Reply To: Vaccine contaminants and safety

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This is a direct challenge to Paul

Reporting of half truths by liars and interpreted by ignorant people is a dangerous thing in the internet. Because you need knowledge to debunk this rubbish.

‘… A conservative estimate based on the research suggests that at least 69% of individuals with an ASD diagnosis have microglial activation or neuroinflammation. Encephalitis, which is defined as inflammation of the brain, is medical diagnosis code G04.90 in the International Classification of Disease, 10th revision; however, children with an ASD diagnosis are not generally assessed for a possible medical diagnosis of encephalitis. This is unfortunate because if a child with ASD has neuroinflammation, then treating the underlying brain inflammation could lead to improved outcomes..’

This is of course a quotation , not referenced on this occasion, but obviously from an anti-vaxxer website which sounds plausible but is not.
“A conservative estimate…” this means nothing, we are not estimating here we need data, is there data to prove this assertion? I doubt it. If so then I need a scientific study not say so to believe this or debate it.

“Encephalitis, which is defined as inflammation of the brain, is medical diagnosis code G04.90 in the International Classification of Disease, 10th revision;
…” NO it is not. G04.09 is
ICD-10-CM Codes › G00-G99 Diseases of the nervous system › G00-G09 Inflammatory diseases of the central nervous system › Sequelae of inflammatory diseases of central nervous system G09
Sequelae of inflammatory diseases of central nervous system G09-
Category G09 is to be used to indicate conditions whose primary classification is to G00-G08 as the cause of sequelae, themselves classifiable elsewhere. The ‘sequelae’ include conditions specified as residuals.

Do you know what this means? No I don’t think you do, you just regurgitate pseudo rubbish.
If you want to look at classifications of encephalitis then you need to look at G-04
Clinical Information
“An inflammatory process involving the brain (encephalitis) and meninges (meningitis), most often produced by pathogenic organisms which invade the central nervous system, and occasionally by toxins, autoimmune disorders, and other conditions.”
and G-05
ICD-10-CM Coding Rules
“G05.3 describes the manifestation of an underlying disease, not the disease itself.”

As to neuroinflammation, you can read all about it here.

A role for immune responses, involving antigen presentation and immune-response-generating cytokines, in neurodegenerative diseases such as Alzheimer’s disease was recognized for a decade before the term neuroinflammation came into widespread use [1, 2]. A PubMed search using “neuroinflammation” as the only key word yields some 300 papers, none before 1995 [3]. While some chronic/remitting neurological diseases, such as multiple sclerosis, have long been recognized as inflammatory, the term neuroinflammation has come to denote chronic, CNS-specific, inflammation-like glial responses that do not reproduce the classic characteristics of inflammation in the periphery but that may engender neurodegenerative events; including plaque formation, dystrophic neurite growth, and excessive tau phosphorylation. In this way, neuroinflammation has been implicated in chronic unremitting neurodegenerative diseases such as Alzheimer’s disease – diseases that historically have not been thought of as inflammatory diseases. This new understanding has come from rapid advances in the field of microglial and astrocytic neurobiology over the past fifteen to twenty years. These advances have led to the recognition that glia, particularly microglia, respond to tissue insult with a complex array of inflammatory cytokines and actions, and that these actions transcend the historical vision of phagocytosis and structural support that has long been enshrined in the term “reactive gliosis.” Microglia are now recognized as the prime components of an intrinsic brain immune system [4], and as such they have become a main focus in cellular neuroimmunology and therefore in neuroinflammation. This is not the inflammation of the adaptive mammalian immune response, with its array of specialized T-cells and the made-to-order antibodies produced through complex gene rearrangements. This is, instead, the innate immune system, upon which adaptive immunity is built [5].

As to autism, I urge you to read this paper, a very good start, even if you just read the abstract below:

Autism spectrum disorder (ASD) is a neurodevelopmental condition of heterogeneous etiology. While it is widely recognized that genetic and environmental factors and their interactions contribute to autism phenotypes, their precise causal mechanisms remain poorly understood. This article reviews our current understanding of environmental risk factors of ASD and their presumed adverse physiological mechanisms. It comprehensively maps the significance of parental age, teratogenic compounds, perinatal risks, medication, smoking and alcohol use, nutrition, vaccination, toxic exposures, as well as the role of extreme psychosocial factors. Further, we consider the role of potential protective factors such as folate and fatty acid intake. Evidence indicates an increased offspring vulnerability to ASD through advanced maternal and paternal age, valproate intake, toxic chemical exposure, maternal diabetes, enhanced steroidogenic activity, immune activation, and possibly altered zinc–copper cycles and treatment with selective serotonin reuptake inhibitors. Epidemiological studies demonstrate no evidence for vaccination posing an autism risk. It is concluded that future research needs to consider categorical autism, broader autism phenotypes, as well as autistic traits, and examine more homogenous autism variants by subgroup stratification. Our understanding of autism etiology could be advanced by research aimed at disentangling the causal and non-causal environmental effects, both founding and moderating, and gene–environment interplay using twin studies, longitudinal and experimental designs. The specificity of many environmental risks for ASD remains unknown and control of multiple confounders has been limited. Further understanding of the critical windows of neurodevelopmental vulnerability and investigating the fit of multiple hit and cumulative risk models are likely promising approaches in enhancing the understanding of role of environmental factors in the etiology of ASD.

So Paul, I urge you to cut out the crap. If you really have a genuine interest in understanding and helping people with ASD then you have to be open minded enough to at least believe that it is really not at all related to vaccination but due to other important factors, and that there are people out there who are genuinely interested in helping autistic people, but it is not the antivaxxers. If you do not even wish to engage with me and answer this important post by me on whatever basis you choose, then you would have exposed yourself as a sham. In which case I suggest that this forum thread should be closed.

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