Rise In Autism Research Articles

Assessing Chemical Intolerance in Parents Predicts the Risk of Autism and ADHD in Their Children.

We sought to replicate our 2015 findings linking chemical intolerance in parents with the risk of their children developing autism and/or ADHD. Drawing upon our 2021 discovery of a strong association between chemical intolerance and mast cells, we propose an explanation for this link. In a population-based survey of U.S. adults, we used the internationally validated Quick Environmental Exposure and Sensitivity Inventory (QEESI) to assess symptom severity and chemical intolerance. Parents were asked how many of their biological children had been diagnosed with autism and/or ADHD. Parents with chemical intolerance scores in the top versus bottom tenth percentile had 5.7 times the risk of reporting a child with autism and 2.1 times for ADHD. High chemical intolerance scores among parents of children with autism, coupled with our 2021 discovery of mast cell activation as a plausible biomechanism for chemical intolerance, suggest that (1) the QEESI can identify individuals at increased risk, (2) environmental counseling may reduce personal exposures and risk, and (3) the global rise in autism and ADHD may be due to fossil-fuel-derived and biogenic toxicants epigenetically "turning on" or "turning off" critical mast cell genes that can be transmitted transgenerationally. It is important to note that this study was observational in nature; as such, further research is needed using controlled trials to confirm causality and explore the proposed mechanism.

The Rise of Autism in Kenya: Implications to the stakeholders in Education – Literature Review

This article explored why autism is on the rise globally and the appropriate measures to take to support them. The article found out that the rise in autism may have been contributed due to improved access to healthcare, the society is enlightened and some expanded diagnostic criteria. The article also found that globally there are about 1 in 160 children with ASD while in Kenya it affects approximately four per cent of the population, while the prevalence of higher autism (H-AUT) was found in 0.63% of adolescents and young adults. The article also found out that learners with ASD in Africa are socially isolated and are never neither diagnosed nor treated and in many parts of the continent, developmental disabilities carry a societal stigma and often are attributed to a curse. The article also found out that learners with autism encounter many challenges in their education such lack of a syllabus, educators who were untrained, negative perspective from peers, inadequate learning materials, improper policies and lawful framework for special needs, and high forecast of caregivers, the time assigned per class and that learners with autism are tremendously disoriented by unorganised surroundings. The article further found that the risk factor of ASD is multi systemic including both hereditary and non-hereditary factors contributing. The article further found that there are education measures and treatment methods for learners with autism and preventive measures for them. The article further found that there are several adequate measures for employees with ASD that can be incorporated by their employers to ensure they work effectively. The article concluded by identifying implications to the stakeholders to the rise of autism including an increased appeal for special education services, modifications of the environment, parental involvement and increased resources, advocacy, training of teachers and collaboration among others

Identification of Best Fit Learning Models Based on Calibration for Better Classification of Autism

This paper is intended to exhibit the novel approach to improve the efficiency of the supervised learning models towards the accuracy of the predictions made to classify the autism from that of the normal subject. The state of the art is about 60-75% of Autism classification accuracy. The early prediction of autism plays a vital role as the rise of autism is alarming. The invasive way to analyze the problem at the earliest would render much support to the Autism Spectrum Disorder (ASD) community. In this work, various supervised learning models are first tested on 1101 subjects with 530 ASD subjects and 571 Normal subjects. The Datasets worked are collected from Autism Brain Imaging Data Exchange (ABIDE) repository. The performance measure is calibrated in terms of Brier score which is an accuracy measure of the predictions in probabilistic way. After assessing in probabilistic way, the statistically emphasized models are then evaluated for the same set of data to validate the prediction model efficiency with their statistical measures made and hence developing the confidence of the model selection for better classification based on probability calibration (CAL). The performance evaluation of the model is tested with probability calibrated assessment and found that for given dataset the SVM and Logistic Regression provided better accuracy measure compared to other considered learning models. It is necessary to frame a hypothesis measure on the dataset before any model is deployed. This approach helps to identify the desired and validated supervised model for the given data samples.

Offline encoding impaired by epigenetic regulations of monoamines in the guided propagation model of autism

