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Strategic Plan Question 2: How Can I Understand What is Happening?

Respondent 1

Matthew J. Carey

a. What issues and topics should be added to the introduction?
"Launch three studies that target the underlying biological mechanisms of co-occurring conditions with autism including seizures/epilepsy, sleep disorders and familial autoimmune disorders by 2012." I applaud the IACC for adding this goal. I would suggest that epilepsy in unquestionably linked with autism and much research with multiple studies should focus upon the link and understanding the subgroups of autistics with epilepsy. One question might involve whether the medications routinely used for epilepsy might react differently in autistics than in those without an ASD.

Respondent 2

K. MacDonald

b. What are the remaining gaps in the subject area covered by this chapter?
Where are the studies involving the gut-brain interaction? Where is the research looking at how various family histories of autoimmune disorders play into ASD (asthma, eczema, diabetes, etc.). Where are the studies for environmental triggers, especially the childhood vaccine program (i.e., fully vaccinated vs. never vaccinated, altered schedule and/or numbers of vaccines). How can you even pretend to try to answer this question if you are too afraid to look in the most obvious places for the answers? There are many gaps, as far as "what is happening to a full 1% of our children."

Respondent 3

b. What are the remaining gaps in the subject area covered by this chapter?
I think we have only scratched the surface of understanding in this area, and much more research needs to be done. Specifically the metabolic and immune system characteristics and co-occurring conditions need further understanding. The subgroups of people with ASD are very interesting when comparing the vast differences in individuals with the same diagnosis.

Respondent 4

John Best

a. What has been learned about the issues covered in this chapter in the past year?
There is only one cause of ASD: mercury. Take all the rest of your [profane language redacted] theories and shove them [profane language redacted]. You can't fool all of us with this nonsense so you might as well cut the [profane language redacted] and start telling the truth. If you don't tell the truth, those of us who know it will continue to expose you for the dishonest [profane language redacted] that you are. Sooner or later, the majority of the general public will realize that you [profane language redacted] are lying to them and they will probably [threatening language redacted].

b. What are the remaining gaps in the subject area covered by this chapter?
You [profane language redacted] have been lying to us for a long time now. Are you stupid enough to think that you can get away with this forever?

Respondent 5

Gail Elbek
Child Health Advocates

a. What has been learned about the issues covered in this chapter in the past year?
"...Much of the current science suggests that the behavioral features of ASD result from atypical brain structure, wiring or connections...found differences in density of white and gray matter...associated seizures...disruptions of the immune system...gene mutations...axon impairment…damage to neurotransmitter systems...gender differences...involved in ASD." THE CAUSE OF THESE CAN BE SCIENTIFICALLY EXPLAINED IN DETAIL...

b. What are the remaining gaps in the subject area covered by this chapter?
IACC GAP: Endocrine disruptors (ED) reprogram expression of genes without mutating deoxyribonucleic acid (DNA) as shown in the case of autism. ED cause greatest risk during prenatal and early postnatal development. ED alter, mimic, block the body's natural hormones. Even at low doses ED can disrupt the body's delicate endocrine system that leads to disease: physiological and neurological...brain signaling fails to occur thus causing the failure to respond. As an established endocrine disruptor, SOY is repeatedly proven in scientific detail to damage multiple neurotransmitter systems proven to cause: autism, mental retardation, cerebral palsy, seizures, stuttering, depression, attention deficit hyperactivity disorder (ADHD), and more. Developmental soy neurological poisoning is also proven to cause: damage to multiple brain structures, neuronal atrophy, depressed brain-derived neurotrophic factor (BDNF), depressed calcium-binding proteins, lost protection against neurodegenerative diseases, depressed cortical neurons, impaired hippocampal dentate gyrus, depressed estrogen receptor neurons, depressed hippocampal neuron axonal outgrowth, damaged estrogen receptor messengers, damaged embryonic neurons and glial cells that support and protect neurons, inhibited RET important for the survival of neuron systems involved in brain development and function. Soy poisoning is also proven to damage the thymus, and cause hypothyroidism to then cause immune system deficiency and adverse neurological effects. Soy phytic acid and multiple heavy metals block essential mineral absorption also necessary for body and brain development. Soy estrogenic ED are known to encourage greater risk to males, explaining the 4 to 1 autism ratio. It is past due that as an "Aspirational Goal" the IACC review existing massive evidence proving extensive neurological soy-damaging effects proven to cause autism and several other mental (and physical) developmental disorders. As the marketing and consumption of soy increased in the United States so has autism and multiple severe and irreversible developmental diseases. This is not coincidence, but soy ED poisoning is the cause! Very low costs for the IACC to review published studies and question exposure history of soy contamination.

