Come to Chicago for Autism One Conference (May 20-24, 2009)

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Join NAA at the Autism One Conference in Chicago!

AUTISM ONE 2009 CONFERENCE - MEMORIAL DAY WEEKEND

BIOMEDICAL RESEARCH & TREATMENT

TRACK SAMPLER

www.autismone.org Sonja Hintz, RN, and Sym Rankin, CRNA, APN present: How to Get Your Mainstream Physician to See Beyond AutismMainstream medical practitioners see autism as a behavioral disorder and often overlook how sick our children really are. They need your help to understand that a child's autistic symptoms result from physical conditions that need medical treatment. This session will focus on becoming an informed advocate for your child's health care. Learn to help your mainstream physician understand the metabolic problems in your child so s/he can become an effective member of your team. This session will review current resources and lab tests, and we'll discuss how to match them with specific behavioral observations. The discussion will include the delivery of anesthesia and the unique risks your child may face. If you

can speak the same language as your pediatrician, gastroenterologist, anesthesiologist or other medical professional, you can guide them to an understanding of biomedical treatments. (To parents and all reading this...it is with heavy heart that we report that in March an adolescent passed away as a direct result of dental surgery at a major hospital. We hope that information in Sonja and Sym's presentation will help prevent other children from facing the same danger. Teri) Woody McGinnis, MD, presents: Neurotoxic brainstem impairment as proposed threshold event in autistic regressionLoss of vocalization, changes in social behavior, and altered gastrointestinal function occur in variable permutations in a significant subset-probably a majority-of children who eventually receive the diagnosis of autism. Regression of an ostensibly well child is at once a great tragedy and mystery of autism, and occurs in the second year of life, after maturation of the protective blood-brain barrier. A number of small areas which cluster around the primitive brainstem fail to develop blood-brain barrier, so may act as portals for entry of a broad class of toxins including mercury, cadmium, herbicide, and MSG. Conceivably, many abnormal findings in autism-most particularly, regression-stem from one or more

toxins entering these areas of brain. In 1964, Rimland was the first to suggest primary brainstem involvement in autism. For the first time in public conference, Dr. McGinnis explains how toxins hypothetically trigger autistic regression, and presents data from examination of relevant areas of brainstem and vagus nerve from children with autism. Aristo Vojdani, PhD, presents: Immunology of AutismThe pathophysiology of dysregulation in autism spectrum disorders can be simplified into four understandable steps. Step One, the environmental triggers, such as viral infection, toxicants and/or dietary proteins and peptides, which contribute to gut inflammation. Step Two, enhanced intestinal permeability, or "leaky gut" is the result. Step Three, immune dysregulation, which manifests itself in the nervous system. Step Four, the patient has neuroinflammation. Before an environmental factor triggers dysfunction in the body, it must first infiltrate a network of immune defenses. Mucosal, humoral and cell-mediated immunity each plays a role, whether defensive or dysregulated, in ASD. Finding a balance of the whole body in order to achieve optimal

immune function is possible through understanding how to up- or down-regulate immune molecules. Mark Corrales, MPP, presents: The importance of research on environmental factors in a highly heritable disorderA growing body of evidence suggests various environmental factors are associated with autism. Over time, it should be possible to translate scientific discoveries into widespread adoption of biomedical interventions or appropriate changes in environmental regulation. However, there is a disconnect between the scientific data needed and the data available. The scientific research on autism has focused almost no resources on environmental factors in autism until very recently. While a wide range of environmental factors have been mentioned in the autism research literature or in the popular press, almost none have been thoroughly investigated. This research gap has been partly due to a widely held assumption

that environment plays almost no role in causing or treating autism -- which in turn relies on a misunderstanding about autism's high heritability, or the idea that autism is simply a genetic disorder. In fact, high heritability does not mean environmental interventions can play only a minor role in prevention or treatment. Genes and environment work together in several basic ways to increase the risk and severity of complex diseases such as autism. Research focused on these areas will be essential for progress in autism treatment and prevention. Lewine, PhD, presents: Epileptiform Activity in the Autistic Brain: Cause, Effect, or Co-MorbidityThe observation that almost 30% of children with autism develop clinical seizures by the time that they reach adolescence is one of the fundamental observations in support of the biological basis of autism. Yet, the relationships between clinical seizures, "sub-clinical" epileptiform activity, and autism are poorly understood. At present it is uncertain if epileptiform activity is simply co-morbid with autism, a consequence of the underlying neurobiological abnormalities of autism, or a possible cause of at least some specific features of autism. In this presentation I will explore the hypothesis that, in many cases, the autistic brain is hyper-excitable and prone to epileptiform discharges because of malfunctions

