News and commentary on the autism epidemic and my beautiful boy who is living with autism.
November 18, 2012
Empirical Data Confirm Autism Symptoms Related to Aluminum and Acetaminophen Exposure
Empirical Data Confirm Autism Symptoms Related to Aluminum and Acetaminophen Exposure
Entropy, November 7, 2012
Stephanie Seneff, Robert M. Davidson and Jingjing Liu
Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA, Internal Medicine Group Practice, PhyNet, Inc., Longview, TX 75604, USA
Abstract: Autism is a condition characterized by impaired cognitive and social skills, associated with compromised immune function. The incidence is alarmingly on the rise, and environmental factors are increasingly suspected to play a role. This paper investigates word frequency patterns in the U.S. CDC Vaccine Adverse Events Reporting System (VAERS) database. Our results provide strong evidence supporting a link between autism and the aluminum in vaccines. A literature review showing toxicity of aluminum in human physiology offers further support. Mentions of autism in VAERS increased steadily at the end of the last century, during a period when mercury was being phased out, while aluminum adjuvant burden was being increased. Using standard log-likelihood ratio techniques, we identify several signs and symptoms that are significantly more prevalent in vaccine reports after 2000, including cellulitis, seizure, depression, fatigue, pain and death, which are also significantly associated with aluminum-containing vaccines. We propose that children with the autism diagnosis are especially vulnerable to toxic metals such as aluminum and mercury due to insufficient serum sulfate and glutathione. A strong correlation between autism and the MMR (Measles, Mumps, Rubella) vaccine is also observed, which may be partially explained via an increased sensitivity to acetaminophen administered to control fever.
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Ah excuse me, but what evidence is there that proves that Autism is characterized in association with compromised immune function? I'm sorry, but that is just plain wrong and invalidates the rest of the abstract. There is no verified and proven connection between issues with immune function and Autism.
Neuroglial activation and neuroinflammation in the brain of patients with autism.
Vargas DL, Nascimbene C, Krishnan C, Zimmerman AW, Pardo CA.
Department of Neurology, Johns Hopkins University School of Medicine, 600 North Wolfe Street, Baltimore, MD 21287, USA.
Ann Neurol. 2005 Feb;57(2):304.
Autism is a neurodevelopmental disorder characterized by impaired communication and social interaction and may be accompanied by mental retardation and epilepsy. Its cause remains unknown, despite evidence that genetic, environmental, and immunological factors may play a role in its pathogenesis. To investigate whether immune-mediated mechanisms are involved in the pathogenesis of autism, we used immunocytochemistry, cytokine protein arrays, and enzyme-linked immunosorbent assays to study brain tissues and cerebrospinal fluid (CSF) from autistic patients and determined the magnitude of neuroglial and inflammatory reactions and their cytokine expression profiles. Brain tissues from cerebellum, midfrontal, and cingulate gyrus obtained at autopsy from 11 patients with autism were used for morphological studies. Fresh-frozen tissues available from seven patients and CSF from six living autistic patients were used for cytokine protein profiling. We demonstrate an active neuroinflammatory process in the cerebral cortex, white matter, and notably in cerebellum of autistic patients. Immunocytochemical studies showed marked activation of microglia and astroglia, and cytokine profiling indicated that macrophage chemoattractant protein (MCP)-1 and tumor growth factor-beta1, derived from neuroglia, were the most prevalent cytokines in brain tissues. CSF showed a unique proinflammatory profile of cytokines, including a marked increase in MCP-1. Our findings indicate that innate neuroimmune reactions play a pathogenic role in an undefined proportion of autistic patients, suggesting that future therapies might involve modifying neuroglial responses in the brain.
Autism: A Brain Disorder, or A Disorder That Affects the Brain?