Respondent 6

Eileen Nicole Simon This link exits the Interagency Autism Coordinating Committee Web site

a. What has been learned about the issues covered in this chapter in the past year?
METABOLOMICS (see PubMed) may be more important than genomic (gene-to-behavior) research. Metabolism is not uniform from person to person. Metabolic variants are probably the norm. How unusual metabolites may affect the brain should be investigated, especially how normally non-harmful metabolites in combination with other factors that are also not injurious to most people. Phenylketonuria (PKU) is a genetic disorder associated with autism, and results from a defective liver enzyme. Phenylpyruvic acid is a toxic abnormal metabolite produced by the defective enzyme in the liver, and this abnormal metabolite clearly affects the brain. Injury from phenylpyruvic acid is probably similar to that caused by alcohol intoxication, valproic acid, and other toxic drugs, and should be investigated in research with laboratory animals.

b. What are the remaining gaps in the subject area covered by this chapter?
Look for a "final common pathway" in the brain that might disrupt language development. Autism is associated with: 1.) TUBEROUS SCLEROSIS and tubers in the temporal lobes, the auditory receptive-area endpoint of the auditory system of the brain; 2.) NEUROFIBROMATOSIS and Schwannoma tumors of the auditory system; 3.) FETAL ALCOHOL SYNDROME from early in gestation leads to major deformities (hamartomas) of the brain and disorganized development of synapse connections; 4.) ALCOHOL exposure late in gestation has been shown to disrupt aerobic metabolism in the auditory system (Vingan, Dow-Edwards, & Riley, 1986); 5.) THALIDOMIDE early in gestation results in major malformations; 6.) The effects of thalidomide and VALPROIC ACID late in gestation should be investigated by the deoxyglucose method as Vingan, et al. (1986) did for alcohol. Reference Vingan, R.D., Dow-Edwards, M.L., & Riley, E.P. (1986). Cerebral metabolic alterations in rats following prenatal alcohol exposure: A deoxyglucose study. Alcoholism, Clinical and Experimental Research, 10(1), 22-26.

Respondent 8

a. What has been learned about the issues covered in this chapter in the past year?
"Research on females with ASD to better characterize clinical, biological and protective features" is so needed. As a mother of both a son and a daughter on the spectrum, I have watched my son receive services throughout his lifetime, that include early intervention, preschool services, an individualized education plan (IEP), and Office of Mental Retardation and Developmental Disabilities (OMRDD) services, while my daughter displays many of the same behaviors, in some cases more severe (i.e., tantruming) and receives very little (i.e., occupational therapy (OT) and speech therapy in the past and no IEP). "Another understudied arena of ASD research is gender differences. Many studies of autism preferentially enroll males, which, due to a 4:1 increased prevalence, are easier to recruit. Without additional information about the biological features of ASD in females, it remains unclear whether the course of ASD is similar and whether currently used interventions are appropriate for females." This made me so happy, so important!!!!!!

Respondent 10

Andrea Payne

b. What are the remaining gaps in the subject area covered by this chapter?
It is very difficult to find information about these areas. I am currently struggling to learn about this as well as to determine the medical persons I need to involve to correctly identify the way my son's body works, especially during periods of stress. Overall, due to the many controversies surrounding autism, saying "autism" in a physician's office is like dropping a flaming "A" into the middle of the room - entire buildings get evacuated!

Respondent 11

G.A. Elbek

b. What are the remaining gaps in the subject area covered by this chapter?
Fetal, infant, and child exposure to soy phytotoxic endocrine disruptors are repeatedly proven to damage multiple most fragile developmental brain systems known to cause a number of brain disorders to include autism. Soy is also proven to cause extensive gastrointestinal damage reported in children with autism. Boys are proven to have greater sensitivity for soy estrogenic endocrine disruptor damage, explaining also the increase of autism in males.

Respondent 13

Rebecca Kotter

b. What are the remaining gaps in the subject area covered by this chapter?
Please devote some resources to investigating the possible dysfunction of mirror neurons in autism. It is possible that functional imaging could become an important tool in early identification of individuals with autism. In addition, functional imaging could play a role in monitoring the success of particular intervention strategies.

