A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States

Dufault, Renee; Lukiw, Walter J.; Crider, Raquel; Schnoll, Roseanne; Wallinga, David; Deth, Richard C.

doi:10.1186/1868-7083-4-6

Cited by 50 publications

(51 citation statements)

References 59 publications

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“…Further, the biological plausibility of these insecticides as a cause of autism has been described and wheat and corn have been identified as the most important sources of OP exposure among U.S. children [19]. However, the temporal trend in total OP insecticide use does not correlate well to the trend in autism.…”

Section: Discussionmentioning

confidence: 99%

A comparison of temporal trends in United States autism prevalence to trends in suspected environmental factors

Nevison

2014

Environ Health

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BackgroundThe prevalence of diagnosed autism has increased rapidly over the last several decades among U.S. children. Environmental factors are thought to be driving this increase and a list of the top ten suspected environmental toxins was published recently.MethodsTemporal trends in autism for birth years 1970–2005 were derived from a combination of data from the California Department of Developmental Services (CDDS) and the United States Individuals with Disabilities Education Act (IDEA). Temporal trends in suspected toxins were derived from data compiled during an extensive literature survey. Toxin and autism trends were compared by visual inspection and computed correlation coefficients. Using IDEA data, autism prevalence vs. birth year trends were calculated independently from snapshots of data from the most recent annual report, and by tracking prevalence at a constant age over many years of reports. The ratio of the snapshot:tracking trend slopes was used to estimate the "real" fraction of the increase in autism.ResultsThe CDDS and IDEA data sets are qualitatively consistent in suggesting a strong increase in autism prevalence over recent decades. The quantitative comparison of IDEA snapshot and constant-age tracking trend slopes suggests that ~75-80% of the tracked increase in autism since 1988 is due to an actual increase in the disorder rather than to changing diagnostic criteria. Most of the suspected environmental toxins examined have flat or decreasing temporal trends that correlate poorly to the rise in autism. Some, including lead, organochlorine pesticides and vehicular emissions, have strongly decreasing trends. Among the suspected toxins surveyed, polybrominated diphenyl ethers, aluminum adjuvants, and the herbicide glyphosate have increasing trends that correlate positively to the rise in autism.ConclusionsDiagnosed autism prevalence has risen dramatically in the U.S over the last several decades and continued to trend upward as of birth year 2005. The increase is mainly real and has occurred mostly since the late 1980s. In contrast, children’s exposure to most of the top ten toxic compounds has remained flat or decreased over this same time frame. Environmental factors with increasing temporal trends can help suggest hypotheses for drivers of autism that merit further investigation.Electronic supplementary materialThe online version of this article (doi:10.1186/1476-069X-13-73) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

A comparison of temporal trends in United States autism prevalence to trends in suspected environmental factors

Nevison

2014

Environ Health

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“…In utero, DNA methylation alters expression of multiple proteins through epigenetics [42] and as a result DNA hypomethylation can lead to an epigenetic reprogramming of the fetal brain to adjust to sulfur deficiency [13,14,43]. It has also been demonstrated that parents of children with ASD have the same impairment in sulfur metabolism observed in ASD [44].…”

Section: Asd Sulfur Metabolism Glutathione and Ammoniamentioning

confidence: 78%

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Seneff¹,

Lauritzen

Davidson³

et al. 2013

Entropy

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This paper makes two claims: (1) autism can be characterized as a chronic lowgrade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is provoked by a systemic deficiency in sulfate, but associated seizures and fever support sulfate restoration. We argue that impaired synthesis of cholesterol sulfate in the skin and red blood cells, catalyzed by sunlight and nitric oxide synthase enzymes, creates a state of colloidal instability in the blood manifested as a low zeta potential and increased interfacial stress. Encephalitis, while life-threatening, can result in partial renewal of sulfate supply, promoting neuronal survival. Research is cited showing how taurine may not only help protect neurons from hypochlorite exposure, but also provide a source for sulfate renewal. Several environmental factors can synergistically promote the encephalopathy of autism, including the herbicide, glyphosate, aluminum, mercury, lead, nutritional deficiencies in thiamine and zinc, and yeast overgrowth due to excess dietary sugar. Given these facts, dietary and lifestyle changes, including increased sulfur ingestion, organic whole foods, increased sun exposure, and avoidance of toxins such as aluminum, mercury, and lead, may help to alleviate symptoms or, in some instances, to prevent autism altogether. OPEN ACCESSEntropy 2013, 15 373

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“…An association between reduced PON1 activity and autism in the United States was reported in [67]. Factors which might have contributed to this deficiency that were considered included excess dietary high fructose corn syrup (HFCS), insufficient dietary magnesium, and exposure to mercury.…”

Section: Methionine Synthase Reactionmentioning

confidence: 98%

Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?

Hartzell

Seneff

2012

Entropy

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Autism is a brain disorder involving social, memory, and learning deficits, that normally develops prenatally or early in childhood. Frustratingly, many research dollars have as yet failed to identify the cause of autism. While twin concordance studies indicate a strong genetic component, the alarming rise in the incidence of autism in the last three decades suggests that environmental factors play a key role as well. This dichotomy can be easily explained if we invoke a heritable epigenetic effect as the primary factor. Researchers are just beginning to realize the huge significance of epigenetic effects taking place during gestation in influencing the phenotypical expression. Here, we propose the novel hypothesis that sulfates deficiency in both the mother and the child, brought on mainly by excess exposure to environmental toxins and inadequate sunlight exposure to the skin, leads to widespread hypomethylation in the fetal brain with devastating consequences. We show that many seemingly disparate observations regarding serum markers, neuronal pathologies, and nutritional deficiencies associated with autism can be integrated to support our hypothesis

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A macroepigenetic approach to identify factors responsible for the autism epidemic in the United States

Cited by 50 publications

References 59 publications

A comparison of temporal trends in United States autism prevalence to trends in suspected environmental factors

A comparison of temporal trends in United States autism prevalence to trends in suspected environmental factors

Is Encephalopathy a Mechanism to Renew Sulfate in Autism?

Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?

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