Brian Shilhavy, Health Results Information
Cleaning the information and discovered this document by my good friend Ginger Taylor. 30 studies showing a connection between vaccines and autism. 30. 30. Do you perceive? A TV, CDC, IOM, AAP and NIH is just eisegesis. Do you need to know the actual kicker? There are 49, I couldn't fit all of them into the attention mark (Facebook).
- 1 Evidence that vaccines may cause autism
- 2 This mistrust was once once more found during HHS hearings
- 3 Contact issues of autistic touch
- 4 1. Hepatitis B Vaccination of newborns and autism in men
- 5 2. Porfyrinuria in Childhood Autistic Dysfunction: Results on Environmental Toxicity
- 6 3. Theoretical Aspects of Autism: Causes – Review
- 7 5. Sex Selective Toxicity of Thimerosal
- 8 . 6. Comparison of Blood and Brain Mercury Levels with Vaccines in Methylmercury or Thimerosal
- 9 11. Validating Autistic Regression with House Movies
- 10 12. Mercury blood levels relate to the analysis of autism: Reassessment of an necessary set of knowledge
- 11 13. Development of Regression and Mitochondrial Dysfunction in Autism
- 12 14. Oxidative stress in autism: elevated levels of 3-nitrotyrosine in the brain
- 13 15. The Big Brain of Autism: The Challenge of General Anxiety
- 14 16. Todisteet myrkyllisyydestä, oksidatiivisesta stressistä ja neuronaalisesta loukkauksesta autismissa
- 15 17. Oxidative Stress in Autism
- 16 18. Thimerosal Neurotoxicity is Associated with Glutathione Depletion: Protection with Glutathione Precursors
- 17 19. Aluminum adjuvant linked to gulf conflict illness induces motor neuron demise in mice
- 18 20. Environmental mercury release, special education rates, and autism disorder: an ecological study of Texa
- 19 21. Autism Spectrum Issues in Relation to Distribution of Hazardous Air Pollutants in the SF Bay Area
- 20 22. A Case Collection of Youngsters with Apparent Mercury Toxic Encephalopathies Manifesting with Medical Signs of Regressive Autistic Dysfunction
- 21 23. Consideration-deficit hyperactivity disorder and blood mercury degree: a case-control research in chinese language youngsters
- 22 24. The Changing Prevalence of Autism In California
- 23 25. Mitochondrial Power-Deficient Endophenotype in Autism
- 24 26. Bridging from Cells to Cognition in Autism Pathophysiology: Biological
- 25 27. Heavy-Metallic Toxicity—With Emphasis on Mercury
- 26 28. Proof of Mitochondrial Dysfunction in Autism and Implications for Remedy
- 27 29. Proximity to point sources of environmental mercury launch as a predictor of autism prevalence
- 28 30. Epidemiology of autism spectrum disorder in Portugal: prevalence, medical characterization, and medical circumstances
Evidence that vaccines may cause autism
There is a frequent false impression that there isn’t a analysis that supports the assumption that vaccines may cause autism. This discussion is usually repeated by the medical employees and the public health authorities who’ve by no means advised you that these studies exist, and in some instances those that refuse to read the info when provided to them, in order that they continue their work beneath the false assumption that the explanation for the vaccine's autism is just "Internet rumor" or the results of one paper revealed in 1998.
This mistrust was once once more found during HHS hearings
Actually, the first research that offered proof that vaccines may cause autism was the first guide ever written on autism. In the 1930s, Leo Kanner, a pediatric psychiatrist, found for greater than ten years the existence of latest forms of neurological symptoms that had never been described in the medical literature by which youngsters have been removed, unofficial and showed comparable strange behaviors. This dysfunction is called "autism". In the paper, Dr. Kanner noted that the onset of the dysfunction started after a small vaccine was given. This publication was revealed in 1943, and proof that vaccination causes extra and more neurological and immunological regression, together with autism, has been put in thus far.
Contact issues of autistic touch
Leo Kanner, University of Johns Hopkins, 1943
”Since 1938, various youngsters whose condition differs so clearly and uniquely has been reported up to now that the merits of each case – and hopefully in the end I get – in detail
All Kanners instances have been born after the introduction of Eli Lilly's new type of water-soluble mercury in the late 1920s, used as an anti-fungal agent in the forest business. a processing product in the timber business and as a disinfectant and antibacterial in the pharmaceutical business as "thimerosal" included in the vaccines.
Early Evidence of Ormation Vaccine / Connection, I like to recommend studying Dr. Bryan Jepson's guide "Changing Autism Course: The Scientific Approach of Parents and Doctors" in addition to Mark Blaxill and Dan Olmseted's New Ebook "The Age of Autism: Mercury, Medicine and Man-made Epidemic".
As testified at the listening to, there’s loads of analysis that helps the vaccine of autism link. I’ve included 49 analysis, and included a printed only during the last ten years of analysis. That is not at all an entire record, but the proven fact that I have compiled in recent times, . the research of the topic has acquired attention I've solely included knowledge associated to autism, does research on other vaccine accidents, of which there are lots of
As you possibly can see, medical professionals attest that the vaccine / autism just isn’t scientifically supported principle is. ignorant of recent science When vaccination selections are made on the basis of an ignorant statement, it means critical potential hurt to the patient, and because the regulation prevents vaccine accidents, it additionally signifies that uninformed medical professionals who make dangerous suggestions can’t be held responsible in any method by providing poor patient info
Mother and father need to know can their youngsters develop autism from their vaccines. If they consider the reply is yes, and the danger of brain injury brought on by vaccination is bigger than the danger brought on by the illness, their proper to reject vaccinations for themselves and their youngsters by coercion.