Respondent 14


a. What has been learned about the issues covered in this chapter in the past year?
How some autistics with seizure disorder may benefit, ironically, from "stimulants like Wellbutrin or Ritalin at LOW doses to encourage frontal lobe activity that may be hindered and causing outbursts of behaviors."

Respondent 16

Family Voices-NJ

b. What are the remaining gaps in the subject area covered by this chapter?
None - we support the goal, and short-/long-term objectives

Respondent 19

a. What has been learned about the issues covered in this chapter in the past year?
There has been some research that indicates Lyme disease, certain retroviruses (XMRV) and vaccine adjuvants (aluminum, mercury from thimerosal) create biological mechanisms for the regressive autism we commonly see today.

b. What are the remaining gaps in the subject area covered by this chapter?
We need to thoroughly explore the connection between these biological factors and Lyme disease, xenotropic murine leukemia virus-related virus (XMRV), and vaccine adjuvants by testing with animal models to see if these could be triggers for regressive autism.

Respondent 20

a. What has been learned about the issues covered in this chapter in the past year?
The pathobiology of autism likely involves a perturbation of the antioxidant system mediated by glutathione. There are multiple inputs to this pathology but it appears to be a chronic condition acquired in the infant/toddler period where the gastrointestinal (GI) tract becomes colonized with a yeast which produces the sulfur containig fungal toxin, gliotoxin. Gliotoxin binds to glutathione, essentially removing large quantities of this vital antioxidant from the circulating pool. This disrupts the crucial metal metabolizing metallothionein system, needed to detoxify metals, particularly in the brain. The triggering event is the administration of acetaminophen, aka Tylenol, to the toddler in the perivaccination period. Acetaminophen reduces any remaining glutathione causing metal intoxication in the child and likely causing neuronal cell death of crucial brain cells at a critical time of neurodevelopment. A screening diagnostic tool would measure glutathione in the infant. Such a test already exists, called the erythrocyte glutathione level.

Respondent 21

b. What are the remaining gaps in the subject area covered by this chapter?
You need to include vaccines as a cause of autism!

Respondent 22

Aimee Doyle

a. What has been learned about the issues covered in this chapter in the past year?
I'm not sure what we've learned about the biology of autism. Seems that every article I read covers some new genetic "breakthrough."

b. What are the remaining gaps in the subject area covered by this chapter?
I want to see significant research on regression. My son developed seizures at 18 months. He developed repetition behaviors. He also regressed and lost language, skills, smiling. His entire development stalled. I would like to see detailed analyses of the medical records of children who regress, so we can figure out what triggered the regression. I would also like to see extensive medical testing during the time of regression -- brain scans, physical exams, laboratory analyses. I would also like to see more research into what happens biologically in adolescence. As an adolescent my son developed self-injurious and aggressive behaviors (which he did not have as a child). He hit his leg so many times it was covered with bruises and all the hair fell off. He would yell at the top of his lungs for hours on end, often in the middle of the night. He developed a severe anxiety disorder. He would hit others. We had no idea what was happening to him and neither did any medical doctor or psychiatrist we consulted. My son is not alone -- many adolescents develop problematic behaviors during this time.

Respondent 23

Age of Autism

a. What has been learned about the issues covered in this chapter in the past year?
Why has the IACC never called for a specific study on the children who regressed? In 2008, Dr. Bernadine Healy, former head of the National Institutes of Health, was on CBS News ( This link exits the Interagency Autism Coordinating Committee Web site) calling for research on the children who became autistic after receiving certain vaccines.

b. What are the remaining gaps in the subject area covered by this chapter?
I would like to know why the IACC can refer to autism as an emerging "national health emergency," at the same - When will autism be officially declared a CRISIS? This report said, "Specifically, we need research that deepens our understanding of ASD, including the complex genetic and environmental factors that play a role in its causation," yet not one particular environmental factor was mentioned. When Insel spoke at MIT last December he made the following comments on the environment: "I said before this isn't just genetics... There have to be environmental factors." "We have barely been able to scratch the surface." "There are something like 80,000 potential toxicants." That was a frightening commentary. How much worse will the autism rate have to get before researchers have a clue where to look? Why is the research money going to endless genetic studies while no one seems to know anything about the triggers in the environment? Time it has done little to address it as an emergency.

Respondent 24

Ray Gallup

b. What are the remaining gaps in the subject area covered by this chapter?
The autoimmune/gastro link and vaccine link to the ASD epidemic.