Clinical Neuropsychiatry, 2005
Martha R. Herbert M.D., Ph.D., Harvard University
Autism is defined behaviorally, as a syndrome of abnormalities involving language, social reciprocity and hyperfocus or reduced behavioral flexibility. It is clearly heterogeneous, and it can be accompanied by unusual talents as well as by impairments, but its underlying biological and genetic basis in unknown. Autism has been modeled as a brain-based, strongly genetic disorder, but emerging findings and hypotheses support a broader model of the condition as a genetically influenced and systemic. These include imaging, neuropathology and psychological evidence of pervasive (and not just specific) brain and phenotypic features; postnatal evolution and chronic persistence of brain, behavior and tissue changes (e.g. inflammation) and physical illness symptomatology (e.g. gastrointestinal, immune, recurrent infection); overlap with other disorders; and reports of rate increases and improvement or recovery that support a role for modulation of the condition by environmental factors (e.g. exacerbation or triggering by toxins, infectious agents, or others stressors, or improvement by treatment). Modeling autism more broadly encompasses previous work, but also encourages the expansion of research and treatment to include intermediary domains of molecular and cellular mechanisms, as well as chronic tissue, metabolic and somatic changes previously addressed only to a limited degree. The heterogeneous biologies underlying autism may conceivably converge onto the autism profile via multiple mechanisms on the one hand and processing and connectivity abnormalities on the other may illuminate relevant final common pathways and contribute to focusing on the search for treatment targets in this biologically and etiologically heterogeneous behavioral syndrome.
Bridging from Cells to Cognition in Autism Pathophysiology: Biological
Pathways to Defective Brain Function and Plasticity
American Journal of Biochemistry and Biotechnology 4 (2): 167-176, 2008
Matthew P. Anderson, Brian S. Hooker and Martha R. Herbert
Departments of Neurology and Pathology, Harvard Medical School/Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, High Throughput Biology Team, Fundamental Science Directorate, Pacific Northwest National Laboratory, Pediatric Neurology/Center for Morphometric Analysis, Massachusetts General Hospital/Harvard Medical School, and
Center for Child and Adolescent Development, Cambridge Health Alliance/Harvard Medical School
Abstract: We review evidence to support a model where the disease process underlying autism may begin when an in utero or early postnatal environmental, infectious, seizure, or autoimmune insult triggers an immune response that increases reactive oxygen species (ROS) production in the brain that leads to DNA damage (nuclear and mitochondrial) and metabolic enzyme blockade and that these inflammatory and oxidative stressors persist beyond early development (with potential further exacerbations), producing ongoing functional consequences. In organs with a high metabolic demand such as the central nervous system, the continued use of mitochondria with damaged DNA and impaired metabolic enzyme function may generate additional ROS which will cause persistent activation of the innate immune system leading to more ROS production. Such a mechanism would self-sustain and possibly progressively worsen. The mitochondrial dysfunction and altered redox signal transduction pathways found in autism would conspire to activate both astroglia and microglia. These activated cells can then initiate a broad-spectrum proinflammatory gene response. Beyond the direct effects of ROS on neuronal function, receptors on neurons that bind the inflammatory mediators may serve to inhibit neuronal signaling to protect them from excitotoxic damage during various pathologic insults (e.g., infection). In autism, over-zealous neuroinflammatory responses could not only influence neural developmental processes, but may more significantly impair neural signaling involved in cognition in an ongoing fashion. This model makes specific predictions in patients and experimental animal models and suggests a number of targets sites of intervention. Our model of potentially reversible pathophysiological mechanisms in autism motivates our hope that effective therapies may soon appear on the horizon.
Possible Immunological Disorders in Autism: Concomitant Autoimmunity and Immune Tolerance
The Egyptian Journal of Immunology, 2006
Maha I. Sh. Kawashti, Omnia R. Amin Nadia G. Rowehy
Microbiology Department, Faculty of Medicine (For Girls), Al Azhar University, Cairo, Egypt, Psychiatry Department, Faculty of Medicine, Cairo University, Cairo, Egypt and Serology Lab King Fahad General Hospital, Jeddah, K.S.A.
Abstract: Autism is a pervasive developmental disorder that affect children early in their life. Immunological disorders is one of several contributing factors that have been suggested to cause autism. Thirty autistic children aged 3-6 years and thirty non-autistic psychologically-free siblings were studied. Circulating IgA and IgG autoantibodies to casein and gluten dietary proteins were detected by enzyme-immunoassays (EIA). Circulating IgG antibodies to measles, mumps and rubella vaccine (M.M.R) and cytomeglovirus were investigated by EIA. Results revealed high seropositivity for autoantibodies to casein and gluten: 83.3% and 50% respectively in autistic children as compared to 10% and 6.7% positivity in the control group. Surprisingly, circulating anti-measles, anti-mumps and anti-rubella IgG were positive in only 50%, 73.3% and 53.3% respectively as compared to 100% positivity in the control group. Anti-CMV IgG was positive in 43.3% of the autistic children as compared to 7% in the control group. It is concluded that, autoimmune response to dietary proteins and deficient immune response to measles, mumps and rubella vaccine antigens might be associated with autism, as a leading cause or a resulting event. Further research is needed to confirm these findings.
