Re: Autism and the Environment (NIEH/CDC spin)

[Guest guest]

I saw her at the recent NIEHS meeting in NC which examined the viability of using the VSD for thimerosal/autism research. She was a panel member. This was the meeting which got started after 8 members of Congress wrote Dr. Schwartz, NIEHS Director.

-----Original Message-----From: EOHarm [mailto:EOHarm ]On Behalf Of schaferatsprynetSent: Wednesday, July 26, 2006 3:35 PMEOHarm Subject: Autism and the Environment (NIEH/CDC spin)

Autism and the Environmentby sEnvironmental Health Perspectives Volume 114, Number 7, July 2006http://www.ehponline.org/docs/2006/114-7/editorial.htmlComment: The first words out of her mouth is spin bs, that it is onlyspeculation that the environment plays role in autism. Then sheasserts that the "'autism gene' or set of genes has not yet beenidentified" as if that's a given. She trots out the hidden hordestheory of percieved increase in autism. The rest is a lot of cheapspeculation that autism is anything but mercury in vaccines. This isfrom an NIEH scientist, whom we are supposed to trust. Note where herfunding comes from, which automatically places any of her autismrelated research into the category of junk science. -LennySpeculation that the environment plays a role in the development ofautism primarily comes from two observations: a) although concordanceamong monozygotic twins is high, it is not perfect, and a specific"autism gene" or set of genes has not yet been identified; and theprevalence of autism is higher than previously thought—if it isrising, the rise might be associated with a shift in the environment.Autism is a complex neurodevelopmental disorder defined by impairedsocial interaction, communication deficits, restricted interests, andrepetitive behavioral patterns. These traits can range from mild tovery severe, and may be accompanied by cognitive impairment and othercomorbidities. The autism spectrum disorder (ASD) classificationincludes three disorders: autistic disorder, Asperger disorder, andpervasive developmental disorder not-otherwise-specified; however,there is no evidence that these diagnostic labels representetiologically homogeneous groups.The high concordance rates among monozygotic twins and recurrence infamilies support a strong genetic contribution to ASDs ( et al.1995; Folstein et al. 1977; Ritvo et al. 1985; Steffenburg et al.1989). There is also a growing acceptance that subtle autism-liketraits, such as atypical communication and aloof personality style,more commonly cluster in the nonautistic family members of individualswith autism than in the general population ( 2000). Thesegregation of the milder traits in family members may indicate thepresence of some, but not all, of the factors (genetic orenvironmental) necessary to develop an ASD.To date, no specific genes or combination of genes have beenconsistently associated with autism. Discrepancies in gene-discoverystudies might be, in part, because ASDs result from a variety ofgene–gene and gene–environment combinations. Despite the lack of aspecific genetic mechanism, most researchers agree that the etiologyof autism is heterogeneous and polygenetic, and for some susceptibleindividuals, might involve environmental triggers.Much of the concern surrounding environmental factors and autism comesfrom the perception that the prevalence of autism is increasing. Therehas clearly been a rise in the number of individuals who are actuallydiagnosed with an ASD; however, there are few systematically collecteddata in the same population over time that can be used to evaluatetrue prevalence rate trends (Fombonne 2003; Rutter 2005). Many factorscould contribute to increases in prevalence estimates over time,including changes in diagnostic criteria, increasing availability ofspecialized diagnostic tools, improved case ascertainment, and truechanges in the prevalence.Real shifts in prevalence could result from environmental changes.Systematically monitoring temporal ASD prevalence trends in the samepopulation over time is a necessary step to identifying true changesin prevalence. However, ecologic associations between environmentalchanges and rising autism rates are not sufficient to infer causationfor such a complex disorder.It is unlikely that one or even a few specific environmental agentsare responsible for the majority of ASDs. It is more likely that someindividuals have enhanced susceptibility to insults from theenvironment that may, in combination with their geneticpredisposition, lead to autism. It is rarely possible to distinguishthese complex relationships by simply evaluating trends in the generalpopulation.The much publicized concern over vaccines and autism has primarilybeen based on such ecologic trends. More rigorous studies evaluatingvaccine-related hypotheses are needed to incorporate individual-levelexposure data, account for alternate exposures to metals, and evaluatesusceptible subgroups of the population. However, attention shouldalso be given to other environmental hypotheses.Other environmental exposures found to be associated with autisminclude thalidomide, valproic acid, and infections such as rubella(Arndt et al. 2005; Chess 1971). These relatively rare exposures havebeen evaluated in small studies that have reported subtle effects.Yet, such findings support the plausibility that exposure to anenvironmental agent during a critical window of development can beassociated with development of an ASD. The characteristic traits ofautism are rarely distinguished before 2–3 years of age, but thecascade of events that leads to autism probably occurs much earlier,most likely during early gestation. Research focused on environmentalexposures during critical periods of neurodevelopment should beprioritized.Little is currently known about the etiology of autism, except that itis complex and multifactorial. The interaction between genetic andnongenetic factors during critical periods of neurodevelopmentwarrants further investigation. Until specific susceptibility genesare discovered, the identification of environmental risk factors thatprimarily affect susceptible subgroups may require us to refine ASDsubgroup classifications using specific phenotypic patterns or theclustering of ASDs in families.Given the complexity of autism, we will not find a magic bullet(genetic or environmental) to blame for most cases. There are probablymany combinations of genes and environmental factors that contributeto the constellation of autistic traits. Future investigations ofhypotheses involving environmental exposures need to carefullycharacterize cases, improve exposure assessment, focus on criticalwindows of neurodevelopment, and ensure sufficient power to conductsubgroup analyses and assess interactions. These considerations havebeen accommodated in a few well-planned epidemiologic studies thatare, or soon will be, in progress. As we await advances in genetic andbehavioral research, these studies offer hope for advancing ourunderstanding of the potential role environmental factors play in thedevelopment of autism.The author declares she has no competing financial interests. L. sUniversity of North Carolina School of Public HealthChapel Hill, North CarolinaE-mail: juliedanielsunc (DOT) eduJulie L. s is an assistant professor of epidemiology andmaternal and child health at the University of North Carolina Schoolof Public Health. She directs the North Carolina Center for Autism andDevelopmental Disabilities Research and Epidemiology, funded by theCenters for Disease Control and Prevention. Her research focuses onperinatal environmental exposures that affect infant/child health anddevelopment. -------------------------------------MORE ON THIS NEXT POST

