Out there thinking - ASD/OCD is an autoimmune response to disease

PANDAS can see that autism can happen at any time, in response to an illness. This research paper goes further linking any immune stressor to physically changing the brain chemistry/biology to improve your chances at living. You actually avoid human contact and wash more often - on a subconscious level. Manifest as ASD and OCD and others.

You have seen the opposite in mice infected with a parasite, who seem more attracted to cats, - https://www.nature.com/news/parasite-makes-mice-lose-fear-of-cats-permanently-1.13777

"The results are novel, as this sensitive and comprehensive testing has revealed how prenatal and early postnatal immune activation may regulate core behavioral signs associated with ASD and certain other developmental disorders through changes in signal flow between different structural components of behavior-driving neural circuits," said Bolshakov. "These findings may be of a significant translational value, as they provide important clues to understanding the mechanisms of these disorders and potentially their treatment."


  • You can't  catch autism. That's  a very faulty and dangerous idea.

    Over-reacting immune system could be a factor, that much I  accept, but that doesn't lead you straight to the cause of autism. 

  • I think that there are many potential contributing factors to the development of autism, genetics especially,

    Genealogy is of course involved, only non-autistic parents have autistic children and autistic parents also have non-autistic children.  

    Consider for instance that:

    More than 15 years after scientists first mapped the human genome, most diseases still cannot be predicted based on one's genes, leading researchers to explore epigenetic causes of disease. But the study of epigenetics cannot be approached the same way as genetics, so progress has been slow. Now, researchers at the USDA/ARS Children's Nutrition Research Center at Baylor College of Medicine and Texas Children's Hospital have determined a unique fraction of the genome that scientists should focus on. Their report, which provides a "treasure map" to accelerate research in epigenetics and human disease, was published in Genome Biology.


    The main epigenetic / external causalities for autism in combination appear to be as follows with these links: high cortisole, high pollution, Low oxygenation, and poor diet

    Psychological and physiological abuse involving violence and or addictions have also been linked to causing Autism.

    but you are very right to emphasise that autism can’t be caught! 

    Just as it is important to emphasise that autism is not genetically predetermined as a condition ~ due to it being environmentally conditioned.

  • There are many contributing factors to autism, none of which are 100% and none of which can be completely ruled out. These include genetics; environmental influences; prenatal issues and many many other factors. As with anything in science, research is ongoing, it is likely that a combination of factors determine whether or not an individual will develop autism as opposed to any one factor on its own.

    Err . . . yes of course, hence my listing a 'group' of factors as 'main' causes that 'appear' in the plural sense including not 'especially' genetic influences (as you previously stated) but more also epigenetic influences (as you also stated just above). Yes?

  • only non-autistic parents have autistic children

    No. Autistic parents can have autistic children, in fact, following a diagnosis of autism a review of a family tree frequently reveals numerous predecessors who manifest autistic traits.

    Additionally a parent may often be diagnosed as autistic following/during diagnosis of their child.

  • only non-autistic parents have autistic children

    No. Autistic parents can have autistic children, in fact, following a diagnosis of autism a review of a family tree frequently reveals numerous predecessors who manifest autistic traits.

    Additionally a parent may often be diagnosed as autistic following/during diagnosis of their child.

    Firstly you missed out the contextaul foundation of my original statement as underlined below:

    Genealogy is of course involved, only non-autistic parents have autistic children and autistic parents also have non-autistic children.

    Which perhaps could have been better worded as stating:

    Genealogy is of course involved, but non-autistic parents also have autistic and or non-autistic children ~ just as autistic parents also have non-autistic and or autistic children.

    So rather than genetics more causing autism, it is genetic programming due to epigenetic conditioning more especially.

    Consider first this extract or the whole article from the Guardian Newspaper back in 2011:

    The Failure of the Genome

    By Jonathan Latham ~ executive director of the Bioscience Resource Project.

    In 2009, one of the few remaining scientifically active leaders of the original genome project, Francis Collins, published a review paper in the scientific journal Nature, along with 26 other prominent geneticists. It was titled Finding the Missing Heritability of Complex Diseases. In it, the authors acknowledged that, despite more than 700 genome-scanning publications and nearly $100bn spent, geneticists still had not found more than a fractional genetic basis for human disease.

    Since the Collins paper was published nothing has happened to change that conclusion. It now seems that the original twin-study critics were more right than they imagined. The most likely explanation for why genes for common diseases have not been found is that, with few exceptions, they do not exist.


    Consider second this extract or the whole article from the Huff Post in 2012:

    A Genome-Sized Media Failure

    By Michael White ~ Biologist, Center for Genome Sciences and Systems Biology, Washington Univ. School of Medicine, St. Louis.

    If you read anything that emerged from the ENCODE media blitz, you were probably told some version of the “junk DNA is debunked” story. It goes like this: When scientists realized that classical, protein-encoding genes make up less than 2% of the human genome, they simply assumed, in a fit of hubris, that the rest of our DNA was useless junk. (You might have also heard this from your high school or college teacher. Your teacher was wrong.) Along came the ENCODE consortium, which found that, far from being useless, junk DNA is packed with functionality. And so everything scientists thought they knew about the genome was wrong, wrong wrong.


    And consider third this extract or the whole article from the scientific journal Nature book review in 2018:

    Genetic Determinism Rides Again

    As professor of the history of medicine at Johns Hopkins University in Baltimore, Maryland ~ Nathaniel Comfort  questions a psychologist’s troubling claims about genes and behaviour.

