects.Setting and Subjects Children with a clinical diagnosis of autism attending the Pfeiffer Treatment Center. RESULTS: Compared with controls, children with autism had significantly higher urinary levels of isoprostane F(2alpha)-VI, 2,3-dinor-thromboxane B(2), and 6-keto-prostaglandin F(1alpha). Lipid peroxidation levels directly correlated with both vascular biomarker ratios. CONCLUSION: Besides enhanced oxidative stress, platelet and vascular endothelium activation also could contribute to the development and clinical manifestations of autism.
Oxidative stress in autism.
Chauhan A, Chauhan V. NYS Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA.
Autism is a severe developmental disorder with poorly understood etiology. Oxidative stress in autism has been studied at the membrane level and also by measuring products of lipid peroxidation, detoxifying agents (such as glutathione), and antioxidants involved in the defense system against reactive oxygen species (ROS). Lipid peroxidation markers are elevated in autism, indicating that oxidative stress is increased in this disease. Levels of major antioxidant serum proteins, namely transferrin (iron-binding protein) and ceruloplasmin (copper-binding protein), are decreased in children with autism. There is a positive correlation between reduced levels of these proteins and loss of previously acquired language skills in children with autism. The alterations in ceruloplas | | |
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