[Guest guest]

I think this is a fair article, actually. She's calling for more research on environmental factors including vaccines. The fact that our nation's scientists are now accepting that environmental triggers plays a role in the autism epidemic is huge. They're finally realizing that autism is not purely genetic. This article is on EHP and read by the folks at NIH and NIEHS. If you read it without prejudice, it looks like a good thing for us.

From: EOHarm [mailto:EOHarm ] On Behalf Of schaferatsprynetSent: Wednesday, July 26, 2006 3:35 PMEOHarm Subject: Autism and the Environment (NIEH/CDC spin)

Autism and the Environmentby sEnvironmental Health Perspectives Volume 114, Number 7, July 2006http://www.ehponline.org/docs/2006/114-7/editorial.htmlComment: The first words out of her mouth is spin bs, that it is onlyspeculation that the environment plays role in autism. Then sheasserts that the "'autism gene' or set of genes has not yet beenidentified" as if that's a given. She trots out the hidden hordestheory of percieved increase in autism. The rest is a lot of cheapspeculation that autism is anything but mercury in vaccines. This isfrom an NIEH scientist, whom we are supposed to trust. Note where herfunding comes from, which automatically places any of her autismrelated research into the category of junk science. -LennySpeculation that the environment plays a role in the development ofautism primarily comes from two observations: a) although concordanceamong monozygotic twins is high, it is not perfect, and a specific"autism gene" or set of genes has not yet been identified; and theprevalence of autism is higher than previously thought—if it isrising, the rise might be associated with a shift in the environment.Autism is a complex neurodevelopmental disorder defined by impairedsocial interaction, communication deficits, restricted interests, andrepetitive behavioral patterns. These traits can range from mild tovery severe, and may be accompanied by cognitive impairment and othercomorbidities. The autism spectrum disorder (ASD) classificationincludes three disorders: autistic disorder, Asperger disorder, andpervasive developmental disorder not-otherwise-specified; however,there is no evidence that these diagnostic labels representetiologically homogeneous groups.The high concordance rates among monozygotic twins and recurrence infamilies support a strong genetic contribution to ASDs ( et al.1995; Folstein et al. 1977; Ritvo et al. 1985; Steffenburg et al.1989). There is also a growing acceptance that subtle autism-liketraits, such as atypical communication and aloof personality style,more commonly cluster in the nonautistic family members of individualswith autism than in the general population ( 2000). Thesegregation of the milder traits in family members may indicate thepresence of some, but not all, of the factors (genetic orenvironmental) necessary to develop an ASD.To date, no specific genes or combination of genes have beenconsistently associated with autism. Discrepancies in gene-discoverystudies might be, in part, because ASDs result from a variety ofgene–gene and gene–environment combinations. Despite the lack of aspecific genetic mechanism, most researchers agree that the etiologyof autism is heterogeneous and polygenetic, and for some susceptibleindividuals, might involve environmental triggers.Much of the concern surrounding environmental factors and autism comesfrom the perception that the prevalence of autism is increasing. Therehas clearly been a rise in the number of individuals who are actuallydiagnosed with an ASD; however, there are few systematically collecteddata in the same population over time that can be used to evaluatetrue prevalence rate trends (Fombonne 2003; Rutter 2005). Many factorscould contribute to increases in prevalence estimates over time,including changes in diagnostic criteria, increasing availability ofspecialized diagnostic tools, improved case ascertainment, and truechanges in the prevalence.Real shifts in prevalence could result from environmental changes.Systematically monitoring temporal ASD prevalence trends in the samepopulation over time is a necessary step to identifying true changesin prevalence. However, ecologic associations between environmentalchanges and rising autism rates are not sufficient to infer causationfor such a complex disorder.It is unlikely that one or even a few specific environmental agentsare responsible for the majority of ASDs. It is more likely that someindividuals have enhanced susceptibility to insults from theenvironment that may, in combination with their geneticpredisposition, lead to autism. It is rarely possible to distinguishthese complex relationships by simply evaluating trends in the generalpopulation.The much publicized concern over vaccines and autism has primarilybeen based on such ecologic trends. More rigorous studies evaluatingvaccine-related hypotheses are needed to incorporate individual-levelexposure data, account for alternate exposures to metals, and evaluatesusceptible subgroups of the population. However, attention shouldalso be given to other environmental hypotheses.Other environmental exposures found to be associated with autisminclude thalidomide, valproic acid, and infections such as rubella(Arndt et al. 2005; Chess 1971). These relatively rare exposures havebeen evaluated in small studies that have reported subtle effects.Yet, such findings support the plausibility that exposure to anenvironmental agent during a critical window of development can beassociated with development of an ASD. The characteristic traits ofautism are rarely distinguished before 2–3 years of age, but thecascade of events that leads to autism probably occurs much earlier,most likely during early gestation. Research focused on environmentalexposures during critical periods of neurodevelopment should beprioritized.Little is currently known about the etiology of autism, except that itis complex and multifactorial. The interaction between genetic andnongenetic factors during critical periods of neurodevelopmentwarrants further investigation. Until specific susceptibility genesare discovered, the identification of environmental risk factors thatprimarily affect susceptible subgroups may require us to refine ASDsubgroup classifications using specific phenotypic patterns or theclustering of ASDs in families.Given the complexity of autism, we will not find a magic bullet(genetic or environmental) to blame for most cases. There are probablymany combinations of genes and environmental factors that contributeto the constellation of autistic traits. Future investigations ofhypotheses involving environmental exposures need to carefullycharacterize cases, improve exposure assessment, focus on criticalwindows of neurodevelopment, and ensure sufficient power to conductsubgroup analyses and assess interactions. These considerations havebeen accommodated in a few well-planned epidemiologic studies thatare, or soon will be, in progress. As we await advances in genetic andbehavioral research, these studies offer hope for advancing ourunderstanding of the potential role environmental factors play in thedevelopment of autism.The author declares she has no competing financial interests. L. sUniversity of North Carolina School of Public HealthChapel Hill, North CarolinaE-mail: juliedanielsunc (DOT) eduJulie L. s is an assistant professor of epidemiology andmaternal and child health at the University of North Carolina Schoolof Public Health. She directs the North Carolina Center for Autism andDevelopmental Disabilities Research and Epidemiology, funded by theCenters for Disease Control and Prevention. Her research focuses onperinatal environmental exposures that affect infant/child health anddevelopment. -------------------------------------MORE ON THIS NEXT POST

[Guest guest]

Hi ,

I am amazed that you consider her remarks to be either fair or of huge significance. That there is an environmental factor to autism is a no-brainer, the option is to state that it is purely genetic and that is simply untenuous if not ridiculous. I do not see in her remarks anything close to admitting to an epidemic.

