Parents all over the world have noted that certain environmental agents can trigger their children's symptoms. For many families, managing the symptoms lies in making some changes in diet.
People with autism are more susceptible to allergies and food sensitivities than the average person; and this is likely due to their impaired immune system. Allergies and food sensitivities can affect one's health and behavior, but are treatable.
The AIA does not suggest that sensitivity to foods is the cause of autism, but it does appear that certain components of foods exacerbate some symptoms of autism.
An excess accumulation of advanced glycation end products (AGEs) has been reported in autism brains. Through their interaction with their putative receptor RAGE, AGEs can promote neuroinflammation, oxidative stress and neuronal degeneration. To shed more light on the possible alterations of the AGEs-RAGE axis in autism, hereto we measured plasma levels of endogenous secretory RAGE (esRAGE) and its proinflammatory ligand S100A9 in 18 young adults with autistic spectrum disorder (ASD) and 18 age- and gender-matched healthy comparison subjects. The Childhood Autism Rating Scale (CARS) was used to assess the severity of autistic symptoms. Significantly reduced levels of esRAGE (P=0.0023) and elevated concentrations of S100A9 (P=0.0012) were found in ASD patients as compared to controls. In autistic patients, there was a statistically significant positive correlation between CARS scores and S100A9 levels (r=0.49, P=0.035), but no significant correlation was seen between esRAGE and S100A9 values (r=-0.23, P=0.34). Our results of a significantly reduced peripheral level of esRAGE coupled with elevated S100A9 point to a subtle but definite dysfunction of the AGEs/RAGE axis in autism that could play a role in the pathophysiology of this disorder.
Prolyl Endopeptidase (PEP, EC 18.104.22.168), a cytosolic endopeptidase, hydrolyses peptide bonds on the carboxyl side of proline residue in proteins with a relatively small molecular weight. It has been shown that altered PEP activity is associated with various psychological diseases such as schizophrenia, mania and depression. Autistic Spectrum Disorders (ASD) are neuropsychiatric and behavioural syndromes affecting social behaviours and communication development. They are classified as developmental disorders. The aim of this study was to examine the hypothesis that PEP activity is also associated with ASDs... Our preliminary finding suggests a role for PEP enzyme in the pathophysiology of autism but further research should be conducted to establish its role in the aetiology of psychiatric and neurological disorders, including autism and related spectrum disorders.
A preliminary sketch of a gut-brain relationship via the anterior insular cortex.
The literature seems to show that food allergies and the possibility of candida should be checked immediately because a significant number of children may be autistic because of these problems which can be controlled through drugs or diet.
Immune abnormalities, including antibodies against the central nervous system, have previously been associated with autism but this is the first study that unequivocally proves such a correlation.
Charity dedicated to obtaining funding for independent research addressing immune and immunogenetic abnormalities in autism.
Gateway to science-based biomedical information and commentaries on autism/PDD.
"It was a literal fluke that we discovered in Singapore -- when our entire family was being treated for parasites -- that this medicine would help Michael's autism. Within hours of being treated he improved dramatically. Now I can tell by looking at him if he has another parasite in him.'
The Center for the Study of Autism (CSA) is located in the Salem/Portland, Oregon area. The Center provides information about autism to parents and professionals, and conducts research on the efficacy of various therapeutic interventions.
Each of the papers and idea-collections on this web page reflects not only a goodly amount of medical research but also reflects the wonderful determination of autism-children's parents who are seeking to find answers
Objective: To explore possible associations between autism spectrum disorders (ASD) and environmental exposures, we linked the California autism surveillance system to estimated hazardous air pollutant (HAP) concentrations compiled by the U.S. Environmental Protection Agency. Methods: Subjects included 284 children with ASD and 657 controls, born in 1994 in the San Francisco Bay area. We assigned exposure level by census tract of birth residence for 19 chemicals we identified as potential neurotoxicants, developmental toxicants, and/or endocrine disruptors from the 1996 HAPs database. Because concentrations of many of these were highly correlated, we combined the chemicals into mechanistic and structural groups, calculating summary index scores. We calculated ASD risk in the upper quartiles of these group scores or individual chemical concentrations compared with below the median, adjusting for demographic factors. Results: The adjusted odds ratios (AORs) were elevated by 50% in the top quartile of chlorinated solvents and heavy metals [95% confidence intervals (CIs) , 1.1-2.1], but not for aromatic solvents. Adjusting for these three groups simultaneously led to decreased risks for the solvents and increased risk for metals (AORs for metals: fourth quartile = 1.7 ; 95% CI, 1.0-3.0 ; third quartile = 1.95 ; 95% CI, 1.2-3.1) . The individual compounds that contributed most to these associations included mercury, cadmium, nickel, trichloroethylene, and vinyl chloride. Conclusions: Our results suggest a potential association between autism and estimated metal concentrations, and possibly solvents, in ambient air around the birth residence, requiring confirmation and more refined exposure assessment in future studies.
If you were to draw names out of a hat to choose a "DAN! Doctor" in Arizona, there's apparently a greater than 60% chance you'd be taking your child to see a naturopath or homeopath.
There is increasing evidence that autism is etiologically a heterogeneous disorder involving neurobiological alteration in central nervous system functioning.
In-depth section concerning the theories of autism. Opioid Excess, Gluten/Casein and Relation to Celiac Disease, Gamma Interferon, Autoimmunity, Viral Infection, Vaccinations and Autism, Intestinal Permeability, Vitamin A Deficiency and Autism, etc.
