A Case Control Study of Mercury Burden In Children With Autistic Spectrum Disorders
Doctors found that autistic patients had high levels of mercury in their blood, and high levels of mercury extreted in their urine after chelation therapy (the removal of heavy metals from the body).
‘This study shows a strong association between increased
urinary mercury concentrations following three days of treatment
with DMSA and the presence of an autistic spectrum disorder. The
statistically significant association persists when vaccinated cases
are compared with matched vaccinated controls.’
They also concluded a direct relationship between mercury in childhood vaccines and autistic disorder.
‘Moreover, our findings appear to confirm previously published
epidemiologic evidence showing a direct association between
increasing mercury from thimerosal-containing childhood
vaccines and neurodevelopment disorders in children. These
studies showed that there was a two to sixfold, statistically
significant increased incidence of neurodevelopment disorders
following an additional 75-100 mcg dosage of mercury from
thimerosal-containing childhood vaccines in comparison to thimerosal-free childhood vaccines.’
(Journal of American Physicians and Surgeons Volume 8 Number 3 Fall 2003).
To see the full study, and other studies relating to mercury and vaccines, please see the website:
and go to the Mercury In Vaccines page.
It’s an website run by a dental nurse who was poisoned after working with mercury in the surgery.
Here is a study in the Lancet, showing that autism and ADD disorders have increased dramatically in recent years and they have admitted they don’t know why:
Recent reports have suggested that the prevalence of autism and related spectrum disorders (ASDs) is substantially higher than previously recognised. We sought to quantify prevalence of ASDs in children in South Thames, UK. METHODS: Within a total population cohort of 56 946 children aged 9-10 years, we screened all those with a current clinical diagnosis of ASD (n=255) or those judged to be at risk for being an undetected case (n=1515). A stratified subsample (n=255) received a comprehensive diagnostic assessment, including standardised clinical observation, and parent interview assessments of autistic symptoms, language, and intelligence quotient (IQ). Clinical consensus diagnoses of childhood autism and other ASDs were derived. We used a sample weighting procedure to estimate prevalence. FINDINGS: The prevalence of childhood autism was 38.9 per 10,000 (95% CI 29.9-47.8) and that of other ASDs was 77.2 per 10,000 (52.1-102.3), making the total prevalence of all ASDs 116.1 per 10,000 (90.4-141.8). A narrower definition of childhood autism, which combined clinical consensus with instrument criteria for past and current presentation, provided a prevalence of 24.8 per 10,000 (17.6-32.0). The rate of previous local identification was lowest for children of less educated parents. INTERPRETATION: Prevalence of autism and related ASDs is substantially greater than previously recognised. Whether the increase is due to better ascertainment, broadening diagnostic criteria, or increased incidence is unclear. Services in health, education, and social care will need to recognise the needs of children with some form of ASD, who constitute 1% of the child population.
Source: Lancet. 2006 Jul 15;368(9531):210-5.
These startling figures amount to:
1 in 84 children is autistic
1 in 54 boys is autistic
1 in 215 girls is autistic
Every day, 19 British children develop autism.
Elevated Immune Response In The Brain Of Autistic Patients
This study determined immune activities in the brain of ASD patients and matched normal subjects by examining cytokines in the brain tissue.
Conclusion: ASD patients displayed an increased innate and adaptive immune response through the Th1 pathway, suggesting that localized brain inflammation and autoimmune disorder may be involved in the pathogenesis of ASD.
Source: J Neuroimmunol. 2009 Jan 19.
VAN UK’s Comment: Autistics showing an auto-immune response points away from the genetic argument put forward by pro-vaccinator’s.
Auto Anti-Bodies Found In Egyptian Autistic Children, Pointing To An Auto-Immune Malfunction As The Cause
Autism may involve an autoimmune pathogenesis in a subgroup of patients. The frequency of anti-nuclear antibodies in 80 autistic children and their relationship to a family history of autoimmunity were studied, compared with 80 healthy, matched children. Children with autism had a significantly higher percent seropositivity of anti-nuclear antibodies (20%) than healthy children (2.5%; P < 0.01). Fifty percent of anti-nuclear antibody-seropositive autistic children had an anti-nuclear antibody titer of ≥1:640 (very high positive); 25%, ≥1:160 (high positive); and the remaining 25%, 1:80. All anti-nuclear antibody-seropositive healthy children had anti-nuclear antibody titers of 1:80. A family history of autoimmunity was significantly higher in autistic children (47.5%) than healthy controls (8.8%; P < 0.001). Anti-nuclear antibody seropositivity was significantly higher in autistic children with a family history of autoimmunity than those without such history (36.8% and 5%, respectively; P < 0.001). Anti-nuclear antibody seropositivity had significant positive associations with disease severity, mental retardation and electroencephalogram abnormalities. Autoimmunity may play a role in a subgroup of children with autism. Further studies are warranted to assess anti-nuclear antibody seropositivity, other markers of autoimmunity (e.g., brain-specific autoantibodies), and the role of immunotherapy in children with autism.