    .It’s never a good time for another bout of genetic determinism, but it’s hard to imagine a worse one than this. Social inequality gapes, exacerbated by climate change, driving hostility towards immigrants and flares of militant racism. At such a juncture, yet another expression of the discredited, simplistic idea that genes alone control human nature seems particularly insidious.

    And yet, here we are again with Blueprint, by educational psychologist Robert Plomin. Although Plomin frequently uses more civil, progressive language than did his predecessors, the book’s message is vintage genetic determinism: “DNA isn’t all that matters but it matters more than everything else put together”. “Nice parents have nice children because they are all nice genetically.” And it’s not just any nucleic acid that matters; it is human chromosomal DNA. Sorry, microbiologists, epigeneticists, RNA experts, developmental biologists: you’re not part of Plomin’s picture.


Reply Children

  • Interesting articles.

    Consider perhaps this one I happened across yesterday (13th of July 2019) from the US National Library of Medicine National Institutes of Health, published in 2015, with the abstract if feeling less studious and the link to the whole paper if feeling more so perhaps:


    Mechanisms of Non-Genetic Inheritance and Psychiatric Disorders.

    Inheritance is typically associated with the Mendelian transmission of information from parents to offspring by alleles (DNA sequence). However, empirical data clearly suggest that traits can be acquired from ancestors by mechanisms that do not involve genetic alleles, referred to as non-genetic inheritance. Information that is non-genetically transmitted across generations includes parental experience and exposure to certain environments, but also parental mutations and polymorphisms, because they can change the parental ‘intrinsic’ environment. Non-genetic inheritance is not limited to the first generation of the progeny, but can involve the grandchildren and even further generations. Non-genetic inheritance has been observed for multiple traits including overall development, cardiovascular risk and metabolic symptoms, but this review will focus on the inheritance of behavioral abnormalities pertinent to psychiatric disorders. Multigenerational non-genetic inheritance is often interpreted as the transmission of epigenetic marks, such as DNA methylation and chromatin modifications, via the gametes (transgenerational epigenetic inheritance). However, information can be carried across generations by a large number of bioactive substances, including hormones, cytokines, and even microorganisms, without the involvement of the gametes. We reason that this broader definition of non-genetic inheritance is more appropriate, especially in the context of psychiatric disorders, because of the well-recognized role of parental and early life environmental factors in later life psychopathology. Here we discuss the various forms of non-genetic inheritance in humans and animals, as well as rodent models of psychiatric conditions to illustrate possible mechanisms.



    And then perhaps in light of the ongoing discussion involving the cortisol / hormonal thing ~ consider this 2016 extract or the whole article 

    Environmental effects and their inheritance

    It is nowadays basically undisputed, and has been shown in animal experiments, that the pattern of epigenetic change in genes can be induced by the environment and passed on to the offspring, although, for obvious reasons, watertight direct evidence cannot be provided for humans. However, plenty of convincing indirect evidence is available. Long-term observations have shown that severe famine experienced by pregnant women not only affects the health of the unborn baby, but also that of the grandchildren. A similar transfer of experiences from fathers to sons and grandsons has also been shown.

    The epigenetic programming of organisms already occurs during early embryonic development. It has been shown in mice that unborn embryos are particularly sensitive to environmental stimuli. This is certainly also true for humans. Children of mothers who have experienced massive domestic violence during pregnancy often reveal epigenetic changes in the gene coding for the glucocorticoid receptor that controls the signalling pathway of the stress hormone cortisol.


    And consider this 2018 extract or the whole article from the same source:

    New method for analysing epigentic modifications ~ in the service of medical progress

    It is not just genetic factors that influence developmental processes and diseases; it is becoming increasingly evident that epigenetic changes play a major role too. Thanks to a new method developed at the University of Stuttgart, epigenetic processes can now be investigated in living cells.

    Over the past decades, much has come to light about the role of genes and gene mutations in the development and progression of diseases. However, the DNA sequence of genes is not the whole story. For many years, researchers have been exploring an aspect that has more impact on gene activity than was originally thought, i.e. the fact that DNA bases can undergo chemical modification without leading to changes in the DNA sequence and thus the blueprint of proteins. Methylation, i.e. the addition of a methyl group to the cytosine base in a DNA strand, is the most common type of epigenetic modification.

    Such superordinate, epigenetic changes play a substantial role in determining whether and to what extent genes are activated or repressed. Some DNA sections are literally peppered with methyl groups, which lead to characteristic patterns. The methylation process is dynamic; many factors including diseases can influence the methylation patterns. And to complicate matters, histones, the proteins that package DNA in chromosomes, can also be methylated. The methylation of histones is a regulator of gene expression, marking genes in DNA to be or not be transcribed.

    Investigating epigenetic changes and influences is therefore an important research activity, especially with regard to diseases such as cancer that have a genetic as well as an environmental component. The expectation is that this research will identify new therapeutic approaches that can be used to specifically interfere with epigenetic modifications. Up until now, however, it has not been possible to detect epigenetic signals live – i.e. in the living cell, for the simple reason that suitable methods were not available.

    Prof. Dr. Albert Jeltsch, who heads up the Department of Biochemistry at the Institute of Biochemistry and Technical Biochemistry at the University of Stuttgart, and his team have delivered a real milestone in the study of epigenetic modifications. Using a sophisticated fluorescence labelling strategy, the researchers can track epigenetic processes over a period of several days or weeks.