It is dangerous to suppose that any one mechanism is applicable to all people with autism and it is possible that with different individuals different aspects come into play and are of relevance.
We found low levels of mercury in the hair and high levels of several other metals like aluminum, antimony, arsenic, and tin in the blood and urine. These children retain mercury, which is toxic to them.
Ribonucleic Acid - it's not just for transferring genetic information between DNA and proteins anymore. This blog will discuss current gossip, news, and major papers within the field. The level of discussion will be quite detailed, yet I hope that non-scientists who are interested in RNA will be able to follow.
The hypothesis explored in this review is that the high levels of serotonin in the blood seen in some autistic children (the so-called hyperserotonemia of autism) may lead to some of the behavioral and cellular changes also observed in the disorder. At early stages of development, when the blood-brain Barrier is not yet fully formed, the high levels of serotonin in the blood can enter the brain of a developing fetus and cause loss of serotonin terminals through a known negative feedback function of serotonin during development. The loss of serotonin innervation persists throughout subsequent development and the symptoms of autism appear. A review of the basic scientific literature on prenatal treatments affecting serotonin is given, in support of this hypothesis, with an emphasis on studies using the serotonin agonist, 5-methoxytryptamine (5-MT). In work using 5-MT to mimic hyperserotonemia, Sprague-Dawley rats are treated from gestational day 12 until postnatal 20. In published reports, these animals have been found to have a significant loss of serotonin terminals, decreased metabolic activity in cortex, changes in columnar development in cortex, changes in serotonin receptors, and "autistic-like" behaviors. In preliminary cellular findings given in this review, the animals have also been found to have cellular changes in two relevant brain regions: 1. Central nucleus of the amygdala, a brain region involved in fear-responding, where an increase in calcitonin gene related peptide (CGRP) was found 2. Paraventricular nucleus of the hypothalamus, a brain region involved in social memory and bonding, where a decrease in oxytocin was found. Both of these cellular changes could result from loss of serotonin innervation, possibly due to loss of terminal outgrowth from the same cells of the raphe nuclei. Thus, increased serotonergic activity during development could damage neurocircuitry involved in emotional responding to social stressors and may have relevance to the symptoms of autism.
The induction of Fos-like immunoreactivity (FLI) was used to determine the brain localization affected by b-casomorphin-7 (b-CM7). Peripheral administration of human b-CM7 at different doses (5, 10 and 30 \#956;g/kg, IV for 1 hour) to rats induced moderate to strong FLI in discrete brain regions including the nucleus accumbens, caudate putamen, ventral tegmental and median raphe nucleus, and orbitofrontal, prefrontal, parietal, temporal, occipital and entorhinal cortex. All of the above areas have been shown to be altered either functionally or anatomically in patients with schizophrenia, and most have been shown to be functionally abnormal in autism. Some of these brain areas are originators or components of dopaminergic, serotoninergic and GABA-ergic pathways, suggesting that b-CM7 can affect the function of all of these systems. The role of some other affected areas in emotional and motivated behavior, social adaptation, hallucinations and delusions suggests that b-CM7, which was found in high concentration in the CSF, blood and urine of patients with either schizophrenia or autism, may be relevant to schizophrenia and autism. Induction of FLI in the above brain areas by a moderate dose (10 \#956;g/kg) of b-CM7 was attenuated significantly, or blocked, by pretreatment with naloxone (2 mg/kg, IP). It is concluded that human b-CM7 can cross the blood-brain barrier, activate opioid receptors and affect brain regions similar to those affected by schizophrenia and autism.
We must think of autism, the developmental disability, as the tip of the iceberg and strive to find brain connections but also defects in other organ systems. I think of it like this: cell wall receptors may remain bound with hormone even after g-protein separates off receptors may be replaced by only a fat oil form (called cis) of Vitamin A, found in liver, kidney, Milkfat and cod liver oil.
Brian Deer bought 60 capsules for £21.15, and on checking the directions learnt that, if the product doesn't work, Dr Bradstreet recommends upping the dose, until parents could be spending £1,000 a year in Sea Buddies alone.
Children with autism have inflammation in their brains, although it is not yet clear whether the inflammation actually causes the condition, researchers said. Tests on the brain tissue of 11 patients with autism who had died and spinal fluid from six living children with autism showed the activation of immune system responses, the team at Johns Hopkins University School of Medicine in Baltimore and the University of Milan found.
It is not necessary to explain how the other deficits in Executive Functioning, referred to earlier, are explicable in terms of this process but it can be done. In the same way, it may be possible to extend the process further to explain the perceived difficulties in Theory of Mind or Central Coherence tasks. We do not see these psychological abnormalities as being "the cause" of autism although they are sometimes described in these terms. Rather, they are symptoms of underlying psychological abnormalities, which may themselves result, in particular difficulties, which will modify the semi-automatic behaviours described above, or behaviours which are not otherwise directly related to these basic biochemically inspired phenomena.
Finally, we totally accept that each person with autism is different. The “symptoms” described above are superimposed upon the characters of individual human beings who have their own personalities and characteristics, foibles, preferences and inconsistencies. In no way are we attempting to define real people in terms of chemically driven automata. We must also consider how each and every one of us is affected to a greater or lesser extent by such forces, which are difficult to explain.
In most diseases the diagnostician does a complete work-up of tests to find out the cause of the illness. From the cause, a treatment protocol is prescribed.