Source: doi:10.1016/j.pediatrneurol.2008.10.017.
Neurodevelopmental Disorders After Thimerosal Containing Vaccines
This study represents the first epidemiological evidence based on tens of millions of doses of vaccine administered in the US, that associates increasing thimerosal from vaccines with neurodevelopmental disorders. Specifically, an analysis of the Vaccine Adverse Event Reporting System database showed statistical increases in the incidence rate of autism, mental retardation and speech disorders after thimerosal containing DTaP vaccines in comparison with thimerosal-free DTaP vaccines.
The male/female ratio indicated that autism (17) and speech disorders (2.3) were reported more in males than females after thimerosal containing DTaP, whereas mental retardation (1.2) was more evenly reported among male and female recipients.
Acute control adverse reactions such as death, vasculitis, seizures, ED visits, gastroenteritis and total adverse reactions were reported similarly after thimerosal and thimerosal free DTaP vaccines. An association between neurodevelopmental disorders and thimerosal containing DTaP vaccines was found.
Source: The Genetic Centers of America, http://mercury-freedrugs.org/docs/NeurodevelopmentalDisordersAfterThimerosal-ContainingVaccines-A%20Brief%20Communication.pdf
AUTISM LISTED AS A SIDE-EFFECT IN DTAP VACCINE LEAFLET!
A Tripedia DTAP manufacturer’s vaccine leaflet listed autism as a side-effect.
On page 11 of the document, it says:
‘Adverse events reported during post-approval use of Tripedia vaccine include idiopathic thrombocytopenic purpura, SIDS, anaphalactic reaction, cellulitis, AUTISM, grand-mal convulsion, encephalopathy, hypotonia, neuropathy, somnolence and apnea.’
See: http://www.vaccineshoppe.com/image.cfm?doc_id=5966&image_type=product_pdf
Study Finds Autism Affects 157 children per 10,000 – or 1 in 66
Prevalence of autism-spectrum conditions: UK school-based population study
Simon Baron-Cohen, BA (Hons), PhD, FBPsS, MPhil (Clinical Psychology)*, Fiona J. Scott, BSc (Hons), PhD, C. Psychol* and Carrie Allison, BA (Hons)*
Autism Research Centre, Department of Psychiatry, Cambridge University
Joanna Williams, BA (Hons), MPhil, PhD
Department of Public Health and Primary Care, Institute of Public Health, Cambridge University
Patrick Bolton, MA, BSc, MBBS, PhD, FRCPsych
Autism Research Centre, Department of Psychiatry, Cambridge University
Fiona E. Matthews, MRC
Biostatistics Unit, Institute of Public Health, Cambridge University
Carol Brayne, MSc, MD, FRCP, FFPHM
Department of Public Health and Primary Care, Institute of Public Health, Cambridge University, UK
Correspondence: Simon Baron–Cohen, University of Cambridge, Autism Research Centre, Department of Psychiatry, Douglas House, 18b Trumpington Road, Cambridge CB2 8AH, UK. Email: sb205@cam.ac.uk
Declaration of interest
F.J.S acted as an expert witness for the diagnosis of autism-spectrum conditions and for the measles, mumps and rubella vaccine litigation, but not for children in the population covered by this study.
Funding
This study was funded by the Shirley Foundation. S.B-C., F.J.M. and J.W. were funded by the Medical Research Council during the period of this work. P.B. was supported by the UK NIHR Biomedical Research Centre for Mental Health at the Institute of Psychiatry, King’s College London, and the South London and Maudsley NHS Foundation Trust.
* These authors contributed equally to the work.
Background
Recent reports estimate the prevalence of autism-spectrum conditions in the UK to be 1%.
Aims
To use different methods to estimate the prevalence of autism-spectrum conditions, including previously undiagnosed cases, in Cambridgeshire.