You will have to forgive me if I don't trust the motives or good faith of CDC funded scientists calling for research into vaccines. Call it a prejudice if you must, I call it prudence.

Lenny

From: EOHarm [mailto:EOHarm ] On Behalf Of FournierSent: Thursday, July 27, 2006 7:21 AMEOHarm Subject: RE: Autism and the Environment (NIEH/CDC spin)

I think this is a fair article, actually. She's calling for more research on environmental factors including vaccines. The fact that our nation's scientists are now accepting that environmental triggers plays a role in the autism epidemic is huge. They're finally realizing that autism is not purely genetic. This article is on EHP and read by the folks at NIH and NIEHS. If you read it without prejudice, it looks like a good thing for us.

From: EOHarm [mailto:EOHarm ] On Behalf Of schaferatsprynetSent: Wednesday, July 26, 2006 3:35 PMEOHarm Subject: Autism and the Environment (NIEH/CDC spin)

Autism and the Environmentby sEnvironmental Health Perspectives Volume 114, Number 7, July 2006http://www.ehponline.org/docs/2006/114-7/editorial.htmlComment: The first words out of her mouth is spin bs, that it is onlyspeculation that the environment plays role in autism. Then sheasserts that the "'autism gene' or set of genes has not yet beenidentified" as if that's a given. She trots out the hidden hordestheory of percieved increase in autism. The rest is a lot of cheapspeculation that autism is anything but mercury in vaccines. This isfrom an NIEH scientist, whom we are supposed to trust. Note where herfunding comes from, which automatically places any of her autismrelated research into the category of junk science. -LennySpeculation that the environment plays a role in the development ofautism primarily comes from two observations: a) although concordanceamong monozygotic twins is high, it is not perfect, and a specific"autism gene" or set of genes has not yet been identified; and theprevalence of autism is higher than previously thought—if it isrising, the rise might be associated with a shift in the environment.Autism is a complex neurodevelopmental disorder defined by impairedsocial interaction, communication deficits, restricted interests, andrepetitive behavioral patterns. These traits can range from mild tovery severe, and may be accompanied by cognitive impairment and othercomorbidities. The autism spectrum disorder (ASD) classificationincludes three disorders: autistic disorder, Asperger disorder, andpervasive developmental disorder not-otherwise-specified; however,there is no evidence that these diagnostic labels representetiologically homogeneous groups.The high concordance rates among monozygotic twins and recurrence infamilies support a strong genetic contribution to ASDs ( et al.1995; Folstein et al. 1977; Ritvo et al. 1985; Steffenburg et al.1989). There is also a growing acceptance that subtle autism-liketraits, such as atypical communication and aloof personality style,more commonly cluster in the nonautistic family members of individualswith autism than in the general population ( 2000). Thesegregation of the milder traits in family members may indicate thepresence of some, but not all, of the factors (genetic orenvironmental) necessary to develop an ASD.To date, no specific genes or combination of genes have beenconsistently associated with autism. Discrepancies in gene-discoverystudies might be, in part, because ASDs result from a variety ofgene–gene and gene–environment combinations. Despite the lack of aspecific genetic mechanism, most researchers agree that the etiologyof autism is heterogeneous and polygenetic, and for some susceptibleindividuals, might involve environmental triggers.Much of the concern surrounding environmental factors and autism comesfrom the perception that the prevalence of autism is increasing. Therehas clearly been a rise in the number of individuals who are actuallydiagnosed with an ASD; however, there are few systematically collecteddata in the same population over time that can be used to evaluatetrue prevalence rate trends (Fombonne 2003; Rutter 