Specializes in the detection and characterization of viruses which have undergone a stealth adaptation to avoid elimination by the immune system
At the present time, on the topic of cerebellar antibodies and autistic syndromes, we may neither accept or reject the hypothesis that nuclear or cytopiasmic Purkinje celis antigens are exposed for some reasons in some cases of autism.
Systemic immune abnormalities have no known relevance to brain dysfunction in autism. In order to find evidence for neuroinflammation, we compared levels of sensitive indicators of immune activation: quinolinic acid, neopterin, and biopterin, as well as multiple cytokines and cytokine receptors, in cerebrospinal fluid and serum from children with autism, to control subjects with other neurologic disorders. In cerebrospinal fluid from 12 children with autism, quinolinic acid (P 0.037) and neopterin (P 0.003) were decreased, and biopterin (P 0.040) was elevated, compared with control subjects. In sera from 35 persons with autism, among cytokines, only tumor necrosis factor receptor II was elevated compared with controls (P < 0.02). Decreased quinolinic acid and neopterin in cerebrospinal fluid are paradoxical and suggest dysmaturation of metabolic pathways and absence of concurrent infection, respectively, in autism. Alternatively, they may be produced by microglia but remain localized and not expressed in cerebrospinal fluid.
Deficits in central executive functioning, probably the ability simultaneously to process more than two pieces of information, lead to problems observed in ASD's. It is possible that secretin and other opioid peptides mediate these processes.
Dr Jang discusses liver damage in a patient who was overdosed with Vitamin A. It would appear that the patient was hers and that she prescribed the high doses of Vitamin A in different forms for a 3 year old boy who became seriously ill and was diagnosed with Vitamin A toxicity this year... What about permanent liver damage? Why does a doctor tell the parents "please keep an eye on the level of vitamin A"? Aren't the doctors supposed to do that if they are prescribing the stuff? More to the point shouldn't doctors know that they shouldn't be giving 3 year olds toxic doses of vitamin A?
Scientists have long thought that autism is a genetic disease. Yet gene research has been unable to identify a specific chromosome or location on a gene that is the site of a primary autism defect.
On the advice of a reader, I went to Dr. Bernard Rimland's "Autism Research Institute" (ARI) website and found the following therapies recommended for the treatment of autism: DMG (dimethly glycine, Betaine); Vitamin B6 and Magnesium; Secretin;
This update includes a new trial (Kuriyama 2002) to bring the total of included studies to three (total n=33). One study, which used a cross-over design (Tolbert 1993) provided insufficient data to conduct an analysis. Another crossover study (Findling 1997) yielded no significant differences between treatment and placebo group performances following the B6 intervention on measures of social interaction, communication, compulsivity, impulsivity, or hyperactivity. The latest study (Kuriyama 2002) was motivated by evidence from epilepsy research and was focussed on a subgroup of children with pervasive developmental disorders (PDDs) who exhibited clinical features similar to those with pyroxidine-dependent epilepsy. This small study (n=8) only measured IQ and 'Social Quotient' and found a statistically significant benefit for IQ (5.2, 95% CI = [0.2 to 10.3]) when in the treated group, by using change scores. Due to the small number of studies, the methodological quality of studies, and small sample sizes, no recommendation can be advanced regarding the use of B6-Mg as a treatment for autism.
BACKGROUND: The neurobiological basis for autism remains poorly understood. Given the role of growth factors in brain development, we hypothesized that epidermal growth factor (EGF) may play a role in the pathophysiology of autism. In this study, we examined whether serum levels of EGF are altered in adult subjects with high-functioning autism. METHODS: We measured serum levels of EGF in the 17 male subjects with high-functioning autism and 18 age-matched healthy male subjects. RESULTS: The serum levels of EGF in the subjects with high-functioning autism (72.4 +/- 102.8 pg/mL [mean +/- SD]) were significantly lower (Mann-Whitney U = 22.0, p < .001) than those of normal control subjects (322.3 +/- 122.0 pg/mL [mean +/- SD]). However, there were no correlations between serum EGF levels and clinical variables in the subjects with autism. CONCLUSIONS: This study suggests that decreased levels of EGF might be implicated in the pathophysiology of high-functioning autism.
Information on ordering the DAN protocol
In this paper it is argued that deficient synthesis of nitric oxide will cause inadequate cortical feature maps and also will result in impaired learning in cerebellum and hippocampus.
Donna Williams is a graduate, lecturer and author... She is also autistic. Her remarkable achievements and - she believes - a carefully controlled diet offer hope to thousands of other sufferers.
In September 1999, the Medical Board of California concluded that Robert Sinaiko, M.D., had "departed from the prevailing standard of practice of medicine" by using antifungal drugs and other questionable methods to treat three adults and a nine-year-old child for nonexistent "Candida" problems. Sinaiko was assessed $49,472.79 for administrative costs and placed on five years' probation with stringent supervisory conditions.
Fudenberg's lack of a license does not appear to have stopped him from offering medical services to the public. His Neuro Immuno Therapeutics Research Foundation Web site offers the following services: review of past medical records ($750 per inch); determining what tests are needed, ordering the tests, and interpreting the tests ($750); and determining which therapy will work (usually 2 hours @ $750/hour).
Bacteria, viruses and parasites may cause mental illnesses like depression and perhaps even autism and anorexia
I feel that all autistic children should be given prescription antifungal medication and a sugar-free diet as an integral part of their management program.