Theoretical aspects of autism: Causes—A review
Journal of Immunotoxicology, January-March 2011, Vol. 8, No. 1 , Pages 68-79
Helen V. Ratajczak, PhD
Autism, a member of the pervasive developmental disorders (PDDs), has been increasing dramatically since its description by Leo Kanner in 1943. First estimated to occur in 4 to 5 per 10,000 children, the incidence of autism is now 1 per 110 in the United States, and 1 per 64 in the United Kingdom, with similar incidences throughout the world. Searching information from 1943 to the present in PubMed and Ovid Medline databases, this review summarizes results that correlate the timing of changes in incidence with environmental changes. Autism could result from more than one cause, with different manifestations in different individuals that share common symptoms. Documented causes of autism include genetic mutations and/or deletions, viral infections, and encephalitis following vaccination. Therefore, autism is the result of genetic defects and/or inflammation of the brain. The inflammation could be caused by a defective placenta, immature blood-brain barrier, the immune response of the mother to infection while pregnant, a premature birth, encephalitis in the child after birth, or a toxic environment.
Familial Clustering of Autoimmune Disorders and Evaluation of Medical Risk Factors in Autism
Neeurology/Johns Hopkins University
Autism is an age-dependent neurologic disorder that is often associated with autoimmune disorders in the patients' relatives. To evaluate the frequency of autoimmune disorders, as well as various prenatal and postnatal events in autism, we surveyed the families of 61 autistic patients and 46 healthy controls using questionnaires. The mean number of autoimmune disorders was greater in families with autism; 46% had two or more members with autoimmune disorders. As the number of family members with autoimmune disorders increased from one to three, the risk of autism was greater, with an odds ratio that increased from 1.9 to 5.5, respectively. In mothers and first-degree relatives of autistic children, there were more autoimmune disorders (16% and 21%) as compared to controls (2% and 4%), with odds ratios of 8.8 and 6.0, respectively. The most common autoimmune disorders in both groups were type 1 diabetes, adult rheumatoid arthritis, hypothyroidism, and systemic lupus erythematosus. Forty-six percent of the autism group reported having relatives with rheumatoid diseases, as compared to 26% of the controls. Prenatal maternal urinary tract, upper respiratory, and vaginal infections; asphyxia; prematurity, and seizures were more common in the autistic group, although the differences were not significant. Thirty-nine percent of the controls, but only 11% of the autistic group, reported allergies. An increased number of autoimmune disorders suggests that in some families with autism, immune dysfunction could interact with various environmental factors to play a role in autism pathogenesis. (J Child Neurol 1999;14:388-394).
J Neuroimmunol. 2012 Oct 27. pii: S0165-5728(12)00305-0. doi: 10.1016/j.jneuroim.2012.10.002. [Epub ahead of print]
The link between some alleles on human leukocyte antigen system and autism in children.
Mostafa GA, Shehab AA, Al-Ayadhi LY.
Department of Pediatrics, Faculty of Medicine, Ain Shams University, Cairo, Egypt; Autism Research and Treatment Center, Al-Amodi Autism Research Chair, Department of Physiology, Faculty of Medicine, King Saud University, Riyadh, Saudi Arabia. Electronic address: email@example.com.