Patients want to be able to make their own knowledge-based vaccine selections because they typically know more about the potential vaccine dangers that even the highest public health authorities make.
1. Hepatitis B Vaccination of newborns and autism in men
Annals of Epidemiology, Vol. 19, No. 9 ABSTRACTS (ACE), September 2009: 651-680,
CM Gallagher, MS Goodman, Diploma Program in Public Health, Stony Brook College Medical Middle, Stony Brook, NY
PURPOSE: Common vaccination of newborn with hepatitis B vaccine was advisable in 1991; Nevertheless, the security results are totally different. The vaccine security assessment staff didn’t report that hepatitis B vaccinations between delivery and febrile episodes or neurological uncomfortable side effects weren’t interconnected. In other studies, constructive mixtures
between hepatitis B vaccination and ear an infection, pharyngitis and persistent arthritis have been noticed; and receiving early intervention / particular schooling (EIS); US youngsters chance samples. Youngsters with Autistic Frequency Disorder (ASD) represent an growing presence for EIS. We estimate the relationship between male neonatal hepatitis B vaccination and ASD dad or mum report.
METHODS: On this cross-sectional research, US chance samples from the Nationwide Well being Interview Survey 1997-2002 datasets have been used. Logistic regression modeling was used to guage the impact of newborn hepatitis B vaccination on ASD danger on boys ages Three to 17 years of age with shot data adapted to race, mom coaching, and the two mother and father' household.
RESULTS: Boys who acquired hepatitis B vaccine during the first month have been 2.94 greater chances for ASD (nZ31 7.486; OR Z 2.94; p Z 0.03; 95% CI Z 1.10, 7 , 90)
in comparison with later or unvaccinated boys. For non-Latin white boys, 61% have been much less more likely to have ASD (ORZ0.39; pZ0.04; 95% CIZ0.16, 0.94) compared to non-white boys.
CONCLUSION: The outcomes recommend that US neonates vaccinated with hepatitis B vaccine had a 3-fold greater danger of ASD; the danger was biggest for white boys.
2. Porfyrinuria in Childhood Autistic Dysfunction: Results on Environmental Toxicity
Robert Natafa, Corinne Skorupkab, Lorene Ametb, Alain Lama, Anthea Springbettc and Richard Lathed, aLaboratoire Philippe Auguste, Paris, France, Affiliation ARIANE, Clichy, France, Division of Statistics, Roslin Institute, Roslin, UK, Pieta Analysis,
This new French research utilizes new and refined measurement of environmental toxicity by assessing porphyrin ranges in autistic youngsters. It offers clear and unambiguous evidence that youngsters with autism spectrum issues are more toxic than their neurotic age groups.
Extract: “Coproporphyrin levels increased in children with autistic disorders compared to control groups… the increase was significant. These data suggest environmental toxicity in childhood autistic disorder.
Abstract: In order to solve a possible autistic environment effect, we conducted a retrospective study of urinary porphyrin levels, a biomarker indicative of ecotoxicity, to 269 children with neurological development and related disorders referred to the Paris Clinic (2002–2004), which included 106 patients. autistic disorder. Urine porphyrin levels, determined by high performance liquid chromatography, were compared with diagnostic groups including internal and external control groups. Coproporphyrin levels were elevated in children with autistic disorder compared to control groups. The height was maintained in the normalization of the aging or control hormone metabolite (uroporphyrin) in the same samples. The height was significant (P <0.001). Porphyrin levels remained unchanged in Asperger's disorder by separating it from an autistic disorder. The atypical molecule esproporforphine, a specific indicator of heavy metal toxicity, was also elevated in autistic disorder (P <0.001), but not significantly in Asperger. The subgroup with autistic disorder was treated with oral dimercaptosuccinic acid (DMSA) to remove heavy metals. After DMSA, urinary excretion of porphyrin was significant (P = 0.002). These data suggest environmental toxicity in childhood autistic disorder.
3. Theoretical Aspects of Autism: Causes – Review
Journal of Immunotoxicology, January-March 2011, Vol. 8, No. 1, pp. 68-79
Helen V. Ratajczak, PhD
Autism, a member of PDD, has grown dramatically since Leo Kanner's description in 1943. The first estimate appears in 4-5 For 10,000 children, the incidence of autism is now 1/110 in the United States and 1/64 in the UK. When retrieving information from the 1943 PubMed and Ovid Medline databases, this report summarizes the results that correlate with the timing of changes in incidence and changes in the environment. Autism can be caused by more than one cause, and different manifestations occur in different individuals with common symptoms. The documented causes of autism are genetic mutations and / or deletions, viral infections, and encephalitis after vaccination. Therefore, autism is the result of brain damage and / or inflammation. Inflammation may be due to deficient placenta, immature blood-brain barrier, maternal immune response to infection during pregnancy, premature labor, encephalitis in the child after birth, or toxic environment.
RELATED INFORMATION:  4. Disconnection of ATP-mediated calcium signal and dysregulated IL-6 secretion in dendritic cells Nanomolar Thimerosal
Environmental Health Outlook, July 2006.
Samuel R. Goth, Ruth A. Chu Jeffrey P. Gregg
shows that very low levels of Thimerosal can contribute to the disregulation of the immune system.
Example: “Our result is that DCs primarily express RyR1 channel complex and that this complex is disconnected at very low THI levels with dysregulated IL-6 secretion enhancement fascinating questions about molecule immune system regulation and possible role of RyR1 complex. the genetic susceptibility of the immune system to mercury.