The children in the program (universal diet and clean room) returned to normal physically, in temperament, in awareness of surroundings and others, in emotions and empathy, and in ability to learn.
If parents don't know or can't decide, I proceed in an orderly fashion through nutritional therapies, to body therapies, through educational and behavior therapies, and through Chinese medicine.
Converging evidence from different lines of investigation puts the initiating injury of autism in the brain stem. Even a perfectly normal cerebral cortex would have to function quite abnormally if it receives abnormal input from lower brain structures.
The neuroendocrine abnormalities of autism are disturbances of the brain-adrenal, -gonadal and -gut axes, accompanied by immunological and gastrointestinal dysfunction.
There would appear to be an increase in the incidence in autism and related disorders and of many other disorders which, at first sight, would appear to be unrelated. Environmental factors must be involved.
There are many possible factors but two important aspects would appear to be the changing patterns of infections and especially those introduced by vaccination programmes and the wholesale use of Organo-Phosphorus insecticides.
Autistic children have been described as having bizarre eating habits, which may lead to situations of clinical or subclinical malnutrition. It is well recognized that dietary factors play an important role in maintaining immune defences. Thus, immunocompetence has been recently shown to be a sensitive and functional measure of the nutritional status. Since, autistic children have been reported to be exceptionally free from infectious diseases, and because of the literature is scarce about the relationships between nutritional status and immunocompetence in this syndrome, the purpose of this work was to find out the nutritional assessment of autistic children by evaluating their immunocompetence. The results were compared to those obtained from a control group. The study involved 20 autistic children ranging in ages from 4 to 12 years, who were diagnosed according to DSM IV (American Psychiatric Association, 1994). The patients were divided into two groups: 1) with eating disorders (EDA) (n=9) and 2) without eating disorders (NEDA) (n=11). Control subjects included 11 healthy children (brothers of the patients) matched by age and sex, who were free of medical, psychiatric, and neurological conditions. Leukocyte and lymphocyte counts were tested. Lymphocyte subsets: CD2, CD3, CD4, CD8, CD19 and CD57 were determined by flow cytometry. No modifications were found in lymphocyte subsets between all the autistic children (n=20) and the control group, but both total number and percentage of CD19 cells were higher in the autistic children. However, when the three groups were compared each other, surprisingly the highest values for CD2, NK and CD19 cells were found in the EDA group. The results suggest that contrary to what was expected, neither EDA nor NEDA show signs of malnutrition, having the highest values of lymphocyte subsets the autistic group with eating disorders. Therefore, there might be some defence mechanisms involved where neurotransmitters could play an important role.
We have examined urine from well over fifteen hundred subjects. Some of these have shown no clinical abnormalities (controls) but the majority have exhibited symptoms of autism or of other disorders related to autism.
No longer can the condition just be considered a psychiatric or neurological disorder, they argued. Autism had to be seen as a systemic illness that has gastrointestinal, immunological, endocrinological, psychological and neurological complications.
On October 17, 2002, FDA investigators accompanied U.S. Marshals in a seizure of dietary supplements making drug claims from the Humphrey Laboratories of Lake Oswego, Oregon, doing business as Kirkman Laboratories. U.S. Marshals seized hundreds of bottles of Kirkman's HypoAllergenic Taurine Capsules after FDA determined that Kirkman had made unsubstantiated claims that the product could treat autism.
SerenAid's labeling suggests that it is useful in improving conditions of autism in children. The labeling suggests that the product is safe and effective for its intended use when, in fact, this has not been established.
You want to know how many research validated treatments there are for autism? Do you want to know how many treatments are considered well established empirically validated? I'll tell you how many: NONE. How about "Probably efficacious?" NONE... When someone says they have a cure, a research validated treatment or a promise of recovery from autism, they are telling a LIE. They are no better than the merchants of terror who institutionalized (and molested) autistic children because of "refrigerator mothers."
The following excerpts are in regard to the use of vitamin B6, magnesium, and/or dimethylglycine (DMG) and are edited from letters shared by our advisory board member, Dr. Bernard Rimland, director of the Autism Research Institute (ARI).
I won't be at all surprised to hear of parents flying off to other countries to have their autistic children treated with stem cells. I won't be surprised to hear that some of the chelation doctors in this country start to offer some form of stem cell therapy, that probably isn't stem cell therapy at all but some telomerase treated cell extract or homeopathic tonic not subject to FDA regulations.
Chronic accumulations of xenobiotic and heavy-metal neurotoxins may encourage the development of autism. The results support the assertion that genetic polymorphisms associated with aberrant hepatic detoxification may be universal among autistic children.
A study carried out by Child Medicine and Language Disorders Section at Ain Shams University showed that goat and camel milk and corn bread regular intake helps in curing autism, a childhood disorder characterized by withdrawal, self-stimulation, cognitive deficits, and language disorders. Dr. Mohamed Baraka, Chairman of Language Disorders Unit said that these milks contain enzymes which are useful in stimulating the cognitive and mental ability of autistic children.
We report on elevated total cholesterol and low-density lipoprotein (LDL) levels in 22 individuals with Asperger syndrome compared with well-matched controls, after accounting for lifestyle variables and clinical symptomatology that could affect them. A potential role for dyslipidemia in the pathogenesis of some forms of autism is discussed.