Respondent 27

a. What has been learned about the issues covered in this chapter in the past year?
the importance of epigenetics/environmental contribution

b. What are the remaining gaps in the subject area covered by this chapter?
1.) the role of metabolic/mitochondrial problems, testing, detection and treatment of them; 2.) the role of transporters of elements toxic and nontoxic of +2 oxidation state (including the EAAT, the ABC- Pg glycoprotein-) and the amino acids transporters; 3.) the role of certain polymorphisms in the management of xenobiotics in general in ASD, related to the cycle of glutathione conjugation (coenzymes and cofactors) and phase I and phase II in the liver in autistic people--in this sense from food additives to pesticides/organophosphorates/polychlorinated biphenyls (PCBs) exposures to antibiotics, at chronic/acute low dose such as the exposure from breathing air, food and water. Role of the thymus in ASD; 4.) the role of nutritional deficiencies in terms of vitamins, amino acids and minerals--mainly essential elements; 5.) the axis hypothalmic-pituitary-adrenal (HPA) in autism. Precocious puberty in ASD, testing and adequate treatment; 6.) the role of gastrointestinal (GI) conditions (enzyme deficiencies, organic dysfunctions, reflux, food intolerances), immune abnormalities (hyper-answers--autoimmunity--and hypo-answers--immune depression--to viruses/bacteria/xenobiotics including all the exposures) and endocrinologic abnormalities in the physiology of the autistic brain. The identification of subgroups considering the concomitant medical problems to the diagnosis of ASD. The role of the gut-immune system-brain axis signaling systems (neuropeptides, growth factors, etc.) and inflammation in ASD and the correlation with genetics and proteomics/metabolism. Please note that my emphasis here is in the view of the concomitant medical problem as a consequence of the interaction of genetics/metabolism plus environment, not as "Causes of ASD" per se. Impact in the development of autistic brain from childhood to adulthood of undetected concomitant medical conditions. Role of epigenetic. Role of stress. Role of epilepsy/seizures. Role of undetected pain in aggression in ASD. Research in detection of GI and neurological conditions related to pain in ASD. Role of the combination of concomitant medical problems in physical symptoms and cognition in ASD. 7.) The combined impact of medical pediatrics management in the GI/immune system of autistic children (from antibiotics to vaccines--overall schedule and overall composition--PLUS chronic exposure to xenobiotics from food, water and air (heavy metals/Al, PCBs, polycyclic aromatic hydrocarbons (PAHs), pesticides, organophosphates) and allergic reactions PLUS common bacterial/viral childhood conditions NOT possible to prevent--such as otitis, pharyngitis, laryngitis, colds, etc.) vs. non-autistic children. The possibility of molecular mimicry in the management of xenobiotics and vaccines as a concomitant medical problem to the ASD diagnosis. The possibility of ribonucleic acid (RNA) viral mutation in vivo and exchange of RNA material in persistent infections due to abnormal immune answers (from wild and non-wild origin) in ASD. Multiple chemical sensitivities in ASD. The importance of a new approach to study the efficiency of nutritional approaches to ASD, considering carefully the anecdotic experience on the topic and the need of the concomitant treatment of the concomitant medical problems to achieve useful data about outcomes. 8.) The development of more specific and high technology techniques to the detection of evasive/hidden or tricky abnormalities in the detection of immune answers/immune abnormalities/proteomics in autistic people. The effect/impact of chronic low doses of xenobiotics of all sources as endocrinological, gastrointestinal and immune disruptors in autistic vs. non-autistic children. Adequate testing in ASD to detect these disruptions. 9.) The impact of the overall health status--physical and psychological--in neurocognition and testing of learning in ASD. Developmental changes in ASD related to biochemistry/brain structure/and cognition. Checking before and after a proper medical treatment based on metabolism/biochemistry treatment plus educational of the differences--if any--in the skills and abilities, strengths and weaknesses, in time. Research to discriminate between placebo effect and natural maturation vs. true effect of medical treatment of concomitant medical conditions in ASD.