Method
We carried out a survey of autism-spectrum conditions using the Special Educational Needs (SEN) register. A diagnosis survey was distributed to participating schools to be handed out to parents of all children aged 5–9 years. The mainstream primary school population was screened for unknown cases.
Results
The prevalence estimates generated from the SEN register and diagnosis survey were 94 per 10 000 and 99 per 10 000 respectively. A total of 11 children received a research diagnosis of an autism-spectrum condition following screening and assessment. The ratio of known:unknown cases is about 3:2 (following statistical weighting procedures). Taken together, we estimate the prevalence to be 157 per 10 000, including previously undiagnosed cases.
Conclusions
This study has implications for planning diagnostic, social and health services.
Source:
The British Journal of Psychiatry (2009) 194: 500-509. doi: 10.1192/bjp.bp.108.059345
Even Tiny Injections of Thimerosal Can Cause Autism
Thimerosal, an ethyl mercury compound, is used worldwide as a vaccine preservative. We previously observed that the mercury concentration in mouse brains did not increase with the clinical dose of thimerosal injection, but the concentration increased in the brain after the injection of thimerosal with lipopolysaccharide, even if a low dose of thimerosal was administered. Thimerosal may penetrate the brain, but is undetectable when a clinical dose of thimerosal is injected;
In conclusion, MT-1 and MT-3 mRNAs but not MT-2 mRNA are easily expressed in the cerebellum rather than in the cerebrum by the injection of low-dose thimerosal. It is thought that the cerebellum is a sensitive organ against thimerosal. As a result of the present findings, in combination with the brain pathology observed in patients diagnosed with autism, the present study helps to support the possible biological plausibility for how low-dose exposure to mercury from thimerosal-containing vaccines may be associated with autism.
Source: Induction of metallothionein in mouse cerebellum and cerebrum with low-dose thimerosal injection, Cell Biology and Toxicology, 0742-2091 (Print) 1573-6822 (Online), 9 April 2009.
1976 Study Showing Smallpox Vaccine Causes Autism!
[Autistic syndrome (Kanner) and vaccination against smallpox (author’s
transl)]
[Article in German]
Eggers C.
3-4 weeks following an otherwise uncomplicated first vaccination against
smallpox a boy, then aged 15 months and last seen at the age of 5 1/2 years,
gradually developed a complete Kanner syndrome. The question whether
vaccination and early infantile autism might be connected is being
discussed. A causal relationship is considered extremely unlikely. But
vaccination is recognized as having a starter function for the onset of
autism.
PMID: 944354
Source: Klin Padiatr. 1976 Mar;188(2):172- 80
Mitochondrial dysfunction, impaired oxidative-reduction activity, degeneration, and death in human neuronal and fetal cells induced by low-level exposure to thimerosal and other metal compounds
Thimerosal (ethylmercurithiosalicylic acid), an ethylmercury (EtHg)-releasing compound (49.55% mercury (Hg)), was used in a range of medical products for more than 70 years. Of particular recent concern, routine administering of Thimerosal-containing biologics/childhood vaccines have become significant sources of Hg exposure for some fetuses/infants. This study was undertaken to investigate cellular damage among in vitro human neuronal (SH-SY-5Y neuroblastoma and 1321N1 astrocytoma) and fetal (nontransformed) model systems using cell vitality assays and microscope-based digital image capture techniques to assess potential damage induced by Thimerosal and other metal compounds (aluminum (Al) sulfate, lead (Pb)(II) acetate, methylmercury (MeHg) hydroxide, and mercury (Hg)(II) chloride) where the cation was reported to exert adverse effects on developing cells. Thimerosal-associated cellular damage was also evaluated for similarity to pathophysiological findings observed in patients diagnosed with autistic disorders (ADs). Thimerosal-induced cellular damage as evidenced by concentration- and time-dependent mitochondrial damage, reduced oxidative-reduction activity, cellular degeneration, and cell death in the in vitro human neuronal and fetal model systems studied. Thimerosal at low nanomolar (nM) concentrations induced significant cellular toxicity in human neuronal and fetal cells. Thimerosal-induced cytoxicity is similar to that observed in AD pathophysiologic studies. Thimerosal was found to be significantly more toxic than the other metal compounds examined. Future studies need to be conducted to evaluate additional mechanisms underlying Thimerosal-induced cellular damage and assess potential co-exposures to other compounds that may increase or decrease Thimerosal-mediated toxicity.