Dendritic cells (DC), a rare cell type that is widely distributed, are potent antigens
which express cells that initiate primary immune responses. DCs rely on intracellular redox
and calcium (Ca2 +) signals for proper development and function, but the relationship between the two signaling systems
is unclear. Thimerosal (THI) is the mercury used
to preserve vaccines, consumer products and experimentally induce Ca2 + release from the
microsomal stock. We tested the ATP-mediated Ca2 + responses of DCs, which were temporarily exposed to
nanomolar THI. Transcriptional and immunocytochemical analyzes indicate immature and mature DCs of the mouse
myeloids (IDCs, MDCs) expressing inositol 1,4,5-trisphosphate
and cyanodine receptor (IP3R, RyR) Ca2 + channels. well-known THI items. IDCs express the RyR1 isoform
in the punctate distribution most densely close to plasma membranes, and
in dendritic processes, while IP3Rs are more widely distributed. RyR1 positively
and negatively regulates purinergic signaling because ryanodine (Ry) blockade (1) recruits
80% more ATP responses, (2) shortened ATP-mediated Ca2 + transitions> 2 times,
(3) and caused a delayed and steady rise (≥ 2-fold) at baseline in Ca2 +. THI (100 nM,
5min) recruits more ATP responses, shortened ATP-mediated Ca2 + shift (≥1.4
times) and produced a delayed rise (≥ 3-fold) at Ca2 + level, mimicking Ry. THI and
Ry together produced additive effects resulting in the removal of IP3R and RyR1
signals. The CPI changed ATP-mediated secretion of IL-6, initially by improving the rate, but
suppressed general cytokine secretion in DC. The DCs are very sensitive to THI,
with one mechanism involving the release of positive and negative regulation of the Ca2 +
signals produced by RyR1
5. Sex Selective Toxicity of Thimerosal
Exp Toxicol Pathol. 2009 Mar 61 (2): 133-6. Epub 2008 Sep 3.
Branch DR, Medical and Laboratory and Pathobiology Departments, University of Toronto, Ontario, Canada
A recent report shows a correlation between the historical use of thimerosal in therapeutic immunizations with the development of autism; however, this association is controversial. Autism occurs approximately four times more often in men than in women; therefore, studies on thimerosal toxicity should take into account gender-selective effects. This study was originally done to determine the maximum tolerated dose (MTD) of thimersosal in male and female CD1 mice. However, during limited MTD studies, it appeared that thimerosal has a differential MTD that depends on whether the mouse is male or female. At doses of 38.4-76.8 mg / kg using 10% DMSO as the diluent from seven of the seven male mice, compared to the seven female mice tested, thimerosal was reset. Although the levels of thimerosal used were very high because we initially only tried to determine MTD, it was completely unexpected to notice the difference between MTD and male mice. Thus, our studies, which do not directly deal with the disputes around thimerosal and autism, and are still preliminary, as the number of mice studied was small, give the first report on sex selective toxicity of thimerosal and show that any future studies on thimerosal toxicity should take into account gender differences
. 6. Comparison of Blood and Brain Mercury Levels with Vaccines in Methylmercury or Thimerosal
Environmental Health Outlook, August 2005.
Thomas Burbacher, PhD [University of Washington].
This study clearly and unequivocally demonstrates that – mercury found in vaccines not only ends up in the brain, but leaves a double amount of inorganic mercury in methylmercury, fish like mercury. This work is groundbreaking because little is known about ethyl mercury, and many health authorities have argued that the mercury contained in vaccines is a "safe species". This study also provides a strong attack on the medical institute's 2004 recommendation that it will no longer be implemented in connection with Mercury Autism
Chapter: “The recently published IOM review (IOM 2004) seems to have abandoned its previous recommendation [of studying mercury and autism] and back to the American Pediatrics Academy of Pediatrics [of removing mercury from vaccines]. This approach is difficult to understand given the current limited knowledge of the toxicokinetics and developmental neurotoxicity of thimerosal, which is (and is) injected into millions of newborns and infants.
RELATED INFORMATION:  7. Increase in Reactive Glues in the Visual Cortex of Macaca Fascicularis following Following Long-Term Methyl Mercury Exposures
Toxicology and Applied Pharmacology, 1994
Charleston JS, Bolender RP, Mottet NK, Body RL, Vahter ME, Burbacher TM, Department of Pathology, School of medicine University of Washington
Neurons, astrocytes, reactive glia, oligodendrocytes, endothelial, and the number of charged leukocytes adult Macaca fascicularis kalsinointisuolen housing after a long-term methylmercury (MeHg) and mercuric chloride. (inorganic mercury, inches mercury) Subclinical exposure has been estimated using the optical volume fractionation histology technique. Four groups of monkeys were exposed to MeHg (50 micrograms Hg / kg body weight / day) by mouth for 6, 12, 18 and 12 months followed by 6 months without exposure (purification group). The fifth group of monkeys was given IHg (HgCl2; 200 micrograms Hg / kg body weight / day) as a constant intravenous infusion through the internal catheter for 3 months. Reactive glia increased significantly for each treatment group, increasing by 72% over 6 months, 152% for 12 months, and 120% for 18-month-old MeHg-exposed groups and the number of reactive glues. the clearance group remained high (89%). The IHg-exposed group showed an increase in the number of reactive glues by 165%. The IHg-exposed group and the purification group had low levels of MeHg in tissue; However, the IHg level was elevated in both groups. These results suggest that IHg may be responsible for an increase in reactive glia. All other cell types, including neurons, did not show a significant change in the amount at a given exposure level and duration. Discussions on the identity and effects of reactive glia cells on long-term neuronal function and survival due to changes in the glial population after subclinical long-term exposure to mercury.