Autism is a complex neurodevelopmental disorder of early onset that is highly variable in its clinical presentation. Although the causes of autism in most patients remain unknown, several lines of research support the view that both genetic and environmental factors influence the development of abnormal cortical circuitry that underlies autistic cognitive processes and behaviors. The role of the immune system in the development of autism is controversial. Several studies showing peripheral immune abnormalities support immune hypotheses, however until recently there have been no immune findings in the CNS. We recently demonstrated the presence of neuroglial and innate neuroimmune system activation in brain tissue and cerebrospinal fluid of patients with autism, findings that support the view that neuroimmune abnormalities occur in the brain of autistic patients and may contribute to the diversity of the autistic phenotypes. The role of neuroglial activation and neuroinflammation are still uncertain but could be critical in maintaining, if not also in initiating, some of the CNS abnormalities present in autism. A better understanding of the role of neuroinflammation in the pathogenesis of autism may have important clinical and therapeutic implications.
The frequency of autoimmune disorders was significantly higher in families of the PDD probands compared with families of both the autoimmune and healthy control probands. Autoimmunity was highest among the parents of PDD probands compared with parents of the healthy control subjects. Hypothyroidism/ Hashimoto's thyroiditis and rheumatic fever were significantly more common in families with PDD probands than in the healthy control families.
BACKGROUND: Precise mechanisms underlying the pathophysiology of autism are currently unknown. Given the major role of glutamate in brain development, we have hypothesized that glutamatergic neurotransmission plays a role in the pathophysiology of autism. In this study, we studied whether amino acids (glutamate, glutamine, glycine, d-serine, and l-serine) related to glutamatergic neurotransmission are altered in serum of adult patients with autism. METHODS: We measured serum levels of amino acids in 18 male adult patients with autism and age-matched 19 male healthy subjects using high-performance liquid chromatography. RESULTS: Serum levels (mean=89.2 muM, S.D.=21.5) of glutamate in the patients with autism were significantly (t=-4.48, df=35, p<0.001) higher than those (mean=61.1 muM, S.D.=16.5) of normal controls. In contrast, serum levels of other amino acids (glutamine, glycine, d-serine, l-serine) in the patients with autism did not differ from those of normal controls. There was a positive correlation (r=0.523, p=0.026) between serum glutamate levels and Autism Diagnostic Interview-Revised (ADI-R) social scores in patients. CONCLUSIONS: The present study suggests that an abnormality in glutamatergic neurotransmission may play a role in the pathophysiology of autism.
We describe a model for investigating disorders of central nervous system development based on neonatal rat infection with Borna disease virus, a neurotropic noncytolytic RNA virus.
The series of 15 cases presented here supports the hypothesis that autism has a toxic etiology.
Parents should avail themselves of every therapy available, because even after the child has undergone a biomedical therapy, he does not have a normal development and needs additional assistance.
Most psychologists are still working on 'top down' verbal-semantic approach to understanding the mind. I prefer the bottom-up approach. Psychology needs to become biologically-oriented.
So, the brains of autistic people are chemically different then the brains of non-autistics. Given that fact, is it a) stupid or b) clever to use a process that alters the chemical composition of the person and which has never undergone any safety trials in regards to autism? There's a whole bunch of people here who need to take a drastic step backwards and do some basic safety trials on what is, irrespective of their beliefs, a poorly understood and potentially dangerous/fatal process.
These extraordinarily adaptable behaviors of ES cells shows that environmental cues not only guide choices between different pathways of differentiation, but in certain cases, they can also stop or start the developmental clock.
We propose that the D-saccharide transport system (or an unknown system, with D- specificity) is utilised in the partitioning of opioid peptides through the blood-brain barrier, and that the D- forms these peptides are active.
This research considers the prevalence of iron deficiency in children with autism and Asperger syndrome and examines whether this will influence guidelines and treatment. Retrospective analysis of the full blood count and, as far as available, serum ferritin measurements of 96 children (52 with autism and 44 with Asperger syndrome) was undertaken. Six of the autistic group were shown to have iron deficiency anaemia and, of the 23 autistic children who had serum ferritin measured, 12 were iron deficient. Only two of the Asperger group had iron deficiency anaemia and, of the 22 children who had their serum ferritin measured, only three were iron deficient. Iron deficiency, with or without anaemia, can impair cognition and affect and is associated with developmental slowing in infants and mood changes and poor concentration in children. This study showed a very high prevalence of iron deficiency in children with autism, which could potentially compromise further their communication and behavioural impairments.
The premise of this theory is that the blockage of fever with antipyretics interferes with normal immunological development in the brain, leading to neurodevelopmental disorders in certain genetically and immunologically disposed individuals.
Autism is characterized by restricted, repetitive behaviors and impairment in socialization and communication. Although no neuropathologic substrate underlying autism has been found, the findings of brain overgrowth via neuroimaging studies and increased levels of brain-derived neurotrophic factor (BDNF) in neuropathologic and blood studies favor an anabolic state. We examined acetylcholinesterase, plasma neuronal proteins, secreted beta-amyloid precursor protein (APP), and amyloid-beta 40 and amyloid-beta 42 peptides in children with and without autism. Children with severe autism and aggression expressed secreted beta-amyloid precursor protein at two or more times the levels of children without autism and up to four times more than children with mild autism. There was a trend for children with autism to show higher levels of secreted beta-amyloid precursor protein and nonamyloidogenic secreted beta-amyloid precursor protein and lower levels of amyloid-beta 40 compared with controls. This favors an increased a-secretase pathway in autism (anabolic), opposite to what is seen in Alzheimer disease. Additionally, a complex relationship between age, acetylcholinesterase, and plasma neuronal markers was found.