BackgroundEnvironmental factors can modify the expression of genes, including those involved in the metabolism of neurotransmitters. Accounting for a control role of monoamine neurotransmitters, the guided propagation (GP) memory model may contribute to investigate the consequences of neuromodulation impairments on development disorders such as autism. A prenatal transient excess of ‘monoamine oxidase A’ enzyme is assumed here to trigger persistent epigenetic regulations that would induce imbalanced metabolisms of synaptic monoamines. When imported into the ‘offline’ encoding cycles of a GP model, the consequent ‘serotoninergic noise’ leads to aberrant memory structures that can be linked with autism symptoms.ResultsIn computer experiments, different levels of uncoupling between representations of monoamines correlate with the amount of impaired GP modules, the severity of irrelevant connections, as well as network overgrowth. Two types of faulty connections are respectively assumed to underlie autism traits, namely repetitive behavior and perceptual oversensitivity. Besides computational modelling, a genetic family-tree shows how the autism sex-ratio can result from combinations of pharmacological and epigenetic features.ConclusionsThese results suggest that the current rise of autism is favored by three possible sources of biological masking: (1) during sleep, when cyclic variations of monoamines may undergo disrupted enzymatic activities; (2) across generations of ‘healthy carriers’ protected by the X-chromosome silencing and a specific genetic variant; (3) early in life, as long as the brain development draws on pools of neurons born when the transient enzymatic excess and its persistent epigenetic regulation overlapped, and as long as the B type of monoamine oxidase does not significantly impact dopamine. A disease-modifying therapy can be derived from this study, which involves relevant biomarkers to be first monitored over several months of clinical trial.

Early Disruption of the Microbiome Leading to Decreased Antioxidant Capacity and Epigenetic Changes: Implications for the Rise in Autism.

Currently, 1 out of every 59 children in the United States is diagnosed with autism. While initial research to find the possible causes for autism were mostly focused on the genome, more recent studies indicate a significant role for epigenetic regulation of gene expression and the microbiome. In this review article, we examine the connections between early disruption of the developing microbiome and gastrointestinal tract function, with particular regard to susceptibility to autism. The biological mechanisms that accompany individuals with autism are reviewed in this manuscript including immune system dysregulation, inflammation, oxidative stress, metabolic and methylation abnormalities as well as gastrointestinal distress. We propose that these autism-associated biological mechanisms may be caused and/or sustained by dysbiosis, an alteration to the composition of resident commensal communities relative to the community found in healthy individuals and its redox and epigenetic consequences, changes that in part can be due to early use and over-use of antibiotics across generations. Further studies are warranted to clarify the contribution of oxidative stress and gut microbiome in the pathophysiology of autism. A better understanding of the microbiome and gastrointestinal tract in relation to autism will provide promising new opportunities to develop novel treatment modalities.

Autism Advocacy: A Network Striving for Equity

In this exploratory case study, we examine the rise of autism on the policy agenda and the new generation of autism advocacy. We focus especially on interconnections between the rhetoric about autism in the media and the emergence and political effectiveness of Autism Speaks, the nation's largest autism advocacy group. We portray how influential social actors frame the story of autism and how they have secured policy victories for youth with autism and their families. Whether issue framing affects policy by motivating network collaboration, or whether collaboration affects how social actors frame issues to affect policy is of fundamental concern in our preliminary analyses. We conclude by discussing implications for new research on the framing of the issue and network development.

The prevalence puzzle: Autism counts

Shifting diagnoses and heightened awareness explain only part of the apparent rise in autism. Scientists are struggling to explain the rest.

New Information That People in High Places Do Not Want Us to Know About Autism

Until the 1930s, the term “autism” was not mentioned in the literature. Until then, vaccination programs did not exist in the United States. Leo Kanner applied the term “early infantile autism,” detailing 11 cases of children born in 1931. He thought these children seemed like they inhabited a world of one, hence the term “autism,” originally derived from Bleuler (1911). Kanner furnished the following description: “aloneness that, whenever possible, disregards, ignores, shuts out anything that comes to the child from the outside.” He initially claimed parents of children with autism were often cold and humorless perfectionists (Kanner, 1943), considering them to be “emotional refrigerators,” a characterization that haunted him, one he deeply regretted and ultimately recanted. There has been a significant rise in autism. Some of this is probably due to looser definitions, widened to include a broad “spectrum” of behaviors. However, even when I tightened up the criteria for inclusion, I still was able to observe a rather sizeable—in fact, dramatic and alarming—increment. Curious about why this might be so, I began to investigate. I discovered a great deal of secrecy, nontransparency, obstructionism, mystification, and even falsification of data in which people in high places were engaged. This article is intended to disclose facts heretofore obscured, hidden, or reassembled in fanciful ways and to raise questions and make scientific statements and social commentary on this highly important issue. Possible sources of toxicity are listed.