2005). Many factorscould contribute to increases in prevalence estimates over time,including changes in diagnostic criteria, increasing availability ofspecialized diagnostic tools, improved case ascertainment, and truechanges in the prevalence.Real shifts in prevalence could result from environmental changes.Systematically monitoring temporal ASD prevalence trends in the samepopulation over time is a necessary step to identifying true changesin prevalence. However, ecologic associations between environmentalchanges and rising autism rates are not sufficient to infer causationfor such a complex disorder.It is unlikely that one or even a few specific environmental agentsare responsible for the majority of ASDs. It is more likely that someindividuals have enhanced susceptibility to insults from theenvironment that may, in combination with their geneticpredisposition, lead to autism. It is rarely possible to distinguishthese complex relationships by simply evaluating trends in the generalpopulation.The much publicized concern over vaccines and autism has primarilybeen based on such ecologic trends. More rigorous studies evaluatingvaccine-related hypotheses are needed to incorporate individual-levelexposure data, account for alternate exposures to metals, and evaluatesusceptible subgroups of the population. However, attention shouldalso be given to other environmental hypotheses.Other environmental exposures found to be associated with autisminclude thalidomide, valproic acid, and infections such as rubella(Arndt et al. 2005; Chess 1971). These relatively rare exposures havebeen evaluated in small studies that have reported subtle effects.Yet, such findings support the plausibility that exposure to anenvironmental agent during a critical window of development can beassociated with development of an ASD. The characteristic traits ofautism are rarely distinguished before 2–3 years of age, but thecascade of events that leads to autism probably occurs much earlier,most likely during early gestation. Research focused on environmentalexposures during critical periods of neurodevelopment should beprioritized.Little is currently known about the etiology of autism, except that itis complex and multifactorial. The interaction between genetic andnongenetic factors during critical periods of neurodevelopmentwarrants further investigation. Until specific susceptibility genesare discovered, the identification of environmental risk factors thatprimarily affect susceptible subgroups may require us to refine ASDsubgroup classifications using specific phenotypic patterns or theclustering of ASDs in families.Given the complexity of autism, we will not find a magic bullet(genetic or environmental) to blame for most cases. There are probablymany combinations of genes and environmental factors that contributeto the constellation of autistic traits. Future investigations ofhypotheses involving environmental exposures need to carefullycharacterize cases, improve exposure assessment, focus on criticalwindows of neurodevelopment, and ensure sufficient power to conductsubgroup analyses and assess interactions. These considerations havebeen accommodated in a few well-planned epidemiologic studies thatare, or soon will be, in progress. As we await advances in genetic andbehavioral research, these studies offer hope for advancing ourunderstanding of the potential role environmental factors play in thedevelopment of autism.The author declares she has no competing financial interests. L. sUniversity of North Carolina School of Public HealthChapel Hill, North CarolinaE-mail: juliedanielsunc (DOT) eduJulie L. s is an assistant professor of epidemiology andmaternal and child health at the University of North Carolina Schoolof Public Health. She directs the North Carolina Center for Autism andDevelopmental Disabilities Research and Epidemiology, funded by theCenters for Disease Control and Prevention. Her research focuses onperinatal environmental exposures that affect infant/child health anddevelopment. -------------------------------------MORE ON THIS NEXT POST