Commercial site offering "RNA derived therapeutics."
Many children with autism spectrum disorders (ASD) display abnormally low levels of total cholesterol, according to a report in the American Journal of Medical Genetics Part B for September. These low levels may play a role in the pathogenesis of ASD. This deficient appears to stem from an inability to produce cholesterol, not from inadequate dietary intake or impaired intestinal absorption, the findings suggest. Previous reports have linked autism with Smith-Lemli-Opitz Syndrome (SLOS), a genetic disorder involving impaired cholesterol synthesis. However, the rate of SLOS and other sterol disorders among ASD patients was unclear.
The misdiagnoses in childhood autism come not in the diagnosis of the condition itself, something that is unmistakable once one has seen a few children with the condition, but from a failure to recognize autism as predominantly an environmental illness.
Autism is a behaviorally defined neurodevelopmental disorder usually diagnosed in early childhood that is characterized by impairment in reciprocal communication and speech, repetitive behaviors, and social withdrawal. Although both genetic and environmental factors are thought to be involved, none have been reproducibly identified. The metabolic phenotype of an individual reflects the influence of endogenous and exogenous factors on genotype. As such, it provides a window through which the interactive impact of genes and environment may be viewed and relevant susceptibility factors identified. Although abnormal methionine metabolism has been associated with other neurologic disorders, these pathways and related polymorphisms have not been evaluated in autistic children. Plasma levels of metabolites in methionine transmethylation and transsulfuration pathways were measured in 80 autistic and 73 control children. In addition, common polymorphic variants known to modulate these metabolic pathways were evaluated in 360 autistic children and 205 controls. The metabolic results indicated that plasma methionine and the ratio of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH), an indicator of methylation capacity, were significantly decreased in the autistic children relative to age-matched controls. In addition, plasma levels of cysteine, glutathione, and the ratio of reduced to oxidized glutathione, an indication of antioxidant capacity and redox homeostasis, were significantly decreased. Differences in allele frequency and/or significant gene-gene interactions were found for relevant genes encoding the reduced folate carrier (RFC 80G > A), transcobalamin II (TCN2 776G > C), catechol-O-methyltransferase (COMT 472G > A), methylenetetrahydrofolate reductase (MTHFR 677C > T and 1298A > C), and glutathione-S-transferase (GST M1). We propose that an increased vulnerability to oxidative stress (endogenous or environmental) may contribute to the development and clinical manifestations of autism.
Defective functioning of metallothionein protein (MT) is a distinctive feature of autism. This abnormality results in impaired brain development and extreme sensitivity to toxic metals and other environmental substances.
I have done testing on patients with virtually every disorder mentioned in The Yeast Connection and found evidence of abnormal microbial metabolites in all of them.
The citations presented here convey principles whereby intra-monocyte infections can affect hematopoiesis, immunity, and the blood-brain barrier.
Private practitioner focusing on immunological treatment
Autistic Syndrome probably is a state of dysfunction induced in the brain by a dysregulated immune system. It could be possible that this dysfunction may occur in individuals that have a genetic predisposition.
It is generally accepted that the earlier a true diagnosis is made the better for the child, the family and those involved around them. This is because effective strategies can only be employed if the true nature of a condition is known.
I was on a panel at a local autism/aspergers conference this past weekend. I'm glad I went, both to represent parents and people on the spectrum, and to keep an eye on what therapists and parents are being sold as autism treatment.
While we currently refer to the social, behavioral and language abnormalities as autism, a more accurate diagnosis for most children with this disorder would be autoimmune or dysimmune encephalopathy.
The way of thinking of some parents of autistic children is quite evident on the "autism biomedical treatment" Internet support groups, where recipes and protocols are exchanged. The advice given by these parents, some of whom say they are quoting their child's DAN! doctor, ends up being contradictory of advice from other parents. Some of the advice is quite frightening. Other advice is patently bizarre. Some responding to the advice express fear of implementing it. Sometimes they implement it in spite of their fears. Worst of all, there are individuals in these groups who end up being seen as real experts whose opinion is equal or superior to that of any doctor who has actually seen the child.
In a previous study we showed that b-casomorphin-7 (b-CM7) is taken up by brain regions relevant to schizophrenia and autism. The present experiment was designed to find whether b-CM7 has any behavioral or analgesic effects in rats. About 65 seconds after treatment with different doses of b-CM7, rats became restless and ran violently, with teeth chattering and with rapid respiration. Seven minutes later, the rats became inactive with less walking, distancing themselves from the other rat in the same cage, and sitting in, or putting their head against, the corner of the cage. The sound response was reduced and social interaction was absent. One hour later, the rats showed hyperdefensiveness. The above behavioral effects of b-CM7 did not occur when rats were pretreated with naloxone (2 mg/kg, IP). The rats receiving saline did not show any behavioral changes throughout the 2 hour period of observation. b-CM7 also demonstrated analgesic effects, which could be blocked by naloxone. The results suggest that b-CM7 may play a role in behavioral disorders such as autism and schizophrenia.