The reason behind the initiation of autoimmunity to brain in some patients with autism is not well understood. There is an association between some autoimmune disorders and specific alleles of human leukocyte antigen (HLA) system. Thus, we examined the frequency of some HLA-DRB1 alleles in 100 autistic children and 100 healthy matched-children by differential hybridization with sequence-specific oligonucleotide probes. The risk of association between acquisition or absence of these alleles and autism and also a history of autoimmune diseases in autistic relatives was studied. Autistic children had significantly higher frequency of HLA-DRB1*11 allele than controls (P<0.001). In contrast, autistic children had significantly lower frequency of HLA-DRB1*03 allele than controls (P<0.001). Acquisition of HLA-DRB1*011 and absence of HLA-DRB1*3 had significant risk for association with autism (odds ratio: 3.21 and 0.17, respectively; 95% CI: 1.65-6.31 and 0.06-0.45, respectively). HLA-DRB1*11 had a significant risk for association with a family history of autoimmunity in autistic children (odds ratio: 5.67; 95% CI: 2.07-16.3). In conclusions, the link of some HLA alleles to autism and to family history of autoimmunity indicates the possible contributing role of these alleles to autoimmunity in some autistic children. Despite a relatively small sample size, we are the first to report a probable protective association of HLA-DRB1*03 allele with autism. It warrants a replication study of a larger sample to validate the HLA-DRB1 genetic association with autism. This is important to determine whether therapeutic modulations of the immune function are legitimate avenues for novel therapy in selected cases of autism.
Autism Res Treat. 2012;2012:959073. Epub 2012 Feb 15.
HLA Immune Function Genes in Autism.
Torres AR, Westover JB, Rosenspire AJ.
Center for Persons with Disabilities, Utah State University, 6804 Old Main Hill, Logan, UT 84322, USA.
The human leukocyte antigen (HLA) genes on chromosome 6 are instrumental in many innate and adaptive immune responses. The HLA genes/haplotypes can also be involved in immune dysfunction and autoimmune diseases. It is now becoming apparent that many of the non-antigen-presenting HLA genes make significant contributions to autoimmune diseases. Interestingly, it has been reported that autism subjects often have associations with HLA genes/haplotypes, suggesting an underlying dysregulation of the immune system mediated by HLA genes. Genetic studies have only succeeded in identifying autism-causing genes in a small number of subjects suggesting that the genome has not been adequately interrogated. Close examination of the HLA region in autism has been relatively ignored, largely due to extraordinary genetic complexity. It is our proposition that genetic polymorphisms in the HLA region, especially in the non-antigen-presenting regions, may be important in the etiology of autism in certain subjects.
Dev Neurobiol. 2012 Oct;72(10):1327-34. doi: 10.1002/dneu.22052. Epub 2012 Sep 4.
Maternal and fetal antibrain antibodies in development and disease.
Fox E, Amaral D, Van de Water J.
Department of Internal Medicine, University of California, Davis, Davis, California 95616, USA.
Recent evidence has emerged indicating that the maternal immune response can have a substantial deleterious impact on prenatal development (Croen et al., : Biol Psychiatry 64:583-588). The maternal immune response is largely sequestered from the fetus. Maternal antibodies, specifically immunoglobulin G (IgG), are passed to the fetus to provide passive immunity throughout much of pregnancy. However, both protective and pathogenic autoantibodies have equal access to the fetus (Goines and Van de Water : Curr Opin Neurol 23:111-117). If the mother has an underlying autoimmune disease or has reactivity to fetal antigens, autoantibodies produced before or during pregnancy can target tissues in the developing fetus. One such tissue is the fetal brain. The blood brainbarrier (BBB) is developing during the fetal period allowing maternal antibodies to have direct access to the brain during gestation (Diamond et al. : Nat Rev Immunol; Braunschweig et al. ; Neurotoxicology 29:226-231). It has been proposed that brain injury by circulating brain-specific maternal autoantibodies might underlie multiple congenital, developmental disorders (Lee et al. : Nat Med 15:91-96). In this review, we will discuss the current state of research in the area of maternal autoantibodies and the development of autism.
J Neuroinflammation. 2012 Aug 17;9:201.
Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: Relation to autoimmunity.
Mostafa GA, Al-Ayadhi LY.
Autism Research and Treatment Center, AL-Amodi Autism Research Chair, Department of Physiology, Faculty of Medicine, King Saud University, Riyadh, Saudi Arabia. firstname.lastname@example.org.
Aside from the skeletal health affection, vitamin D deficiency has been implicated as a potential environmental factor triggering for some autoimmune disorders. Vitamin D might play a role in the regulation of the production of auto-antibodies. Immunomodulatory effects of vitamin D may act not only through modulation of T-helper cell function, but also through induction of CD4+CD25high regulatory T-cells. We are the first to investigate the relationship between serum levels of 25-hydroxy vitamin D and anti-myelin-associated glycoprotein (anti-MAG) auto-antibodies in autistic children.