[Guest guest]

What is the definition of epidemic"?A sudden marked INCREASE IN NUMBERS, or a SUDDEN LARGE INCREASE IN NUMBERS CAUSED by an INFECTIOUS AGENT? RE: Autism and the Environment (NIEH/CDC spin)Hi ,I am amazed that you consider her remarks to be either fair or of huge significance. That there is an environmental factor to autism is a no-brainer, the option is to state that it is purely genetic and that is simply untenuous if not ridiculous. I do not see in her remarks anything close to admitting to an epidemic You will have to forgive me if I don't trust the motives or good faith of CDC funded scientists calling for research into vaccines. Call it a prejudice if you must, I call it prudence. LennyFrom: EOHarm [mailto:EOHarm ] On Behalf Of FournierSent: Thursday, July 27, 2006 7:21 AMEOHarm Subject: RE: Autism and the Environment (NIEH/CDC spin)I think this is a fair article, actually. She's calling for more research on environmental factors including vaccines. The fact that our nation's scientists are now accepting that environmental triggers plays a role in the autism epidemic is huge. They're finally realizing that autism is not purely genetic. This article is on EHP and read by the folks at NIH and NIEHS. If you read it without prejudice, it looks like a good thing for us.From: EOHarm [mailto:EOHarm ] On Behalf Of schaferatsprynetSent: Wednesday, July 26, 2006 3:35 PMEOHarm Subject: Autism and the Environment (NIEH/CDC spin)Autism and the Environmentby sEnvironmental Health Perspectives Volume 114, Number 7, July 2006http://www.ehponline.org/docs/2006/114-7/editorial.htmlComment: The first words out of her mouth is spin bs, that it is onlyspeculation that the environment plays role in autism. Then sheasserts that the "'autism gene' or set of genes has not yet beenidentified" as if that's a given. She trots out the hidden hordestheory of percieved increase in autism. The rest is a lot of cheapspeculation that autism is anything but mercury in vaccines. This isfrom an NIEH scientist, whom we are supposed to trust. Note where herfunding comes from, which automatically places any of her autismrelated research into the category of junk science. -LennySpeculation that the environment plays a role in the development ofautism primarily comes from two observations: a) although concordanceamong monozygotic twins is high, it is not perfect, and a specific"autism gene" or set of genes has not yet been identified; and theprevalence of autism is higher than previously thought—if it isrising, the rise might be associated with a shift in the environment.Autism is a complex neurodevelopmental disorder defined by impairedsocial interaction, communication deficits, restricted interests, andrepetitive behavioral patterns. These traits can range from mild tovery severe, and may be accompanied by cognitive impairment and othercomorbidities. The autism spectrum disorder (ASD) classificationincludes three disorders: autistic disorder, Asperger disorder, andpervasive developmental disorder not-otherwise-specified; however,there is no evidence that these diagnostic labels representetiologically homogeneous groups.The high concordance rates among monozygotic twins and recurrence infamilies support a strong genetic contribution to ASDs ( et al.1995; Folstein et al. 1977; Ritvo et al. 1985; Steffenburg et al.1989). There is also a growing acceptance that subtle autism-liketraits, such as atypical communication and aloof personality style,more commonly cluster in the nonautistic family members of individualswith autism than in the general population ( 2000). Thesegregation of the milder traits in family members may indicate thepresence of some, but not all, of the factors (genetic orenvironmental) necessary to develop an ASD.To date, no specific genes or combination of genes have beenconsistently associated with autism. Discrepancies in gene-discoverystudies might be, in part, because ASDs result from a variety ofgene–gene and gene–environment combinations. Despite the lack of aspecific genetic mechanism, most researchers agree that the etiologyof autism is heterogeneous and polygenetic, and for some susceptibleindividuals, might involve environmental triggers.Much of the concern surrounding environmental factors and autism comesfrom the perception that the prevalence of autism is increasing. Therehas