OBJECTIVE: Determine the effect of a moderate dose multivitamin/mineral supplement on children with autistic spectrum disorder. DESIGN: Randomized, double-blind, placebo-controlled 3-month study. SUBJECTS: Twenty (20) children with autistic spectrum disorder, ages 3-8 years. RESULTS: A Global Impressions parental questionnaire found that the supplement group reported statistically significant improvements in sleep and gastrointestinal problems compared to the placebo group. An evaluation of vitamin B(6) levels prior to the study found that the autistic children had substantially elevated levels of B6 compared to a control group of typical children (75% higher, p < 0.0000001). Vitamin C levels were measured at the end of the study, and the placebo group had levels that were significantly below average for typical children, whereas the supplement group had near-average levels. DISCUSSION: The finding of high vitamin B(6) levels is consistent with recent reports of low levels of pyridoxal-5-phosphate and low activity of pyridoxal kinase (i.e., pyridoxal is only poorly converted to pyridoxal-5-phosphate, the enzymatically active form). This may explain the functional need for high-dose vitamin B(6) supplementation in many children and adults with autism.
A growing number of scientists believe that developmental and neurological toxins could be partly responsible for the increased incidence of a range of physical and mental effects in children.
Creating and implementing a treatment program for autism is not easy, but -- as more and more parents are reporting -- it can be done. It is, in any case, certainly worthwhile to try.
Dallas-lawyer Brian R. Arnold wrote Playtex Products, Inc. in January alleging that a toddler became seriously ill and, eventually, "began to exhibit autistic behavior," after drinking from a plastic spill-proof cup made by Playtex... Dr. Cave, who runs a "holistic" general practice in Baton Rouge, diagnosed the child with "dysbiosis," a serious sounding medical condition. Dysbiosis means one's intestinal bacteria are somehow out of "balance." Dr. Cave says dysbiosis is associated with behavioral disorders and autism in children... William Shaw, Ph.D., who runs the Great Plains Laboratory, reported that the child had elevated levels of yeast by-products, indicating a "yeast/fungal overgrowth of the gastrointestinal tract." Dr. Shaw says such yeast infections cause autism Even giving Dr. Shaw's theory the benefit of doubt, the bacteria found on the Playtex cup was not the same kind that was found in the child.
Where on Earth did anyone get the idea that ignoring things like chronic diarrhea or Asthma is part of neurodiversity? ... if your child has a diagnosis for all of the above (physical conditions) (and I mean a diagnosis from an actual Doctor, not a quack who'll wheel out a diagnosis because they're 'excited' about trying their brand new pet theory out) then go right ahead and treat them -- to do otherwise would be insane. However, don't make the mistake of thinking that a diagnosis of these things is equitable to a diagnosis of autism.
With each new intervention that came along, we expanded our definition of acceptable risks. "Maybe this is something we wouldn't normally give to a child of this age but if it helps the benefit will offset the risk. Right? There are a lot of other parents doing these things and it isn't really blind experimentation on children, not really. Not as long as other parents have tried it and it didn't hurt their child." Each new intervention felt like the treadmill was turned up another notch. Support and encouragement from other parents kept us going, much like the encouragement from unknown bar patrons in the bad joke. "It helped? Increase the dose" or "If that worked you really have to try this thing." Where does it end? Where do you stop? Just keep going until your child is typical, is injured, or worse? It becomes almost like a gambling addiction. "I know this one will be the winner! Just one more roll baby and then we can scoop up our winnings and go home winners!" But there's always the chance with any experiment the outcome will be worse than expected.
The number and variation of factors emerging from the current study, suggests that the metabolic hypothesis of autism does provide a platform to explain why the aetiology of autism spectrum disorders may have eluded medical science at present.
Among Brian Deer's findings was that Andrew Wakefield had filed patent claims for a vaccine and a possible cure for autism, based on a fringe theory of "transfer factors". His collaborator and "co-inventor" was Hugh Fudenberg, who claimed in a 2004 interview with Brian Deer to cure autistic children with his own bone marrow. Here is Fudenberg's record with the South Carolina board of medical examiners. In November 1995, he was banned indefinitely from prescribing.
The biological causes of autism are unknown. Since the early 1960s, the most consistent pathophysiological finding in autistic individuals has been their statistically elevated blood 5-hydroxytryptamine (5-HT, serotonin) levels. However, many autistic individuals have normal blood 5-HT levels, so this finding has been difficult to interpret. The serotonin transporter (SERT) controls 5-HT uptake by blood platelets and has been implicated in autism, but recent studies have found no correlation between SERT polymorphisms and autism. Finally, autism is considered a brain disorder, but studies have so far failed to find consistent serotonergic abnormalities in autistic brains. A simple mathematical model may account for these paradoxes, if one assumes that autism is associated with the failure of a molecular mechanism that both regulates 5-HT release from gut enterochromaffin cells and mediates 5-HT signaling in the brain. Some 5-HT receptors may play such a dual role. While the failure of such a mechanism may lead to consistent abnormalities of synaptic transmission with no alteration of brain 5-HT levels, its effects on blood 5-HT levels may appear paradoxical.
It must be constantly born in mind that we are dealing with individual people whose autism may be the consequence of a variety of aetiologies. The effects of medication and other therapies appear to differ markedly between individuals.
Nothing will make you stop and say "Wait a minute. I want to try that!" like a report of a non-verbal child gaining speech in a short period of time. To the parent of such a child it must seem like nothing short of a miracle, especially when changes occur within a few days of the new therapy. How can anyone convince that parent it was a coincidence or just the child's time to start talking? If I found myself in that position I'd like to think I would consider other possibilities but if Therapy-X fit right in with a preconceived idea or hypothesis, it might be tough to change my mind.