Source: Toxicological & Environmental Chemistry, Volume 91, Issue 4 June 2009 , pages 735 – 749
State legislations that limit the use of thimerosal in vaccines for pregnant women and their infants
Thimerosal is a mercurial preservative that was widely used in vaccines in the United States and Europe until 2001. By 1999, expanding recommendations for infant vaccinations indicated that United States children who received a complete series of vaccines that contained thimerosal received up to 187.5 μg of ethyl mercury during the first six months of life. This cumulative exposure could exceed the United States Environmental Protection Agency’s recommended safe intake level, estimated in 1997, to be no more than 0.1 μg of mercury per kilogram of body weight per day. This observation lead to a recommendation by the American Academy of Pediatrics that thimerosal is removed to all vaccines that are administered to infants in the United States. Realizing the potential dangers of thimerosal in vaccines, six states have enacted legislations that have limited the amount of thimerosal that can be used in vaccines in their States (Iowa, California, New York, Missouri, Delaware and Washington). In 1987, Congress established the Vaccine Injury Compensation Program to provide compensation to family of individuals who suffer injuries from vaccines. Until recently, these judgments have been paid only to families of non-autistic children who received complications due to the vaccines. In 2008, the Government conceded its first vaccine-autism case in Federal Court. Scientific studies of this autistic child suggested that the autism was related to a mitochondrial disorder. The Federal Government should enact legislation that prohibits the use of thimerosal in vaccines given to pregnant women and their infants.
Sources: Journal of Pediatric Infectious Diseases, Volume 4, Number 3 / 2009.
VAN UK’S Comment: Why are they discussing legislation to protect babies when they introduced a flu shot for infants at that time and the new swine flu jab has thimerosal in it?
Universal new-born Hepatitis B immunization was recommended in 1991; however, safety
findings are mixed. The Vaccine Safety Datalink Workgroup reported no association between hepatitis B vaccination at birth and febrile episodes or neurological adverse
events. Other studies found positive hepatitis B vaccination and ear infection, pharyngitis, and
chronic arthritis; as well as receipt of early intervention/special education services (EIS); in probability samples of U.S. children. Children with autistic spectrum disorder(ASD) comprise a growing caseload for EIS. We evaluated
the association between hepatitis B vaccination of male neonates and parental report of ASD.
METHODS: This cross-sectional study used U.S. probability samples obtained from National Health Interview Survey 1997–2002 datasets. Logistic regression modeling was used to estimate the effect of neonatal hepatitis B vaccination on
ASDrisk amongboys age 3–17 years with shot records, adjusted for race, maternal education, and two-parent household.
RESULTS:Boys who received the hepatitis B vaccine during the first month of life had 2.94 greater odds for ASD (nZ31 of 7,486; OR Z 2.94; p Z 0.03; 95% CI Z 1.10, 7.90)compared to later- or unvaccinated boys.Non-Hispanic white
boys were 61% less likely to have ASD(ORZ0.39; pZ0.04;95% CIZ0.16, 0.94) relative to non-white boys.
CONCLUSION: Findings suggest that U.S. male neonates vaccinated with hepatitis B vaccine had a 3-fold greater risk of ASD; risk was greatest for non-white boys.
Source: Annals of Epidemiology, vol.19, no. 9, September 2009: 651-680.
Rise in Autism is REAL!
For the 2006 surveillance year, 2,757 (0.9%) of 307,790 children aged 8 years residing in the 11 ADDM sites were identified as having an ASD, indicating an overall average prevalence of 9.0 per 1,000 population (95% confidence interval [CI] = 8.6–9.3). ASD prevalence per 1,000 children aged 8 years ranged from 4.2 in Florida to 12.1 in Arizona and Missouri, with prevalence for the majority of sites ranging between 7.6 and 10.4. For 2006, ASD prevalence was significantly lower in Florida (p<0.001) and Alabama (p<0.05) and higher in Arizona and Missouri (p<0.05) than in all other sites. The ratio of males to females ranged from 3.2:1 in Alabama to 7.6:1 in Florida. ASD prevalence varied by type of ascertainment source, with higher average prevalence in sites with access to health and education records (10.0) compared with sites with health records only (7.5). Although parental or professional concerns regarding development before age 36 months were noted in the evaluation records of the majority of children who were identified as having an ASD, the median age of earliest documented ASD diagnosis was much later (range: 41 months [Florida]–60 months [Colorado]). Of 10 sites that collected data for both the 2002 and 2006 surveillance years, nine observed an increase in ASD prevalence (range: 27%–95% increase; p<0.01), with increases among males in all sites and among females in four of 11 sites, and variation among other subgroups.