in inhibitory GABA systems and/or excitatory glutamine systems. Through normal mechanisms of cortical plasticity and learning, these discharges become self-reinforcing and lead to epileptogenic neural circuits that are no longer able to support normal function and which, through axonal connections, disrupt normal processing in other networks. In some cases, the critically disruptive epileptiform activity may be triggered by other factors including abnormal signaling pathways, abnormal immunological responses, or environmental toxins. The presence of epileptiform activity is a common thread linking almost all of the genetic conditions associated with autism [e.g., tuberous sclerosis complex, Fragile-X, etc.] and also a common finding in conditions of environmental toxicity [e.g., mercury poisoning]. Using functional brain imaging data from magnetoencephalography [a noninvasive method for recording the magnetic signals generated by the brain's electrical

activity], I will provide evidence that auditory and language cortices are especially prone to the development of epileptogenic circuits in autism, and that this is specifically related to language dysfunction. Finally, I will explore how suppression of epileptiform activity in the autistic brain can lead to improvements in language skills and a reduction of autistic features. , MD, presents: TILT: A New Slant on AutismParents of children with autism often suspect environmental and food triggers. Their doctors may disagree--they simply do not see it. In the late 1800s, it was the emergence of the germ theory that enabled physicians and scientists to consider and conduct research into the origins of infectious diseases. As with the germ theory, TILT is a recently published, scientific theory of disease that offers a new framework for understanding how everyday exposures can make you sick--and you won't even know how it happened! By understanding how TILT works, you can find out exactly what is making you ill and make the changes essential for getting well and staying well. This newly described disease mechanism involves two steps, and because they

are often subtle and spaced apart in time, this mechanism has escaped notice. Like the germ theory of disease and the immune theory, TILT is also a theory of disease, one that explains the connection between our exposures and common chronic health conditions that are on the rise. "TILT" stands for "Toxicant-Induced Loss of Tolerance." Chronic conditions ranging from autism to ADHD, asthma and autoimmune disorders, chronic fatigue, migraines, depression and addictive behaviors such as overeating leading to obesity, and substance abuse, may result from this invisible two-stage disease process. Theoharis Theoharides, MD, PhD, presents: Mast cells disrupt the gut-blood-brain barriers and contribute to autismMany autism spectrum disorder (ASD) patients have a history of "allergic" symptoms and food intolerance, suggesting activation of mast cells, now recognized as master regulators of the immune system. Activation of intestinal and brain mast cells by immune, infectious, stress or toxic triggers could lead to gut-blood-brain-barrier disruption, permitting brain inflammation and autism. This is more likely to occur in children up to 3 years old, who are more susceptible to infections, and when their gut-blood-brain barriers are still developing. Moreover, perinatal stress has been associated with ASD development, and we have shown that corticotropin-releasing hormone (CRH) secreted

under stress and during premature labor can induce mast cells to release vascular endothelial growth factor (VEGF), which increases blood-brain-barrier permeability. We have also shown that mercury causes release of VEGF from human mast cells. Mast cells are critical in the disease mastocytosis, characterized by an increased number of hypersensitive mast cells in many tissues. Children with mastocytosis also present with skin allergies, diarrhea, learning disabilities, hyperactivity and difficulty focusing, reminiscent of ASD. A survey of the Mastocytosis Society's members (www.tsmforacure.org) indicated that the rate of autism in children with mastocytosis is at least 10-fold

higher than that reported for the general population. Mastocytosis patients also have high blood levels of interleukin-6 (IL-6), which has recently been implicated in an "animal model" of autism, and which we have shown derives entirely from mast cells. We have also shown that the naturally occurring flavonoids luteolin and quercetin can inhibit human mast cell release of IL-6 and other inflammatory molecules. MORE RESEARCH. MORE HOPE.www.autismone.org Think Autism. Think Cure. ®

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