8. Neurogenic activation and neuroinflammation in autism patients' brain
Annals of Neurology, February 2005.
Diana L. Vargas, MD [Johns Hopkins University].
This study was conducted independently and a different method was used as Dr. Herbert (see above) reached the same conclusion: the brain of autistic children suffers from inflammation.
Extract: “Because this neuroinflammatory process appears to be associated with a continuous and chronic mechanism of CNS dysfunction, potential therapeutic measures should focus on the management of its adverse effects and ultimately on the clinical course of autism. "
9. Autism: Brain Disorder or Brain Disorder
Clinical Neuropsychiatry, 2005
Martha R. Herbert, MD, Ph.D., Harvard University
Autism is defined as a behavioral abnormality syndrome of language, social reciprocity and hyperfunction or reduced behavioral flexibility. It is clearly heterogeneous and can involve both unusual talents and impairments, but the underlying biological and genetic basis of the unknown. Autism is modeled on a brain-based, strongly genetic disorder, but evolving observations and hypotheses support the wider model of space as genetically active and systemic. These include imaging, neuropathology, and psychological evidence of spreading (and not just specific) brain and phenotypic properties; postnatal development and chronic persistence (e.g., gastrointestinal, immune, recurrent infection) of brain, behavior and tissue changes (e.g., inflammation) and symptoms of physical illness; overlap with other disorders; and reports of rate increase and healing or recovery that support the role of modulation of the environment with environmental factors (e.g., exacerbation or triggering of toxins, infectious agents or other stressors or treatment improvement). Autism modeling extends beyond previous work, but also encourages research and care to expand intermediate regions of molecular and cellular mechanisms, as well as chronic tissue, metabolic, and somatic changes that have previously been shown to a limited number. The heterogeneous biology underlying the autism may think of approaching the autism profile through a number of mechanisms, and on the other hand, treatment and connectivity disorders can illuminate the relevant final joint pathways and promote the focus on seeking therapeutic goals in this biologically and etiologically heterogeneous behavior. syndrome.
10. Activation of methionine synthase with insulin-like growth factor-1 and dopamine: target for neurodevelopmental toxins and Thimerosal
Molecular Psychiatry, July 2004.
Richard C. Deth, PhD [Northeastern University].
how thimerosal inhibits methylation, a key factor in cellular communication and development.
“Strong inhibition of this route [methylation] with ethanol, lead, mercury, aluminum and thimerosal suggests that it may be an important target for neurodevelopmental toxins.”
11. Validating Autistic Regression with House Movies
Archive of Common Psychiatry, 2005
Emily Werner, PhD; Geraldine Dawson, PhD, University of Washington
Objective To examine an autistic regression-related parental report utilizing behavioral knowledge encoded in youngsters with autism spectrum disorder (ASD) in comparison with typical 12 and 24 month improvement.
Design Residence recordings of the first and second birthday celebrations of 56 youngsters have been collected from mother and father of ASD's young youngsters who had or had not reported regression historical past and sometimes creating nations. Youngster conduct was coded with sugars from a toddler's analysis and regression history. An older interview, which gathered info on the return of oldsters' early symptoms from delivery, additionally offered info
Regulation Members have been recruited from multidisciplinary autism analysis at a big university.
Members Fifteen youngsters with ASD regression, 21 youngsters with early-stage autism, and 20 sometimes creating youngsters and their mother and father.
Key Outcomes Measures for Baby Communicating, Social, Affective, Repetitive Behaviors and Toy Clips Encoded in Toddler Video Tapes First and Second Birthday Celebration
Evaluation of outcomes revealed that youngsters with ASD regression are comparable in widespread attention and extra frequent use of words and babble compared to typical 12-month-old youngsters. In contrast, youngsters with ASD with early onset of signs and no regression confirmed much less widespread attention and communication conduct at 12 months of age. At the age of 24 months, both ASD teams confirmed less use of phrases, noises, pronouncements, social viewing, and concentrating on than the sometimes creating 24-month-olds.
Parental interview knowledge recommend that some youngsters with regression had problem in regulatory conduct before regression occurred.
Conclusion This research confirms the existence of an early autistic regression
UPDATE: After Poling, this has grow to be a well-liked link, so I update it for extra analysis and better info so you’ll find and learn articles your self. Under is a partial record, the addition of which continues.
12. Mercury blood levels relate to the analysis of autism: Reassessment of an necessary set of knowledge
Journal of Baby Neurology, Vol. 22, No. 11, 1308-1311 (2007)
M. Catherine DeSoto, PhD, Robert T. Hitlan, Department of Psychology, College of North Iowa, Cedar Falls, Iowa
Excerpt: “We have reassessed the information originally reported by Ip et al. in 2004 and have found that the original p-value was incorrect and that there is a significant link between the blood levels of the mercury and the diagnosis of the frequency disorder of autism. In addition, hair sample analysis results provide some support for the idea that autistic individuals may be less effective and more varied in removing mercury from the blood.
The question of what leads to an apparent increase in autism is very important. As with the connection between aspirin and heart attack, a small effect can have significant health effects. If there is a connection between autism and mercury, it is absolutely essential that the first reports of the question have not misrepresented that there is no link. We have reassessed the data set originally reported by Ip et al. in 2004 and have found that the original p-value was incorrect and that there is a significant link between the blood levels of the mercury and the diagnosis of the frequency disorder of autism. In addition, the hair sample analysis results provide some support for the idea that autistic individuals may be less effective and more varied in removing mercury from the blood.