Interpretation: In 2006, on average, approximately 1% or one child in every 110 in the 11 ADDM sites was classified as having an ASD (approximate range: 1:80–1:240 children [males: 1:70; females: 1:315]). The average prevalence of ASDs identified among children aged 8 years increased 57% in 10 sites from the 2002 to the 2006 ADDM surveillance year. Although improved ascertainment accounts for some of the prevalence increases documented in the ADDM sites, a true increase in the risk for children to develop ASD symptoms cannot be ruled out. On average, although delays in identification persisted, ASDs were being diagnosed by community professionals at earlier ages in 2006 than in 2002.
Public Health Actions: These results indicate an increased prevalence of identified ASDs among U.S. children aged 8 years and underscore the need to regard ASDs as an urgent public health concern. Continued monitoring is needed to document and understand changes over time, including the multiple ascertainment and potential risk factors likely to be contributing. Research is needed to ascertain the factors that put certain persons at risk, and concerted efforts are essential to provide support for persons with ASDs, their families, and communities to improve long-term outcome.
Source: MMWR, December 18, 2009 / 58(SS10);1-20
Clinical Presentation and Histologic Findings at Ileocolonoscopy in Children with Autistic Spectrum Disorder and Chronic Gastrointestinal Symptoms – Replica Andrew Wakefield Study
This study doesn’t mention if MMR was given but it does replicate Andrew Wakefield’s findings that children with autism have gastrointestinal disease
Background: Children with developmental disorders experience chronic gastrointestinal symptoms.
Aims: To examine the nature of these gastrointestinal symptoms and histologic findings in children with autism spectrum/developmental disorders and ileocolonic disease.
Methods: Chart review. 143 autism spectrum/developmental disorder patients, with chronic gastrointestinal symptoms, undergoing diagnostic ileocolonoscopy.
Results: Diarrhea was present in 78%, abdominal pain in 59% and constipation in 36%. Ileal and/or colonic lymphonodular hyperplasia (LNH), defined as the presence of an increased number of enlarged lymphoid follicles, often with hyperactive germinal centers, was present in 73.2%. Terminal ileum LNH presented visually in 67% and histologically in 73%. Colonic LNH was multifocal and presented histologically in 32%. Ileal and/or colonic inflammation presented in 74%, consisting primarily of active or chronic colitis (69%). Ileal inflammation presented in 35%. Presence of LNH significantly predicted mucosal inflammation. Patients with ileal and/or colonic LNH had lower mean/median age than those without; patients with ileal and/or colonic inflammation had lower mean/median age than those without. There was a significant association between ileo and/or colonic inflammation or LNH, and onset of developmental disorder; plateaued or regressive onset conferred greater risk than early onset.
Conclusions: Patients with autism or related disorders exhibiting chronic gastrointestinal symptoms demonstrate ileal or colonic inflammation upon light microscopic examination of biopsy tissue. Further work is needed to determine whether resolution of histopathology with appropriate therapy is accompanied by GI symptomatic and cognitive/behavioral improvement.
Source: http://www.la-press.com/clinical-presentation-and-histologic-findings-at-ileocolonoscopy-in-ch-a1816
Retracting Wakefield’s Article From the Lancet Does Not Make the Vaccine and Autism Issue Go Away
Dr. Andrew Wakefield is one of the most vilified medical practitioners of recent times, and now he carries the extremely rare dishonor of a retraction in The Lancet, on the paper he co-authored in 1998 suggesting a potential link between autism, bowel disease and Measles-Mumps-Rubella (MMR) vaccine.
I believe that the public lynching and shaming of Dr. Wakefield is unwarranted and overwrought, and that history will ultimately judge who was right and who was wrong about proposing a possible association between vaccination and regressive autistic spectrum disorder (ASD).
Wakefield’s critics can condemn, retract, decry and de-license all they want, but that does nothing to stop or alter the march of science, which has come a long way over the past 12 years, and especially in the last year or two. The evidence that autism is increasing at alarming rates, and that some thing (or things) in our environment is wreaking havoc on a vulnerable one-percent of all US children is now so irrefutable that, finally, the federal government is climbing aboard the environmental research bandwagon – way late, but better than never.