Serum levels of 25-hydroxy vitamin D and anti-MAG auto-antibodies were measured in 50 autistic children, aged between 5 and 12 years, and 30 healthy-matched children. Serum 25-hydroxy vitamin D levels 10-30 ng/mL and < 10 ng/mL were defined as vitamin D insufficiency and deficiency, respectively.
Autistic children had significantly lower serum levels of 25-hydroxy vitamin D than healthy children (P < 0.001) with 40% and 48% being vitamin D deficient and insufficient, respectively. Serum 25-hydroxy vitamin D had significant negative correlations with Childhood Autism Rating Scale (P < 0.001). Increased levels of serum anti-MAG auto-antibodies were found in 70% of autistic patients. Serum 25-hydroxy vitamin D levels had significant negative correlations with serum levels of anti-MAG auto-antibodies (P < 0.001).
Vitamin D deficiency was found in some autistic children and this deficiency may contribute to the induction of the production of serum anti-MAG auto-antibodies in these children. However, future studies looking at a potential role of vitamin D in the pathophysiology and treatment of autism are warranted.
J Neuroinflammation. 2012 Jul 2;9:158.
Elevated serum levels of interleukin-17A in children with autism.
Al-Ayadhi LY, Mostafa GA.
Department of Physiology, Autism Research and Treatment Center, Al-Amodi Autism Research Chair, Faculty of Medicine, King Saud University, Riyadh, Saudi Arabia.
The T-helper (Th)1/Th2 dichotomy dominated the field of immune regulation until interleukin (IL)-17-expressing T cells (Th17) were proposed to be a third lineage of helper T cells, the key players in the pathogenesis of autoimmune disorders. Autoimmunity to brain tissue may play a pathogenic role in autism. IL-17A is a pro-inflammatory cytokine that has been shown to play an important role in various autoimmune neuroinflammatory diseases. The aim of this study was to measure serum levels of IL-17A in relation to the degree of the severity of autism.
Serum IL-17A levels were measured by ELISA in 45 children with autism and 40 matched healthy controls.
Children with autism had significantly higher serum IL-17A levels than healthy controls (P <0.001), with increased serum levels of IL-17A found in 48.9% of the autism group. Patients with severe autism had significantly higher serum IL-17A levels than those with mild to moderate autism (P=0.01), and raised serum IL-17A levels were significantly more common in children with severe autism (67.9%) than in those with mild to moderate autism (17.6%), P=0.001.
Serum IL-17A levels were raised in the group with autism, and the levels correlated significantly with the severity of autism. This is the first study to measure levels of IL-17A in relation to the severity of autism, to our knowledge. Further research, with a larger subject population, is warranted to determine whether the increase of serum IL-17A levels plasma has a pathogenic role in autism, and whether anti- IL-17A therapy could be useful.
BMC Pediatr. 2012 Jul 2;12:89. doi: 10.1186/1471-2431-12-89.
Perinatal stress, brain inflammation and risk of autism-Review and proposal.
Angelidou A, Asadi S, Alysandratos KD, Karagkouni A, Kourembanas S, Theoharides TC.
Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Molecular Physiology and Pharmacology, Tufts University School of Medicine and Tufts Medical Center, Boston, MA 02111, USA. email@example.com.
Autism Spectrum Disorders (ASD) are neurodevelopmental disorders characterized by varying deficits in social interactions, communication, and learning, as well as stereotypic behaviors. Despite the significant increase in ASD, there are few if any clues for its pathogenesis, hampering early detection or treatment. Premature babies are also more vulnerable to infections and inflammation leading to neurodevelopmental problems and higher risk of developing ASD. Many autism "susceptibility" genes have been identified, but "environmental" factors appear to play a significant role. Increasing evidence suggests that there are different ASD endophenotypes.