Regarding the Rise in Autism: Vaccine Safety Doubt, Conditions of Inquiry, and the Shape of Freedom

Abstract Beginning in the 1980s in the United States, a growing number of parents of children diagnosed with autism and other problems related to neurodevelopment began to suspect that their children's conditions were caused by, or somehow related to, vaccinations. By the early 21st century, the idea that something about childhood vaccinations are the cause, may be the cause, or may be one contributing factor in the apparently rising numbers of children with neurodevelopmental problems had spread widely. This article traces parent anxiety about a connection between autism and vaccines. It illustrates the ways in which a large number of parents think about potential risks of vaccines and make decisions about immunizing their children. It focuses on their doubt and responsibilities, and shows how they negotiate their relationship to medical expertise and the ethics of citizenship. Overall, this article explores the rise of autism into public awareness—as a mutable object of knowledge, a protean disease category, and an exemplar of the condition of uncertainty today—to show the limits of risk assessment as a way of managing life. [risk assessment, subjectivity, ethic of care, technologies of doubt]

Commentary: Diagnostic change and the increased prevalence of autism

Commentary: Diagnostic change and the increased prevalence of autism

Commentary: Fact and artefact in the secular increase in the rate of autism

King and Bearman sought to determine whether the increased prevalence of an autism diagnosis in California was due to diagnostic substitution of autism in place of mental retardation (MR). They make good use of systematic administrative data from the California Department of Developmental Services between 1992 and 2005 for this purpose, with the conclusion that changes in diagnostic practices accounted for a quarter of the observed increase in diagnosed autism over this time period. They discuss this finding as reflecting diagnostic substitution or accretion, but it is clear that there was almost no substitution. Thus, in 95% of the cases the change was from ‘pure’ MR to MR plus autism. Figure 3 in King & Bearman indicates a substantial increase in MR between 1992 and 2005, although the proportional increase for autism was greater. Most of the rise applied to ‘pure’ autism, about a quarter to ‘pure’ MR being changed to MR and autism, and very little to MR being replaced by autism. In other words, the main change in diagnostic practice concerned an increased willingness to note co-morbidity. Given that the increase in ‘pure’ autism between 1992 and 2005 was huge (from 4446 to 28 046 cases)—a much greater rise than for co-morbidity (3210–10 410), it is dubious whether the latter increase does much to help in resolving the key basic issue of whether there has been a true increase over time in the incidence of autism. That is particularly so when the available evidence suggests that the main rise has not predominantly involved autism associated with intellectual disability; rather, it seems to have particularly involved autism in individuals with non-verbal IQ in the normal range. King and Bearman quite properly pointed out that they could not examine that suggestion in their dataset. Nevertheless, the consequence is that their main focus was off-target with respect to the observed rise. Almost all reviews have concluded that a substantial part of the rise in the rate of diagnosed autism has been due to a combination of better ascertainment and a broadening of the diagnostic concept, but has there been, in addition, a true rise in incidence? In my view, we simply do not know. The rise has been seen in Europe, the USA and Japan, but there is a geographic variability in whether the main rise began in the 1970s and 80s, or rather in the 1990s. The claims that the so-called ‘epidemic’ of autism was due to either the measles–mumps–rubella (MMR) vaccine or mercury-containing preservative thimerosal that used to be present in many vaccines are not supported by the evidence. Most crucially, in Japan, where MMR was discontinued at a time when it remained in wide use in other countries, the removal of MMR was not followed by any fall in the rate of autism, or even by a reduction in the rate of rise. Similarly, the discontinuation of use of thimerosal in Scandanavia was not followed by any change in the rising rate of autism. Nevertheless, these findings do not rule out a risk effect from other prenatal or postnatal toxins or other hazards. Large-scale prospective epidemiological/longitudinal studies with good biological measures and good diagnostic procedures are needed to test that possibility. The ongoing MoBa study of mothers and babies in Norway constitutes one good example of what is needed in that connection. It should be added that the factor responsible for a real rise in autism (if that truly has occurred) need not necessarily be a specific environmental hazard. The trigger could be a rising age of parenthood, given the evidence that high paternal age is associated with an increased rate of autism in the offspring. How might that operate? One possibility is that it increases the rate of developmental perturbations such as copy number variation (i.e. submicroscopic substitutions or deletion) or minor congenital anomalies or chromosomal anomalies, all of which have been found to be more common in autism. Whilst there is value in considering the role of changing concepts and better ascertainment in the observed rise in the rate of diagnosed autism, and there is still uncertainty on whether or not there has been a true rise in incidence, the greater the need is for hypothesis-testing focused research on possible causal mechanisms that could lead to changes in incidence. MRC SGDP Centre, PO 80, Institute of Psychiatry, King’s College London, De Crespigny Park, Denmark Hill, London SE5 8AF, UK. E-mail: camilla.azis@kcl.ac.uk Published by Oxford University Press on behalf of the International Epidemiological Association

Is autism reversible?