clearly been a rise in the number of individuals who are actuallydiagnosed with an ASD; however, there are few systematically collecteddata in the same population over time that can be used to evaluatetrue prevalence rate trends (Fombonne 2003; Rutter 2005). Many factorscould contribute to increases in prevalence estimates over time,including changes in diagnostic criteria, increasing availability ofspecialized diagnostic tools, improved case ascertainment, and truechanges in the prevalence.Real shifts in prevalence could result from environmental changes.Systematically monitoring temporal ASD prevalence trends in the samepopulation over time is a necessary step to identifying true changesin prevalence. However, ecologic associations between environmentalchanges and rising autism rates are not sufficient to infer causationfor such a complex disorder.It is unlikely that one or even a few specific environmental agentsare responsible for the majority of ASDs. It is more likely that someindividuals have enhanced susceptibility to insults from theenvironment that may, in combination with their geneticpredisposition, lead to autism. It is rarely possible to distinguishthese complex relationships by simply evaluating trends in the generalpopulation.The much publicized concern over vaccines and autism has primarilybeen based on such ecologic trends. More rigorous studies evaluatingvaccine-related hypotheses are needed to incorporate individual-levelexposure data, account for alternate exposures to metals, and evaluatesusceptible subgroups of the population. However, attention shouldalso be given to other environmental hypotheses.Other environmental exposures found to be associated with autisminclude thalidomide, valproic acid, and infections such as rubella(Arndt et al. 2005; Chess 1971). These relatively rare exposures havebeen evaluated in small studies that have reported subtle effects.Yet, such findings support the plausibility that exposure to anenvironmental agent during a critical window of development can beassociated with development of an ASD. The characteristic traits ofautism are rarely distinguished before 2–3 years of age, but thecascade of events that leads to autism probably occurs much earlier,most likely during early gestation. Research focused on environmentalexposures during critical periods of neurodevelopment should beprioritized.Little is currently known about the etiology of autism, except that itis complex and multifactorial. The interaction between genetic andnongenetic factors during critical periods of neurodevelopmentwarrants further investigation. Until specific susceptibility genesare discovered, the identification of environmental risk factors thatprimarily affect susceptible subgroups may require us to refine ASDsubgroup classifications using specific phenotypic patterns or theclustering of ASDs in families.Given the complexity of autism, we will not find a magic bullet(genetic or environmental) to blame for most cases. There are probablymany combinations of genes and environmental factors that contributeto the constellation of autistic traits. Future investigations ofhypotheses involving environmental exposures need to carefullycharacterize cases, improve exposure assessment, focus on criticalwindows of neurodevelopment, and ensure sufficient power to conductsubgroup analyses and assess interactions. These considerations havebeen accommodated in a few well-planned epidemiologic studies thatare, or soon will be, in progress. As we await advances in genetic andbehavioral research, these studies offer hope for advancing ourunderstanding of the potential role environmental factors play in thedevelopment of autismThe author declares she has no competing financial interests. L. sUniversity of North Carolina School of Public HealthChapel Hill, North CarolinaE-mail: juliedanielsunc (DOT) eduJulie L. s is an assistant professor of epidemiology andmaternal and child health at the University of North Carolina Schoolof Public Health. She directs the North Carolina Center for Autism andDevelopmental Disabilities Research and Epidemiology, funded by theCenters for Disease Control and Prevention. Her research focuses onperinatal environmental exposures that affect infant/child health anddevelopment. -------------------------------------MORE ON THIS NEXT POST