This long-overdue paradigm shift will leave many in the scientific community with some proverbial but nonetheless uncomfortable egg on their increasingly irrelevant faces: Those who have protested with shrill certainty that autism is almost purely genetic, and not environmental in nature, and therefore not really increasing at all, will hopefully recede from the debate.
And that begs a nagging question: If those people were dead wrong about environmental factors in autism, could they also be mistaken in their equally heated denials about a possible vaccine-autism link? More bluntly, why should we heed them any longer?
We need to examine a host of environmental factors (air, water, food, medicine, household products and social factors) and how they might interact with vulnerable genes to create the varying collection of symptoms we call “autism.” But these triggers almost have to be found in every town of every county of every state in the land – from Maine to Maui.
Are vaccines the only contributing factors to autism? Of course not. Other pharmaceutical products like thalidomide and valporic acid, as well as live mumps virus, have been associated with increased autism risk in prenatal exposures, so we already know that a variety of drugs and bugs can likely make a child autistic.
But, there are now at least six published legal or scientific cases of children regressing into ASD following vaccination – and many more will be revealed in due time.
There was the case of Hannah Poling, in federal vaccine court, in which the government conceded that Hannah’s autism was caused by vaccine-induced fever and overstimulation of the immune system that aggravated an asymptomatic and previously undetected dysfunction of her mitochondria. Hannah received nine vaccines in one day, including MMR.
Then there was the Bailey Banks case, in which the court ruled that Petitioners had proven that MMR had directly caused a brain inflammation illness called “acute disseminated encephalomyelitis” (ADEM) which, in turn, had caused PDD-NOS, an autism spectrum disorder, in Bailey.
And last September, a chart review of children with autism and mitochondrial disease, published in the Journal of Child Neurology, looked at 28 children with ASD and mitochondrial disease and found that 17 of them (60.7%) had gone through autistic regression, and 12 of the regressive cases had followed a fever. Among the 12 children who regressed after fever, a third (4) had fever associated with vaccination, just like Hannah Poling.
The authors reported that “recommended vaccination schedules are appropriate in mitochondrial disease,” although “fever management appears important for decreasing regression risk.”
That conclusion, however, is not supported by some of the world’s leading experts on mitochondrial disease, including Dr. Douglas Wallace, a professor of pediatrics and biological chemistry at UC Irvine, and director of its Center for Molecular & Mitochondrial Medicine and Genetics. “We have always advocated spreading the immunizations out as much as possible because every time you vaccinate, you are creating a challenge for the system” in people with mito disorders, Dr. Wallace, who was recently named to the National Academies of Science, testified at a federal vaccine safety meeting.
The possibility that vaccines and mitochondrial disease might be related to autism was also supported in another chart review published in PLoS Online. The authors wrote that mitochondrial autism is not at all rare, and said that, “there might be no difference between the inflammatory or catabolic stress of vaccinations and that of common childhood diseases, which are known precipitants of mitochondrial regression.”
In fact, they added, “Large population-based studies will be needed to identify a possible relationship of vaccination with autistic regression in persons with mitochondrial cytopathies.”
Another fact that gets little attention in this never-ending debate is that more than 1,300 cases of vaccine injuries have been paid out in vaccine court, in which the court ruled that childhood immunizations caused encephalopathy (brain disease), encephalitis (brain swelling) and/or seizure disorders. Encephalopathy/encephalitis is found in most if not all ASD cases, and seizure disorders in about a third of them.
If we know that vaccines can cause these injuries, is it not reasonable to ask if they can cause similar injuries that lead to autism? (Stay tuned as those 1,300 cases come under closer scrutiny).
Fortunately, the federal government seems to be getting serious about identifying ALL potnetial environmental factors that could contribute to autism, including a few studies that take in vaccines and the mercury-containing preservative thimerosal. And President Obama’s brand-new budget includes increased spending for autism research at NIH, including money to help identify environmental factors that contribute to ASD.
Meanwhile, the National Vaccine Advisory Committee has unanimously endorsed a CDC proposal to study autism as a possible “clinical outcome” of vaccination, and has recommended several more studies pertaining to vaccines and autism, including a feasability study on analyzing vaccinated vs. unvaccinated populations.