INTRODUCTION Autism is a neurodevelopmental disorder characterized by limited ability to interact and communicate with others (1). Autism affects all races, ethnic groups and socioeconomic levels, with males experiencing this disorder 2 to 6.5 times more commonly than females (1). More recently, autism is referred to as ‘autism spectrum disorder’ (ASD), as afflicted individuals manifest varied signs and symptoms and with differing severity. Some people with milder forms of autism are able to function, while others with severe forms of the disorder are completely disabled. Although the American Academy of Pediatrics (AAP) has concluded that ‘ASDs, similar to other neurodevelopmental disabilities, are generally not ‘curable’ and chronic management is required’ (2), this paper respectfully proposes the viewpoint that some cases (not all) of autism are, in fact, reversible. Recent literature suggests that the incidence of autism has climbed by over 1500% in <20 years from a rate of around 1:2500 in the mid 1980s to a rate of 1:150 by 2002 (3)—with reported rates as high as 1:94 in some areas of America (1). Hypothetically, a 20% increase in cancer or 25% increase in heart disease might provoke clamour for an explanation; the colossal rise in autism, however, is sometimes passed off as incidental. Although many believe the ASD escalation represents better and earlier diagnosis, improved public awareness and expanding criteria to fulfil the diagnosis, these changes do not appear to adequately account for the rapid rise (4). It is possible that some of the escalating prevalence of ASD reflects an escalating prevalence of one or more causative determinants. Accordingly, to reverse the rising incidence in population groups, it is necessary to identify and diminish the prevalence of such determinants. To reverse ASD within an individual, it is necessary to reverse the cause within that person if possible.

The Rise in Autism and the Mercury Myth

The Rise in Autism and the Mercury Myth

The rise in autism and the role of age at diagnosis.

Autism prevalence in California, based on individuals eligible for state-funded services, rose throughout the 1990s. The extent to which this trend is explained by changes in age at diagnosis or inclusion of milder cases has not been previously evaluated. Autism cases were identified from 1990 through 2006 in databases of the California Department of Developmental Services, which coordinates services for individuals with specific developmental disorders. The main outcomes were population incident cases younger than age 10 years for each quarter, cumulative incidence by age and birth year, age-specific incidence rates stratified by birth year, and proportions of diagnoses by age across birth years. Autism incidence in children rose throughout the period. Cumulative incidence to 5 years of age per 10,000 births rose consistently from 6.2 for 1990 births to 42.5 for 2001 births. Age-specific incidence rates increased most steeply for 2- and 3-year olds. The proportion diagnosed by age 5 years increased only slightly, from 54% for 1990 births to 61% for 1996 births. Changing age at diagnosis can explain a 12% increase, and inclusion of milder cases, a 56% increase. Autism incidence in California shows no sign yet of plateauing. Younger ages at diagnosis, differential migration, changes in diagnostic criteria, and inclusion of milder cases do not fully explain the observed increases. Other artifacts have yet to be quantified, and as a result, the extent to which the continued rise represents a true increase in the occurrence of autism remains unclear.

Prenatal influences on brain dopamine and their relevance to the rising incidence of autism

The incidence of autism has risen 10-fold since the early 1980s, with most of this rise not explainable by changing diagnostic criteria. The rise in autism is paradoxical in that autism is considered to be one of the most genetically determined of the major neurodevelopmental disorders and should accordingly either be stable or even declining. Because a variety of epigenetic influences, particularly those occurring during the prenatal period, can override or masquerade as genetic influences, these should be considered as prime contributors to the recent increase of autism. Prenatal influences on dopamine activity are especially well-documented, including the effects of maternal psychosocial stress, maternal fever, maternal genetic and hormonal status, use of certain medications, urban birth, and fetal hypoxia. All of these factors have been implicated in the genesis of autism, which is characterized by a "hyperdopaminergic" state based on evidence from monkey and human behavioral studies, pharmacological studies in humans, and a left-hemispheric predominance of both dopamine and autistic-like symptoms. Chronically high maternal levels of dopamine caused by the pressures of increasingly urbanized societies and by changing maternal demographics such as increased workforce participation, educational achievement level, and age at first birth, may be especially significant epigenetic contributors to the recent autism rise.

New study fails to find link between MMR and autism

A new study published in the British Medical Journal failed to find any temporal link between the rise in autism and the prevalence of MMR vaccine usage. The report, based on a time trend analysis of data from the UK general practice database, studied children aged 12 or younger diagnosed with autism in 1988–1999, with further analysis of boys aged 2–5 years born between 1988 and 1993. They found that the rate of autism rose sevenfold from 0.3 cases per 10 000 people per year to 2.1 cases per 10 000 people per year. Analysis of 2–5-year-old boys born between 1988 and 1993 showed that the rate of autism quadrupled, whereas the prevalence of MMR vaccination remained stable at over 95%. Lead author Dr James Kaye, of the Boston University School of Medicine, concludes that, ‘…because the incidence of autism among 2–5-year-olds increased markedly among boys born in each year separately from 1988 to 1993, while MMR vaccine coverage was over 95% for successive annual birth cohorts, the data provide evidence that no correlation exists between the prevalence of MMR vaccination and the rapid increase in the risk of autism over time.’ The authors suggest that increase in recorded diagnoses of autism could be caused by increased awareness of the condition among parents and general practitioners, changing criteria or environmental factors. Br. Med. J. (2001) HM