We review relevant literature suggesting in utero inflammation can lead to preterm labor, while insufficient development of the gut-blood-brain barriers could permit exposure to potential neurotoxins. This risk apparently may increase in parents with "allergic" or autoimmune problems during gestation, or if they had been exposed to stressors. The presence of circulating auto-antibodies against fetal brain proteins in mothers is associated with higher risk of autism and suggests disruption of the blood-brain-barrier (BBB). A number of papers have reported increased brain expression or cerebrospinal fluid (CSF) levels of pro-inflammatory cytokines, especially TNF, which is preformed in mast cells. Recent evidence also indicates increased serum levels of the pro-inflammatory mast cell trigger neurotensin (NT), and of extracellular mitochondrial DNA (mtDNA), which is immunogenic. Gene mutations of phosphatase and tensin homolog (PTEN), the negative regulator of the mammalian target of rapamycin (mTOR), have been linked to higher risk of autism, but also to increased proliferation and function of mast cells.
Premature birth and susceptibility genes may make infants more vulnerable to allergic, environmental, infectious, or stress-related triggers that could stimulate mast cell release of pro-inflammatory and neurotoxic molecules, thus contributing to brain inflammation and ASD pathogenesis, at least in an endophenotype of ASD patients.
Getting tired. Do some reading on your own:
As I said, no verified or proven connection. Only speculation based in narrow band guesswork.
*Neuroglial activation and neuroinflammation in the brain of patients with autism.
Numbers studied total 17 only, including 11 no longer alive. Useless report.
*Autism: A Brain Disorder, or A Disorder That Affects the Brain?
No evidence. Irrelevant to the point I'm making.
*Bridging from Cells to Cognition in Autism Pathophysiology: Biological
DNA damage in children will result in instant death, so this abstract is rubbish.
*Possible Immunological Disorders in Autism: Concomitant Autoimmunity and Immune Tolerance
Emphasis on "possible". Egypt does not have the facilities to provide a strong case for the argument. 60 subjects in the study are still not enough. And the abstract even admits that more research would be needed to confirm the findings.
*Theoretical aspects of autism: Causes—A review
Another speculation piece, emphasis on "theoretical". I know that the theory with encephalitis has already been proven wrong (don't have a link handy at present). The same applies to the idea of the blood brain barrier being an issue, which is connected to the thimerosal theory and has been well and truly debunked multiple times.
*Familial Clustering of Autoimmune Disorders and Evaluation of Medical Risk Factors in Autism
Age dependent? Sorry, but that's a lie. Autism is lifelong. A rubbish report on that basis alone.
*The link between some alleles on human leukocyte antigen system and autism in children.
Another one from Egypt. It admits to a small sample size even though the number is 200 combined, and like before it wants more study for confirmation.
*HLA Immune Function Genes in Autism.
This is clearly another speculation piece, concentrating on auto immune issues as seperate to Autism and only speculates a link.
*Maternal and fetal antibrain antibodies in development and disease.
This goes way wider than just Autism. It speaks of general issues with mothers with already existing immune issues with NO connection to Autism. It simply speaks of the auto immune issues in general being passed on through a lack of natural protection from antibodies. That's a general threat not exclusive to Autism and the report makes no attempt to prove the link other than a brief unrelated reference at the end.
*Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: Relation to autoimmunity
Now we have a study from Saudi Arabia, who are in the same position on facilities as Egypt AND take the same line of caution. Vitamin D deficiencies can be an issue for Autistics, but then that's true for every child who prefers video and computer games to going outdoors for instance. The numbers used were not balanced (80 subjects with 50 on one side and 30 on the other). Once more study is done, I'm sure it will be found that the issues this abstract is speculating are exclusive to Autism are in fact general issues.
*Elevated serum levels of interleukin-17A in children with autism.
Saudi again, and similar numbers with another imbalance although not as bad as the previous study. It also refuses to be specific or final in it's conclusions.
*Perinatal stress, brain inflammation and risk of autism-Review and proposal
The summary of this shows a much wider range of issues to auto immune issues are being considered as worthy of note.
That is enough to show me that doing further reading on that link will simply show that you believe that speculation is enough to prove a case. It's not. You have failed to convince me and I'm not really surprised. Auto immune issues are seperate to Autism and while one may cause issues when the other is present, that's normal for any two conditions that clash with each other. It doesn't prove that they are linked.
"Ah excuse me, but what evidence is there that proves that Autism is characterized in association with compromised immune function? I'm sorry, but that is just plain wrong and invalidates the rest of the abstract."
Really? You don't keep up with autism research, do you? The connection between the immune system and autism left the fringes of the autism world and entered the world mainstream medicine more than a few years ago.