13. Development of Regression and Mitochondrial Dysfunction in Autism
Journal of Child Neurology / Volume 21, Issue 2, February 2006
Jon S. Poling, MD, PhD, Neurology and Neurosurgery Department
Johns Hopkins Hospital  It appears that 38% of the patients with Kennedy Krieger Institute autism had one sign of impaired oxidative phosphorylation (mitochondrial dysfunction), and 47% had another marker.
Extract: “Children with (mitochondrial-related) dysfunctional cellular energy metabolism may be more prone to exposure to autistic regression at the age of 18-30 months if they also have infections or immunizations at the same time. "
14. Oxidative stress in autism: elevated levels of 3-nitrotyrosine in the brain
Elizabeth M. Sajdel-Sulkowska, – Department of Psychiatry, Harvard Medical School  Looks Possible the connection between the mercury and the young brain of autism. The sign of oxidative stress in the autistic brain problem was 68.9% higher than the controls (statistically significant result), while the mercury content was 68.2% higher.
Example: Preliminary data suggest that oxidative stress, its relationship to environmental factors, and its possible antioxidant attenuation in autism. "
15. The Big Brain of Autism: The Challenge of General Anxiety
Neuroscientist, Part 11, Issue 5, 2005.
Martha Herbert, MD, Doctor of Harvard University
This research helps to reverse the idea that autistic brain brain children are simply wired in different ways way, and states that "neuroinflammation appears to be present in autistic brain tissue from childhood to adulthood." Dr. Herbert suggests that chronic illness or an external environmental source (such as heavy metals) can cause inflammation.
Excerpt: "Oxidative stress, inflammation of the brain and microgliosis have been documented much in the context of toxic exposures, including various heavy metals … awareness that brain and autistic diseases in children may be due to chronic biomedical abnormalities such as inflammation, the possibility of relevant biomedical interventions opens up. may be well ahead of the child's maximal sensitivity window as it is now assumed that all deficits are due to fixed early developmental changes in nervous architecture, is now weakened.
The most repeated observation of the neuroanatomy of autism – a tendency to abnormally large brains – has been shown to be paradoxical in relation to the specificity of the abnormalities in the three behavioral regions that determine autism. We now know a lot of things about this phenomenon, including the brain of autism growing rapidly after birth, and then slowly growing in a few short years that only younger but not older brains are larger in autism than in control that the White substance disproportionately affects this volume growth and non- a formal pattern referring to postnatal pathology, that functional connectivity in autistic brain regions is reduced and that neuroinflammation (including microgliosis and astroglioosis) appears to be present in autistic brain tissue from childhood to adulthood. In addition to these permissive brain tissues and functional abnormalities, there are theories of general or widespread neural data processing or signal co-ordination abnormalities (such as weak central sensitivity, impaired complex processing, and sub-connectivity) allegedly supporting specific observable behavioral characteristics. autism. Tämä havaintojen ja mallien lähentyminen viittaa siihen, että autismin funktiona ja patofysiologiassa on otettava huomioon järjestelmien ja kroonisten tautien perustuva uudelleenformulointi, ja se avaa mahdollisuuden uusiin hoitotavoitteisiin.
16. Todisteet myrkyllisyydestä, oksidatiivisesta stressistä ja neuronaalisesta loukkauksesta autismissa
Journal of Toxicology and Environmental Health, marras-joulukuu 2006.
Janet Kern, Anne Jones, Psykiatrian laitos, University of Texas Southwestern Medical Center Dallasissa, Dallasissa
”Tässä artikkelissa käsitellään todisteita siitä, että jotkut autistiset lapset voivat tulla autistisiksi hermosolujen kuolemasta tai aivovauriosta joskus synnytyksen jälkeen syntymän seurauksena; ja käsittelee hypoteeseja, että toksisuus ja oksidatiivinen stressi voivat olla syynä hermosolujen loukkaamiseen autismissa… artikkelissa käsitellään sitä, mikä voi tapahtua kehityskulun aikana, ja monista tekijöistä, jotka saattavat olla vuorovaikutuksessa ja jotka tekevät näistä lapsista alttiimpia myrkyllisyydelle, oksidatiiviselle stressille, ja neuronaalinen loukkaus. ”
Autismin Amerikan yhdistyksen mukaan autismia pidetään nyt epidemiana. Epidemiologisten tutkimusten ja hallituksen raporttien osoittaman autismin määrän kasvu merkitsee ulkoisten tai ympäristötekijöiden merkitystä, jotka saattavat muuttua. Tässä artikkelissa käsitellään todisteita siitä, että jotkut autistiset lapset voivat tulla autistisiksi hermosolujen kuolemasta tai aivovauriosta joskus synnytyksen jälkeen syntymän seurauksena; ja käsittelee hypoteeseja, että toksisuus ja oksidatiivinen stressi voivat olla syynä hermosolujen loukkaamiseen autismissa. Artikkelissa kuvataan ensin
autismissa, Purkinjen solujen fysiologiassa ja haavoittuvuudessa havaittu Purkinjen solujen menetys ja todisteet postnataalisten solujen häviämisestä. Toiseksi artikkelissa kuvataan autismin lisääntynyttä aivojen määrää ja sitä, miten se voi liittyä Purkinjen solujen häviöön. Third, the proof for toxicity and oxidative
stress is covered and the potential involvement of glutathione is mentioned. Lastly, the article discusses what may be occurring over the course of improvement and the multiple elements which will interaction and make these youngsters more weak to toxicity, oxidative stress, and neuronal insult.
17. Oxidative Stress in Autism
Abha Chauhan, Ved Chauhan
This research supplies a useful overview of the rising evidence supporting the link between oxidative stress and autism.