And over at the government’s leading autism research panel, the Inter-Agency Autism Coordinating Committee (IACC), the Chairman, National Institute of Mental Health Director Dr. Thomas Insel, recently told me that that better diagnosis and reporting could not “explain away this huge increase” in ASD cases.
“There is no question that there has got to be an environmental component here,” Insel said.
I asked him if the IACC would ever support direct research into vaccines and autism, now that CDC has rasied the estimated ASD rate from 1-in-150 to 1-in-110, in just two years. “I think what you are going to see with this update is that there is a recognition that we need to look at subgroups who might be particularly responsive to environmental factors,” he answered.
So what might those factors include? Well, it turns out that the IACC has unanimously recommend research to determine if certain sub-populations are more susceptible to environmental exposures such as “immune challenges related to naturally occurring infections, vaccines or underlying immune problems.”
Nobody seriously thinks that the retraction of The Lancet article, and the international flogging of Dr. Andrew Wakefield, will do anything to make this debate go away. And they are right.
Source: by David Kirby, The Huffington Post, 3 February 2010.
Mitochondrial Disease in Autism Spectrum Disorder Patients: A Cohort Analysis
Recently, there has been increased concern regarding a possible causative role of vaccinations in autistic children with an underlying mitochondrial cytopathy [35], [36]. For one of our 25 patients, the child’s autism/neurodevelopmental deterioration appeared to follow vaccination [12], [36]. Although there may have been a temporal relationship of the events in this case, such timing does not prove causation. That said, there might be no difference between the inflammatory or catabolic stress of vaccinations and that of common childhood diseases, which are known precipitants of mitochondrial regression [37]. Large, population-based studies will be needed to identify a possible relationship of vaccination with autistic regression in persons with mitochondrial cytopathies.
Source: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0003815
Mercury Increases Susceptibility to Infectious Diseases and Makes Auto-Immune Conditions Worse
Mercury has often been implicated as the culprit for a variety of health issues, from being a possible source of developmental disorders like autism, due to the mercury preservative in vaccines, to being potentially toxic for tuna-ingesting sushi-lovers.
And though mercury poisoning often receives much of the publicity, it is a little known fact that mercury, in the form found in marine wildlife and in many workplaces, can cause severe autoimmune responses and even increase the body’s susceptibility to infectious diseases.
“Research on mercury as an immunotoxic agent is relatively new, and these are the first studies to demonstrate effects on immune modulation in humans,” said Ellen Silbergeld, the senior author of the study and a professor of Environmental Health Studies at Hopkins’ Bloomberg School of Public Health.
Mercury exposure can occur in a variety of settings, and the researchers first started considering the relationship between the immune system and mercury after studying Amazonian gold miners who use the metal.
According to Silbergeld, one of the red flags that triggered their hypothesis was the increased incidence of malaria in the miners and others living in this region. “We’ve shown associations between mercury exposures and increased susceptibility to malarial infections in both experimental models and human populations.”
When mice were exposed to inorganic mercury, the researchers found that it changed the pattern of cytokine release, which are compounds that function as signaling molecules in the immune system. Mercury exposure caused more pro-inflammatory cytokines and fewer anti-inflammatory cytokines to be released.
“There is evidence that mercury can increase risks of both autoimmune disease and certain infectious diseases,” Silbergeld said. “These consequences may involve a set of fundamental mechanisms in which the proinflammatory response is not counterbalanced.”
This imbalance could increase inflammation when the organism is exposed to infectious disease agents. Increased inflammatory responses could in turn raise the risk of susceptibility to infectious diseases. Additionally, for people with autoimmune disorders, mercury exposure could further worsen their conditions.
Other research suggests a correlation between mercury exposure, inflammation and cardiovascular disease. This is only one of many possible instances in which mercury may play a role in the development of chronic diseases.
Genetic factors may also play a role in an individual’s immune response to mercury exposure. When genetically susceptible mice were exposed to mercury, they developed an autoimmune disease similar to lupus. “Given the importance of genetics in immunobiology, this may be an important area of research in understanding differences in population responses to mercury,” Silbergeld said.
Although much more research needs to be done to investigate the mechanism behind this phenomenon, Silbergeld hypothesizes that mercury acts on a certain type of receptor, known as the TL4 receptor, to alter the release of cytokines.
Even low levels of mercury were enough to generate this immune response, and the amounts used in the experiment were well within the range of mercury exposure in the United States.