There is a very substantial body of evidence that the immune system is altered, comprised, or otherwise skewed in people with autism and that these findings are significantly more common in people with autism than the general population.
To be convinced all you have to do is open your mind and start reading on pubmed.
I don't read speculation, which is what is on PubMed. I want proven connections confirmed by multiple other studies. They do not exist. If you are like Ginger Taylor and rely in speculation then I feel sorry for you. You must lead an extremely paranoid life, sir.
Well then thank you for visiting Mr. Gregory. Have a nice day.
I see. You are firmly challenged and are unable to respond with valid evidence. Thank you for confirming this.
So, let me get this straight.
You call the premier repository of peer-reviewed research "speculation", said that anyone who reads it must "lead an extremely paranoid life", demand as your standard of proof "multiple other studies" that apparently are not contained in the repository of "speculation", and think that anyone who can't live up to this mythical standard of evidence is "unable to respond with valid evidence" when "firmly challenged"?
Wow, I didn't know it was possible to pack so much crazy into three short comments.
Now, if you are done waiting for the Truth Of Autism to be delivered on stone tablets from the mountaintop, why don't you spend some time learning what you already presume you know.
Every single one of those studies refuses to make the link directly. Therefore it is speculation. Where's the smoking gun? Nowhere and that's because the link has not been proven. The truth of Autism has been delivered by the Vaccine Court with the defeating of the Autism Omnibus. If it was anything otherwise the result would have been different. Don't forget, in that Court you don't have to prove anything 100 percent. It's just 50 percent and a feather as they say, and the petitioners couldn't even do that. So the genetic belief still holds the floor.
This is not crazy. This is sensible. What's crazy is to rely on speculation to explain something that I guess you don't want to know about. PubMed is a research tool for experts. You are not an expert. I don't try to be, but I know a lack of cast iron evidence when I see it. And I have the confidence in myself to say it in my name instead of some sawed off screen name that depicts a dead pop star.
There is no "smoking gun" for any aspect of autism.
Take for example the idea that autism is "genetic" - there is a widespread belief that autism is extremely heritable and that most cases of autism have a large genetic component. But if you went looking for the "smoking gun" that "proves" the link between certain genetic modifications and autism you wouldn't be able to find it.
You can find associations with an extremely small number of causes, you can find certain mutations that cause the behaviors of autism, but you can't find anything that is linked to the majority of cases of autism. Therefore, by your own criteria, autism cannot be genetic.
I am not sure what to even make of nonsense like this -
"The truth of Autism has been delivered by the Vaccine Court with the defeating of the Autism Omnibus."
To assume that the omnibus "proved" that there was no link between the immune system and autism is dead wrong. The cases heard before the court were about vaccines - not about the immune system. And the presumption that any judge's decision carries the same weight as actual studies of the immune system or that the judges in the onmibus were in any way, shape, or form experts on autism or the immune system is just utterly absurd.
As for comments like this -
"And I have the confidence in myself to say it in my name instead of some sawed off screen name that depicts a dead pop star."
Well, I don't know what to tell you, my initials are my initials. If you look at letters and see a dead pop star, well that's your problem.
As for you having "confidence" in yourself, well, you really shouldn't. Your ignorance of autism is quite breathtaking. And I'm not just saying that because, in my secret identify as Michael Jackson's cadaver, I don't breath. I'm saying that because you clearly don't seem to know that much about autism, how to interpret research, or links between the immune system and autism. But if you're proud of your ignorance then good for you.
Your ignorance is what is breathtaking as you clearly do not know speculation when you read it. I repeat that there is no proof that there is any connection between autism causation and immune system issues. Vaccines are related to the immune system which is why the Autism Omnibus is relevant.
You do not know what you are talking about so I suppose it's best if you don't use your real name. If you did your name would be wrecked. Perhaps you are aware of this and it's why you won't connect your real name to your comments.
I seriously doubt you are even a qualified person to interpret those reports, as well as failing at comprehension when it comes to recognizing speculation when you read it.
Should you respond in continued insulting terms I shall know for certain that I am dealing with a deluded loony.
I'm glad I found this site. It sure has a lot of helpful information regarding autism. beta prostate
Yes there are absolutely scores of peer-reviewed papers that correlate immune dysfunction and Autism. I don't have time to get into it, but look it up. And not on Google.
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