Respondent 28

J. Fenech

a. What has been learned about the issues covered in this chapter in the past year?
More than enough money has been spent strictly on the genetic aspect of ASD. Enough already. Let's start looking at what is happening to the child before it is born. Does the mother have a history of illness where she is constantly on antifungals, other drugs, etc.? What drugs were given in utero (absolutely including any vaccinations)? Was the mother given any catch-up immunizations while in the hospital (shedding from this and also transmission through breast milk)? IS THERE A TEST TO SEE HOW STRONG THE IMMUNE SYSTEM OF THE BABY IS WHEN IT IS BORN?

b. What are the remaining gaps in the subject area covered by this chapter?
My daughter is now 17 years old. We have done just about every therapy that is known to man to help her. After years and years of applied behavior analysis (ABA), speech therapy, etc., I finally convinced my pediatrician to go to an autism conference (after eight years of begging). He came home from the conference and immediately started my daughter on methylcobalamin with glutathione. Within days, my child's language was coming out faster than we could take in (age 10). Prior to this, it was like pulling teeth to get two or three words from her. So, what happened to her body's production of gluatathione? Did the hepatitis B shot damage her production of it?? So, if her detoxification system didn't work properly from the time of her hepatitis B shot (at two weeks old?), what did this do to her developing brain and neurological system? I want to know and you should too.

Respondent 39

Ann-Mari Pierotti
American Speech-Language-Hearing Association

b. What are the remaining gaps in the subject area covered by this chapter?
Supporting the development of research that addresses the efficacy of existing interventions aimed at mitigating behavioral and medical challenges should be a top priority. Specifically, research designed to contrast highly structured treatment (i.e., ABA) with other approaches aimed at improving social contextually- based communication and the comprehension and production of spoken language, as well as examining the change in outcomes associated with the frequency, intensity and duration of treatment.

Respondent 40

b. What are the remaining gaps in the subject area covered by this chapter?
The link between vaccines and autism needs to be explored much more thoroughly. The neurotoxins in vaccines (e.g. aluminum, mercury) cannot be good for a developing infant. The fact that so many ASD kids have allergies suggests vaccines may be causing an immune or autoimmune reaction.

Respondent 43

Michael Framson

a. What has been learned about the issues covered in this chapter in the past year?
The "What we know" section alludes to the possibility of a biological basis of ASD but goes on to say that little evidence exists for such a basis outside of a transient pattern of brain growth. Multiple studies have been published the past 2 years documenting metabolic, immune, and neurological abnormalities that offer additional support for biological underpinnings of the disorder. Zecavati and Spence (2009) review neurometabolic disorders and dysfunction found in ASD. Enstrom (2009) identifies altered innate immunity capable of initiating and perpetuating autoimmune responses. Li (2009) documents an elevated immune response in the brains of autistic patients. Wills (2009) reports on detection of autoantibodies to neural cells of the cerebellum in the plasma of subjects with autism spectrum disorders. Sajdel-Sulkowska (2009)reports an increase in cerebellar neurotrophin-3 and oxidative stress markers in autistic cerebella. James (2009) continues to expand her finding of oxidative stress, documenting cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism. Palmeieri (2010) provides additional support for mitochondrial dysfunction in autism along with Shoffner (2009), who links fever and mitochondrial dysfunction with the development of ASD. Weissman (2008) argues that defective mitochondrial oxidative phosphorylation is an additional pathogenetic basis for a subset of individuals with autism. This section of the plan is in need of updates in an effort to focus research initiatives more specifically on these new novel findings since they also may provide insight into the development of effective therapeutic strategies and possible etiology of the disorder.

b. What are the remaining gaps in the subject area covered by this chapter?
THIS IS SO CRITICAL IACC. SAFE MINDS EXPRESSES THESE POINTS CLEARLY. Although there was an objective added last year that focuses on the prospective characterization of children with reported regression, it is imperative that this objective include intensive evaluations of infants and toddlers during the reported timeframe of regression. These evaluations must include detailed historical data, extensive physical exams, brain imaging, and laboratory parameters that elucidate the function of a wide range of metabolic, immunologic, and toxicologic parameters in an effort to understand the mechanisms and responsible agents driving these regressions. In addition, many parents have opted to bank cord blood. A secondary research opportunity is to compare cord-blood parameters to those obtained during regression in order to identify what has changed in the child over time, including genetic analysis of both samples in an effort to identify epigenetic alterations, de novo mutations, copy number variation (CNV) aberrations, and potential environmental exposures. Existing databases of phenotype characteristics (behaviors and core deficits) should be expanded to include a list of cooccurring medical differences including CNS, sensory/perceptual, metabolic, immunologic, and gastrointestinal variations found in people with ASD. Attention to metabolic alterations should address detoxification pathways, cell signaling, methylation, apoptosis, growth factors, and porphyrin profiles. There should be a determination of how these characteristics change over time. Rigorous and independent studies on autism prevalence rates over time and across geographies are needed to determine the extent of the apparent autism epidemic, the role of changes in diagnostic practices, the extent to which environmental factors play a causal role in any increase, and what future services might be needed, given the true increase in autism rates.