Excerpt: “Upon completion of this article, participants should be able to: 1. Be aware of laboratory and clinical evidence of greater oxidative stress in autism. 2. Understand how gut, brain, nutritional, and toxic status in autism are consistent with greater oxidative stress. 3. Describe how anti-oxidant nutrients are used in the contemporary treatment of autism.”
18. Thimerosal Neurotoxicity is Associated with Glutathione Depletion: Protection with Glutathione Precursors
Neurotoxicology, Jan 2005.
S. Jill James, PhD [University of Arkansas].
This current research demonstrates that Thimerosal lowers or inhibits the body’s potential to supply Glutathione, an antioxidant and the body’s main cellular-level defense towards mercury.
Excerpt: “Thimerosal-induced cytotoxicity was associated with depletion of intracellular Glutathione in both cell lines…The potential effect of Glutathione or N-acetylcysteine against mercury toxicity warrants further research as possible adjunct therapy to individuals still receiving Thimerosal-containing vaccines.”
Neuromolecular Drugs, 2007
Christopher Shaw, Ph.D. [Department of Ophthalmology and Program in Neuroscience, University of British Columbia, Vancouver, British Columbia, Canada]
This research demonstrates the extreme toxicity of the aluminum adjuvant used as a preservative in vaccines.
Excerpt: “testing showed motor deficits in the aluminum treatment group that expressed as a progressive decrease in strength measured…Significant cognitive deficits in water-maze learning were observed in the combined aluminum and squalene group…Apoptotic neurons were identified in aluminum-injected animals that showed significantly increased activated caspase-3 labeling in lumbar spinal cord (255%) and primary motor cortex (192%) compared with the controls. Aluminum-treated groups also showed significant motor neuron loss (35%) and increased numbers of astrocytes (350%) in the lumbar spinal cord.
20. Environmental mercury release, special education rates, and autism disorder: an ecological study of Texa
Health & Place, 2006
Raymond F. Palmer, University of Texas Health Science Center
This study demonstrated the correlation between environmental mercury and autism rates in Texas.
Excerpt: “On average, for each 1,000 lb of environmentally released mercury, there was a 43% increase in the rate of special education services and a 61% increase in the rate of autism. The association between environmentally released mercury and special education rates were fully mediated by increased autism rates. This ecological study suggests the need for further research regarding the association between environmentally released mercury and developmental disorders such as autism.”
21. Autism Spectrum Issues in Relation to Distribution of Hazardous Air Pollutants in the SF Bay Area
Environmental Health Views – Vol. 114 No. 9, September, 2006
Gayle Windham, Div. of Environmental and Occupational Illness Management, California Department of Well being Providers
284 ASD youngsters & 657 controls, born in 1994 in Bay Area, have been assigned exposure levels by delivery tract for 19 chemical compounds. Dangers for autism have been elevated by 50% in tracts with the highest chlorinated solvents and heavy metals. The very best danger compounds have been mercury, cadmium, nickel, trichloroethylene, and vinyl chloride, and the danger from heavy metals was virtually twice as excessive as solvents.
Excerpt: “Our results suggest a potential association between autism and estimated metal concentrations, and possibly solvents, in ambient air around the birth residence.”
22. A Case Collection of Youngsters with Apparent Mercury Toxic Encephalopathies Manifesting with Medical Signs of Regressive Autistic Dysfunction
Journal of Toxicology and Environmental Well being, 2007
David A. Geier, Mark R. Geier
This research reviewed the case histories and medical profiles of 9 autistic youngsters and concluded that eight of the 9 youngsters have been mercury toxic and this toxicity manifested itself in a fashion in line with Autism Spectrum Issues.
Excerpt: “…these previously normally developing children suffered mercury toxic encephalopathies that manifested with clinical symptoms consistent with regressive ASDs. Evidence for mercury intoxication should be considered in the differential diagnosis as contributing to some regressive ASDs.”
Impairments in social relatedness and communication, repetitive behaviors, and stereotypic abnormal motion patterns characterize autism spectrum issues (ASDs). It’s clear that whereas genetic elements are essential to the pathogenesis of ASDs, mercury exposure can induce immune, sensory, neurological, motor, and behavioral dysfunctions just like traits defining or related to ASDs. The Institutional Assessment Board of the Institute for Continual Sicknesses (Workplace for Human Research Protections, U.S. Department of Health and Human Providers, IRB quantity IRB00005375) accepted the present research. A case collection of 9 sufferers who introduced to the Genetic Centers of America for a genetic/developmental analysis are mentioned. Eight of nine patients (one affected person was found to have an ASD resulting from Rett’s syndrome) (a) had regressive ASDs; (b) had elevated ranges of androgens; (c) excreted vital quantities of mercury submit chelation challenge; (d) had biochemical evidence of decreased perform in their glutathione pathways; (e) had no recognized vital mercury exposure besides from Thimerosal- containing vaccines/Rho(D)-immune globulin preparations; and (f) had alternate causes for their regressive ASDs ruled out. There was a big dose-response relationship between the severity of the regressive ASDs observed and the complete mercury dose youngsters acquired from Thimerosal-containing vaccines/Rho (D)- immune globulin preparations. Based mostly upon differential diagnoses, 8 of 9 sufferers examined have been exposed to vital mercury from Thimerosal-containing biologic/vaccine preparations throughout their fetal/infant developmental durations, and subsequently, between 12 and 24 mo of age, these beforehand normally creating youngsters suffered mercury toxic encephalopathies that manifested with medical signs in line with regressive ASDs. Proof for mercury intoxication ought to be thought-about in the differential analysis as contributing to some regressive ASDs.