A wide range of abnormalities has been reported in autistic brains, but these abnormalities may be the result of an earlier underlying developmental alteration that may no longer be evident by the time autism is diagnosed. The most consistent biological finding in autistic individuals has been their statistically elevated levels of 5-hydroxytryptamine (5-HT, serotonin) in blood platelets (platelet hyperserotonemia). The early developmental alteration of the autistic brain and the autistic platelet hyperserotonemia may be caused by the same biological factor expressed in the brain and outside the brain, respectively. Unlike the brain, blood platelets are short-lived and continue to be produced throughout the life span, suggesting that this factor may continue to operate outside the brain years after the brain is formed. The statistical distributions of the platelet 5-HT levels in normal and autistic groups have characteristic features and may contain information about the nature of this yet unidentified factor.... At least some biological factors, the abnormal function of which leads to the development of the autistic brain, may regulate the release of 5-HT from the gut years after birth. If the present model is correct, it will allow future efforts to be focused on a limited number of gene candidates, some of which have not been suspected to be involved in autism (such as the 5-HT4 receptor gene) based on currently available clinical and experimental studies.
CCID has performed viral cultures on blood samples from well over 100 autistic children. In greater than 80% of the samples, a marked cytopathic effect (CPE) has occurred. The strongly positive CPE is similar to that induced by stealth-adapted viruses.
Adverse-events factors are capable of inducing CNS damage regardless of the person's genetics. These factors are independent of cognition genes, even as the adverse-events factors affect cognition, emotional expression, and behaviors.
Interventions involving manipulations in diet are being increasingly used for autism spectrum disorders. Professionals who do not consider such interventions are in danger of missing the boat and failing to meet the needs of their clients.
Re Internet survey of treatments used by parents of children with autism.
"In the search for promising novel therapies in autism, there is the potential for parents to be manipulated and children to be harmed." You said it, buster. (Review of Placebo Effects in Developmental Disabilities: Implications for Research and Practice by Adrian Sandler.)
Ever since I began the Herculean (some might say Quixotic) task of exposing the quackery and pseudoscience surrounding autism, I have had people ask me, "Are you the same Jim Laidler who used to talk about chelation at autism conferences?" To them, the idea that I could once have been an impassioned supporter of the very thing I am now trying to debunk is hard to fathom. Well, everyone has something in their past that they are embarrassed about -- and that is mine. I consider myself to be a very scientific person. While growing up, I was skeptical and inquiring and naturally gravitated to the sciences. My first brushes with pseudoscience and quackery in medical school left me convinced that "it could never happen to me." I was sure that my background and training would keep me from making the same mistake as "those people." I was wrong.
Stem cells for autism!! Why not?? This is so scary. The scary part is the way parents are pressured by quacks to do something NOW!!! for their babies, BEFORE IT'S TOO LATE!! Remember, "Cure Autism Now" and "Defeat Autism Now!" and "Defeat Autism Yesterday"? Yeah. Desperation, plus pressure, plus available cash, plus the nebulous belief that death is better than autism--equals bad news for the child, good news for the quack.
TIPOgen is an in vitro diagnostic development company that will use modern and novel proteomic approaches to identify sets of molecules (biomarkers). These biomarkers will have the utility to predict autism spectrum disorders (ASDs) earlier and prognose the outcome of behavioral treatments for ASDs. TIPOgen will be the basis for one of the first dedicated research modalities in the world for ASDs. The hope is that through TIPOgen research and diagnostics better autism therapies may be forged.
Excess or deficiency of natural trace elements has been implicated in the etiology of autism. This study explores whether concentration levels of toxic metals in the hair of children with autism significantly differ from those of age- and sex-matched healthy controls. In-hair concentration levels of antimony, uranium, arsenic, beryllium, mercury, cadmium, lead and aluminum from 40 boys with autism and 40 healthy boys were determined by Perkin-Elmer mass spectrometry. The children with autism had significantly (p < 0.001) higher in-hair concentration levels of lead, mercury and uranium. There was no significant difference between the two groups in the other five toxic elements. The ratio between nutritional elements and toxic metals among children with autism was within the normal range. The possible sources of the toxic metals are discussed. Such testing is informative but at present the practical implications in terms of diagnosis and clinical management are limited.
While only speculatively, it can be suggested that there is a rural/suburban bias in the incidence of ASD. This fits with the hypothesis of the possibility of environmental factors (such as OP pesticides) contributing to the formation of IAG.
We support the hypothesis that autism could be the consequence of the action of peptides of exogenous origin affecting neurotransmission within the Central Nervous System.
Autism is the consequence of a metabolic disorder, whereby biologically active peptides derived mainly from gluten and/or casein in the diet are not broken down correctly, and through problems with gut permeability, are excessively present in the blood.
In my view, autism is the absence, or profound diminution of the intensity, of the innate biological drive to connect with other human beings. Researchers in cognitive neuroscience might refer to this as an impaired affiliative drive.
Chelation is still "topical", it has a lot of people "talking it up" at the moment and, as a result, will rate higher. As parents experience the inevitable "treatment failures" and see the cycles of the disorder coming around again, they will become disenchanted with chelation and it will gradually fall from favor. If we could go back and see the poll numbers for secretin during its heyday, we would see - I suspect - much the same result. High "effectiveness" numbers when everyone was talking about how secretin was going to "cure" autistic children, followed by a slide from grace as the studies after study showed no effect.
WCAP aims to develop programs and educational materials to redefine autism as a complex but treatable condition, and seeks to redefine autism as a multi-systemic medical condition with environmental causal factors.