Respondent 45

a. What has been learned about the issues covered in this chapter in the past year?
This chapter fails to go into depth on the possible environmental triggers, such as bisphenol A (BPA), flu vaccines, and xenotropic murine leukemia virus-related virus (XMRV).

b. What are the remaining gaps in the subject area covered by this chapter?
Potential triggers of ASD under investigation: estrogen mimickers such as BPA, XMRV, ultrasound, etc.

Respondent 47

Duke Crestfield

a. What has been learned about the issues covered in this chapter in the past year?
Finer and different MNS characteristics in ASD people.

b. What are the remaining gaps in the subject area covered by this chapter?
There are lots of simple mirror neuron system (MNS) tests that can be done, but little systematic work. Indications are that ASD people have much stronger MNS with other ASD people than with neurotypicals (NT's), and that the MNS can be developed through increased oxytocin activation, primarily through touch.

Respondent 50

Theresa K. Wrangham

b. What are the remaining gaps in the subject area covered by this chapter?
Research goals in the plan continue to focus on structural differences instead of asking what causes the structural differences. The plan remains heavy in genetic focus. Genetics is funded well privately and federal funds would be better used in the underfunded environmental sciences of this plan, particularly given that genetic studies only indicate to date that a very small percentage of ASD is likely to be strictly genetic. Please use these funds to explore environmental triggers.

Respondent 52

b. What are the remaining gaps in the subject area covered by this chapter?
Aspirational Goal, Research Opportunities. Current: "Research on unique strengths and abilities..." CONSIDER: More specifically, what skills and exceptionalities are seen in a significant majority of autistic spectrum individuals (e.g., types of memory, sense of location/direction, etc.) -- not savant or temporary skills but commonly present and sustained over time. (My non-savant autistic son, and others with autism, can show no preference for letters/simple sentences appearing up or down/inverted; can locate a destination after one visit and much time has elapsed, and after appearing to not pay much attention to where he was going in the first place -- What is this remarkable internal compass about ??, etc.) From this study, we may (1) gain insight into distinct and global brain functioning, and (2) develop programs of intervention -- learning and vocational -- to capitalize on these assets. CONSIDER: While effort is targeting markers and phenomena specific to autism, we may also be able to gain insight and consider intervention that has been successful with other conditions with overlapping symptomology. For example, Alzheimer's, learning disability, attention deficit disorder (ADD), etc. LUMINOSITY is a software program developed as a brain exercise for Alzheimer patients. It has since been used also with Traumatic Brain Injury, etc.

Respondent 54

Rebecca Estepp

a. What has been learned about the issues covered in this chapter in the past year?
Update "What we know" section for new evidence supporting a biological basis for ASD - Zecavati & Spence (2009) - neurometabolic dysfunction; Enstrom (2009) - altered innate immunity; Li (2009) - elevated immune response in brain; Wills (2009) - autoantibodies to cerebellum neurons; Sajdel- Sulkowska (2009) - increase in cerebellar neurotrophin-3/oxidative stress markers; James (2009) - glutathione redox imbalance; Palmeieri (2010), Weissman (2008), Shoffner (2010) - mitochondrial dysfunction.

b. What are the remaining gaps in the subject area covered by this chapter?
(a) Expand objective F to include intensive evaluations during regression: medical history; physical exams; brain imaging; laboratory metabolic, immunologic, and toxicologic parameters to understand mechanisms and responsible agents; comparison of cord blood with regression blood samples to identify time changes, including genetic/epigenetic and toxicologic. (b) Expand phenotype databases to include medical differences and time changes, e.g. central nervous system (CNS), sensory/perceptual, metabolic (including detox pathways, cell signaling, methylation, apoptosis, growth factors, porphyrin profiles), immunologic, and GI variations. (c) Rigorous studies on prevalence over time and across geographies: determine extent of epidemic, role of diagnostic changes/environment, future services needed given real increase.

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Please note that respondent numbers are not sequential due to the fact that some respondents did not provide an answer to each question or sub-question. Some respondents indicated that they wished to have their name and/or affiliation be associated with their response, and in those cases, the information is provided at the top of the response.

Typographical and spelling errors have been corrected and abbreviations lengthened to facilitate searching the document. Every effort was made to avoid altering the meaning of the comments. Responses that referenced an individual respondent's earlier responses (e.g. "See above.") and did not contain additional information were omitted to make this working document more concise. Profane, abusive and/or threatening language, and personally identifiable information have been redacted.

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