23. Consideration-deficit hyperactivity disorder and blood mercury degree: a case-control research in chinese language youngsters
Neuropediatrics, August 2006 – P.R. Kong [Department of Pediatrics and Adolescent Medicine, The University of Hong Kong].
This research demonstrates that blood mercury levels are greater for youngsters with ADHD.
Excerpt: “There was significant difference in blood mercury levels between cases and controls, which persists after adjustment for age, gender and parental occupational status. The geometric mean blood mercury level was also significantly higher in children with inattentive and combined subtypes of ADHD. High blood mercury level was associated with ADHD. Whether the relationship is causal requires further studies.”
24. The Changing Prevalence of Autism In California
Journal of Autism and Developmental Issues, April 2003
Mark F. Blaxill, David S. Baskin, and Walter O. Spitzer
This research helps to refute the supposition made by some researchers that autism’s epidemic might solely be on account of “diagnostic substitution”.
Excerpt: “They have suggested that ‘diagnostic substitution’ accounts for an apparent increase in the incidence of autism in California that is not real. This hypothesized substitution is not supported by proper and detailed analyses of the California data.”
25. Mitochondrial Power-Deficient Endophenotype in Autism
American Journal of Biochemistry and Biotechnology 4 (2): 198-207, 2008
J. Jay Gargus and Faiqa Imtiaz
Division of Physiology and Biophysics and Department of Pediatrics, Section of Human Genetics, Faculty of Drugs, College of California, Irvine, Arabian Diagnostics Laboratory, King Faisal Specialist Hospital and Research Centre
While proof points to a multigenic etiology of most autism, the pathophysiology of the disorder has yet to be outlined and the underlying genes and biochemical pathways they subserve remain unknown. Autism is taken into account to be influenced by a mixture of varied genetic, environmental and immunological elements; extra lately, proof has steered that elevated vulnerability to oxidative stress could also be concerned in the etiology of this multifactorial disorder. Moreover, current studies have pointed to a subset of autism related to the biochemical endophenotype of mitochondrial power deficiency, recognized as a delicate impairment in fat and carbohydrate oxidation. This phenotype is analogous, however extra delicate than these seen in basic mitochondrial defects. In some instances the beginnings of the genetic underpinnings of those mitochondrial defects are emerging, comparable to delicate mitochondrial dysfunction and secondary carnitine deficiency noticed in the subset of autistic sufferers with an inverted duplication of chromosome 15q11-q13. As well as, rare instances of familial autism associated with sudden toddler dying syndrome (SIDS) or associated with abnormalities in mobile calcium homeostasis, corresponding to malignant hyperthermia or cardiac arrhythmia, are beginning to emerge. Such special instances recommend that the pathophysiology of autism might comprise pathways which might be immediately or not directly involved in mitochondrial power production and to additional probe this connection three new avenues appear worthy of exploration: 1) metabolomic medical studies scary managed cardio train stress to increase the biochemical phenotype, 2) high-throughput expression arrays to instantly survey exercise of the genes underlying these biochemical pathways and Three) model techniques, either based mostly upon neuronal stem cells or model genetic organisms, to find novel genetic and environmental inputs into these pathways
26. Bridging from Cells to Cognition in Autism Pathophysiology: Biological
Pathways to Defective Mind Perform and Plasticity
American Journal of Biochemistry and Biotechnology four (2): 167-176, 2008
Matthew P. Anderson, Brian S. Hooker and Martha R. Herbert
Departments of Neurology and Pathology, Harvard Medical Faculty/Beth Israel Deaconess Medical Middle, Harvard Institutes of Drugs, Excessive Throughput Biology Group, Elementary Science Directorate, Pacific Northwest National Laboratory, Pediatric Neurology/Middle for Morphometric Analysis, Massachusetts Basic Hospital/Harvard Medical Faculty, and Middle for Youngster and Adolescent Improvement, Cambridge Well being Alliance/Harvard Medical Faculty
Abstract: We evaluation evidence to help a mannequin where the disease process underlying autism might begin when an in utero or early postnatal environmental, infectious, seizure, or autoimmune insult triggers an immune response that increases reactive oxygen speci es (ROS) production in the brain that leads to DNA injury (nuclear and mitochondrial) and metabolic enzyme blockade and that these inflammatory and oxidative stressors persist past early improvement (with potential further exacerbations), producing ongoing practical consequences. In organs with a high metabolic demand resembling the central nervous system, the continued use of mitochondria with broken DNA and impaired metabolic enzyme perform might generate further ROS which can cause persistent activation of the innate immune system resulting in extra ROS production. Such a mechanism would self-sustain and probably progressively worsen. The mitochondrial dysfunction and altered redox signal transduction pathways found in autism would conspire to activate each astroglia and microglia. These activated cells can then provoke a broad-spectrum proinflammatory gene response. Past the direct effects of ROS on neuronal perform, receptors on neurons that bind the inflammatory mediators might serve to inhibit neuronal signaling to guard them from excitotoxic injury throughout numerous pathologic
insults (e.g., an infection). In autism, over-zealous neuroinflammatory responses couldn’t solely affect neural developmental processes, but might more considerably impair neural signaling involved in cognition in an ongoing trend. This model makes specific predictions in patients and experimental animal fashions and suggests quite a lot of targets sites of intervention. Our mannequin of probably reversible pathophysiological mechanisms in autism motivates our hope that effective therapies might quickly appear on the horizon.