[Guest guest]

Research into chelators, biochemical processes to enhance excretion of heavy metals and immune dysfunction/disregulation will help.

You cure/prevent autism in general by changing the vaccine protocol to something more rational (think Japan), much less damaging and avoid heavy metal toxicities in the environment. This is scientifically extremely easy to do.

You cure a mercury poisoned person through chelation, enhancing the natural biochemical processes available to detoxify and you restore appropriate immune regulation.

Anything else, with minor exception, should be in a superhero comic book.

RE: Autism and the Environment (NIEH/CDC spin)

I respectfully disagree. This article is mixing up good with the bad; kind of like sugar coated poison. In some ways it kind of reminds me of the CAA movement...lets be as vague as possible and chasing these windmills around and around. I do not appreciate that. Mercking up the waters and confusing this very simple issue that a neurotoxin causes neurodevepmental disorders does not help our children get a proper diagnosis and get better. Why can't we promote more research into mercury chelators instead of the genetic stuff.

The research from France is specific proof of the"enviromental factor". Eli Lilly's MSDS clearly states that Thimerosal is 49.6% mercury and it alters genetic material. Mercury poisoing is not genetic... mercury alters genetic material. It is like saying lets study a forest and see if there are trees in it. Maybe the abilitly to excrete poison might be somewhat genetic to some degree but poison is poison.

We need to stay on the right track for our kids.

Fournier <wendysweb> wrote:

I think this is a fair article, actually. She's calling for more research on environmental factors including vaccines. The fact that our nation's scientists are now accepting that environmental triggers plays a role in the autism epidemic is huge. They're finally realizing that autism is not purely genetic. This article is on EHP and read by the folks at NIH and NIEHS. If you read it without prejudice, it looks like a good thing for us.

From: EOHarm [mailto:EOHarm ] On Behalf Of schaferatsprynetSent: Wednesday, July 26, 2006 3:35 PMEOHarm Subject: Autism and the Environment (NIEH/CDC spin)