27. Heavy-Metallic Toxicity—With Emphasis on Mercury
John Neustadt, ND, and Steve Pieczenik, MD, PhD
Conclusion: Metals are ubiquitous in our surroundings, and publicity to them is inevitable. Nevertheless, not all individuals accumulate toxic ranges of metals or exhibit signs of metallic toxicity, suggesting that genetics play a task in their potential to wreck well being. Metallic toxicity creates multisystem dysfunction, which seems to be mediated primarily by means of mitochondrial injury from glutathione depletion.
Accurate screening can improve the probability that sufferers with potential metallic toxicity are recognized. Probably the most accurate screening technique for assessing chronic-metals exposure and metals load in the physique is a provoked urine check.
28. Proof of Mitochondrial Dysfunction in Autism and Implications for Remedy
American Journal of Biochemistry and Biotechnology 4 (2): 208-217, 2008
Daniel A. Rossignol, J. Jeffrey Bradstreet, Worldwide Youngster Improvement Resource Middle,
Abstract: Classical mitochondrial illnesses happen in a subset of individuals with autism and are often brought on by genetic anomalies or mitochondrial respiratory pathway deficits. Nevertheless, in many instances of autism, there’s proof of mitochondrial dysfunction (MtD) without the basic features associated with mitochondrial disease. MtD seems to be more widespread in autism and presents with less extreme indicators and symptoms. It isn’t associated with discernable mitochondrial pathology in muscle biopsy specimens despite goal proof of lowered mitochondrial functioning. Exposure to environmental toxins is the doubtless etiology for MtD in autism. This dysfunction then contributes to quite a few diagnostic signs and comorbidities observed in autism together with: cognitive impairment, language deficits, irregular power metabolism, persistent gastrointestinal problems, abnormalities in fatty acid oxidation, and elevated oxidative stress. MtD and oxidative stress may clarify the high male to female ratio present in autism resulting from elevated male vulnerability to those dysfunctions.
Biomarkers for mitochondrial dysfunction have been recognized, however appear extensively under-utilized regardless of obtainable therapeutic interventions. Nutritional supplementation to decrease oxidative stress together with elements to enhance decreased glutathione, in addition to hyperbaric oxygen remedy (HBOT) characterize supported and rationale approaches. The underlying pathophysiology and autistic signs of affected individuals can be anticipated to both improve or stop worsening once efficient remedy for MtD is carried out.
29. Proximity to point sources of environmental mercury launch as a predictor of autism prevalence
Health & Place, 2008
Raymond F. Palmer, Stephen Blanchard, Robert Wooden
University of Texas Well being Science Middle, San Antonio Department of Household and Group Drugs, Our Woman of the Lake College, San Antonio Texas, Chair, Department of Sociology
This research ought to be seen as hypothesis-generating – a primary step in analyzing the potential position of environmental mercury and childhood developmental issues. Nothing is understood about specific exposure routes, dosage, timing, and individual susceptibility. We suspect that persistent low-dose exposures to varied environmental toxicants, including mercury, that occur during crucial home windows of neural improvement amongst genetically vulnerable youngsters (with a diminished capability for metabolizing amassed toxicants) might improve the danger for developmental issues resembling autism. Efficiently identifying the particular mixture of environmental exposures and genetic susceptibilities can inform the improvement of targeted prevention intervention methods.
30. Epidemiology of autism spectrum disorder in Portugal: prevalence, medical characterization, and medical circumstances
Developmental Drugs & Baby Neurology, 2007
Guiomar Oliveira MD PhD, Centro de Desenvolvimento da Criança, Hospital Pediátrico de Coimbra; Assunção Ataíde BSc, Direcção Regional de Educação do Centro Coimbra;
Carla Marques MSc, Centro de Desenvolvimento da Criança, Hospital Pediátrico de Coimbra; Teresa S Miguel BSc, Direcção Regional de Educação do Centro, Coimbra;
Ana Margarida Coutinho BSc, Instituto Gulbenkian de Ciência, Oeiras; Luísa Mota-Vieira PhD, Unidade de Genética e Patologia moleculares, Hospital do Divino Espírito Santo, Ponta Delgada, Açores; Esmeralda Gonçalves PhD; Nazaré Mendes Lopes PhD, Faculdade de Ciências e Tecnologia, Universidade de Coimbra; Vitor Rodrigues MD PhD; Henrique Carmona da Mota MD PhD, Faculdade de Medicina, Universidade de Coimbra, Coimbra; Astrid Moura Vicente PhD, Instituto Gulbenkian de Ciência, Oeiras, Portugal.
*Correspondence to first writer at Hospital Pediátrico de Coimbra, Av Bissaya Barreto, 3000-Zero76 Coimbra, Portugal. E-mail: [email protected]
Summary: The objective of this research was to estimate the prevalence of autistic spectrum disorder (ASD) and determine its medical characterization, and medical circumstances in a paediatric inhabitants in Portugal. A faculty survey was carried out in elementary faculties, concentrating on 332 808 school-aged youngsters in the mainland and 10 910 in the Azores islands. Referred youngsters have been instantly assessed using the Diagnostic and Statistical Guide of Mental Issues (4th edn), the Autism Diagnostic Interview–Revised, and the Childhood Autism Score Scale. Medical history and a laboratory investigation was performed. In parallel, a systematic multi-source search of youngsters recognized to have autism was carried out in a restricted region. The global prevalence of ASD per 10 000 was 9.2 in mainland, and 15.6 in the Azores, with intriguing regional differences. A variety of related medical circumstances was documented in 20%, with an unexpectedly high fee of mitochondrial respiratory chain issues.
Unique Source: Lisa Joyce Goes – Facebook Notes
*Article originally appeared in Well being Influence News. Reprinted with permission.
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