Autism and the Environmentby sEnvironmental Health Perspectives Volume 114, Number 7, July 2006http://www.ehponline.org/docs/2006/114-7/editorial.htmlComment: The first words out of her mouth is spin bs, that it is onlyspeculation that the environment plays role in autism. Then sheasserts that the "'autism gene' or set of genes has not yet beenidentified" as if that's a given. She trots out the hidden hordestheory of percieved increase in autism. The rest is a lot of cheapspeculation that autism is anything but mercury in vaccines. This isfrom an NIEH scientist, whom we are supposed to trust. Note where herfunding comes from, which automatically places any of her autismrelated research into the category of junk science. -LennySpeculation that the environment plays a role in the development ofautism primarily comes from two observations: a) although concordanceamong monozygotic twins is high, it is not perfect, and a specific"autism gene" or set of genes has not yet been identified; and theprevalence of autism is higher than previously thought—if it isrising, the rise might be associated with a shift in the environment.Autism is a complex neurodevelopmental disorder defined by impairedsocial interaction, communication deficits, restricted interests, andrepetitive behavioral patterns. These traits can range from mild tovery severe, and may be accompanied by cognitive impairment and othercomorbidities. The autism spectrum disorder (ASD) classificationincludes three disorders: autistic disorder, Asperger disorder, andpervasive developmental disorder not-otherwise-specified; however,there is no evidence that these diagnostic labels representetiologically homogeneous groups.The high concordance rates among monozygotic twins and recurrence infamilies support a strong genetic contribution to ASDs ( et al.1995; Folstein et al. 1977; Ritvo et al. 1985; Steffenburg et al.1989). There is also a growing acceptance that subtle autism-liketraits, such as atypical communication and aloof personality style,more commonly cluster in the nonautistic family members of individualswith autism than in the general population ( 2000). Thesegregation of the milder traits in family members may indicate thepresence of some, but not all, of the factors (genetic orenvironmental) necessary to develop an ASD.To date, no specific genes or combination of genes have beenconsistently associated with autism. Discrepancies in gene-discoverystudies might be, in part, because ASDs result from a variety ofgene–gene and gene–environment combinations. Despite the lack of aspecific genetic mechanism, most researchers agree that the etiologyof autism is heterogeneous and polygenetic, and for some susceptibleindividuals, might involve environmental triggers.Much of the concern surrounding environmental factors and autism comesfrom the perception that the prevalence of autism is increasing. Therehas clearly been a rise in the number of individuals who are actuallydiagnosed with an ASD; however, there are few systematically collecteddata in the same population over time that can be used to evaluatetrue prevalence rate trends (Fombonne 2003; Rutter 2005). Many factorscould contribute to increases in prevalence estimates over time,including changes in diagnostic criteria, increasing availability ofspecialized diagnostic tools, improved case ascertainment, and truechanges in the prevalence.Real shifts in prevalence could result from environmental changes.Systematically monitoring temporal ASD prevalence trends in the samepopulation over time is a necessary step to identifying true changesin prevalence. However, ecologic associations between environmentalchanges and rising autism rates are not sufficient to infer causationfor such a complex disorder.It is unlikely that one or even a few specific environmental agentsare responsible for the majority of ASDs. It is more likely that someindividuals have enhanced susceptibility to insults from theenvironment that may, in combination with their geneticpredisposition, lead to autism. It is rarely possible to distinguishthese complex relationships by simply evaluating trends in the generalpopulation.The much publicized concern over vaccines and autism has primarilybeen based on such ecologic trends. More rigorous studies evaluatingvaccine-related hypotheses are needed to incorporate individual-levelexposure data, account for alternate exposures to metals, and evaluatesusceptible subgroups of the population. However, attention shouldalso be given to other environmental hypotheses.Other environmental exposures found to be associated with autisminclude thalidomide, valproic acid, and infections such as rubella(Arndt et al. 2005; Chess 1971). These relatively rare exposures havebeen evaluated in small studies that have reported subtle effects.Yet, such findings support the plausibility that exposure to anenvironmental agent during a critical window of development can beassociated with development of an ASD. The characteristic traits ofautism are rarely distinguished before 2–3 years of age, but thecascade of events that leads to autism probably occurs much earlier,most likely during early gestation. Research focused on environmentalexposures during critical periods of neurodevelopment should beprioritized.Little is currently known about the etiology of autism, except that itis complex and multifactorial. The interaction between genetic andnongenetic factors during critical periods of neurodevelopmentwarrants further investigation. Until specific susceptibility genesare discovered, the identification of environmental risk factors thatprimarily affect susceptible subgroups may require us to refine ASDsubgroup classifications using specific phenotypic patterns or theclustering of ASDs in families.Given the complexity of autism, we will not find a magic bullet(genetic or environmental) to blame for most cases. There are probablymany combinations of genes and environmental factors that contributeto the constellation of autistic traits. Future investigations ofhypotheses involving environmental exposures need to carefullycharacterize cases, improve exposure assessment, focus on criticalwindows of neurodevelopment, and ensure sufficient power to conductsubgroup analyses and assess interactions. These considerations havebeen accommodated in a few well-planned epidemiologic studies thatare, or soon will be, in progress. As we await advances in genetic andbehavioral research, these studies offer hope for advancing ourunderstanding of the potential role environmental factors play in thedevelopment of autism.The author declares she has no competing financial interests. L. sUniversity of North Carolina School of Public HealthChapel Hill, North CarolinaE-mail: juliedanielsunc (DOT) eduJulie L. s is an assistant professor of epidemiology andmaternal and child health at the University of North Carolina Schoolof Public Health. She directs the North Carolina Center for Autism andDevelopmental Disabilities Research and Epidemiology, funded by theCenters for Disease Control and Prevention. Her research focuses onperinatal environmental exposures that affect infant/child health anddevelopment. -------------------------------------MORE ON THIS NEXT POST

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