“Mercury is a highly toxic agent, in all its forms – not just methyl mercury, which is the major form to which we are exposed,” Silbergeld said. She also stresses that stricter regulations should be put into place to reduce our exposure, which frequently occurs in the form of fish consumption.
“There is certainly an important need for individuals to evaluate their own exposure risks and to consume fish prudently, but even more importantly, national and international actions are long overdue to reduce inputs of mercury into the environment that result in contamination of fish,” she said.
This study puts the notion of mercury toxicity in a very different light, by suggesting that it may specifically target the immune system in order to inflict damage. “The concept that environmental toxicants could modify human immune response opens up new areas for research on these types of complex . . . interactions,” Silbergeld said.
Source: The John Hopkins Newsletter, by Tiffany NG, 4 February 2010.
DELAYED ACQUISITION OF NEONATAL REFLEXES IN NEWBORN PRIMATES RECEIVING A THIMEROSAL-CONTAINING HEPATITIS B VACCINE INFLUENCE OF GESTATIONAL AGE AND BIRTH WEIGHT
This study examined whether acquisition of neonatal reflexes and sensorimotor skills in newborn
3 rhesus macaques (Macaca mulatta) is influenced by receipt of the single neonatal dose of Hepatitis B
4 (HB) vaccine containing the preservative thimerosal (Th). HB vaccine containing a standardized
5 weight-adjusted Th dose was administered to male macaques within 24 hours of birth (n=13).
6 Unexposed animals received saline placebo (n=4) or no injection (n=3). Infants were raised identically
7 and tested daily for acquisition of 9 survival, motor, and sensorimotor reflexes by a blinded observer.
8 In exposed animals there was a significant delay in the acquisition of three survival reflexes: root, snout
9 and suck, compared with unexposed animals.
Our findings provide an important rationale for determining what factors in the HB vaccine may be
16 responsible for these clinical observations. This should also include aluminum hydroxide which is
17 used as an adjuvant in many vaccines, including the HB vaccine formulation used for this study.
18 Studies are underway to examine this, and the consequences of repeated and/or additional vaccine
19 exposures on the natural course of neurodevelopment.
Source: Hewitson L, Houser LA, Stott C, Sackett G, Tomko JL,Atwood D, Blue L, White ER, Wakefield AJ, Delayed Acquisition of Neonatal
Reflexes in newborn Primates receiving A Thimerosal-containing HepatitiS B
Vaccine: influence of gestational age and Birth weight, Neurotoxicology (2008),
doi:10.1016/j.neuro.2009.09.008
http://www.rescuepost.com/files/hewitson-et-al-09-primate-hbv-study.pdf
Mercury May Contribute to ASD
Background
Mercury is known to be neurotoxic, but its effects on the immune system are less well known. Mast cells are involved in allergic reactions, but also in innate and acquired immunity, as well as in inflammation. Many patients with Autism Spectrum Disorders (ASD) have “allergic” symptoms; moreover, the prevalence of ASD in patients with mastocytosis, characterized by numerous hyperactive mast cells in most tissues, is 10-fold higher than the general population suggesting mast cell involvement. We, therefore, investigated the effect of mercuric chloride (HgCl2) on human mast cell activation.
Methods
Human leukemic cultured LAD2 mast cells and normal human umbilical cord blood-derived cultured mast cells (hCBMCs) were stimulated by HgCl2 (0.1-10 microM) for either 10 min for beta-hexosaminidase release or 24 h for measuring vascular endothelial growth factor (VEGF) and IL-6 release by ELISA.
Results
HgCl2 induced a 2-fold increase in beta-hexosaminidase release, and also significant VEGF release at 0.1 and 1 microM (311+/-32 pg/10*6 cells and 443+/-143 pg/10*6 cells, respectively) from LAD2 mast cells compared to control cells (227+/-17 pg/10*6 cells, n=5, p<0.05). Addition of HgCl2 (0.1 microM) to the proinflammatory neuropeptide substance P (SP, 0.1 microM) had synergestic action in inducing VEGF from LAD2 mast cells. HgCl2 also stimulated significant VEGF release (360 +/- 100 pg/10*6 cells at 1 microM, n=5, p<0.05) from hCBMCs compared to control cells (182 +/-57 pg/10*6 cells), and IL-6 release (466+/-57 pg/10*6 cells at 0.1 microM) compared to untreated cells (13+/-25 pg/10*6 cells, n=5, p<0.05). Addition of HgCl2 (0.1 microM) to SP (5 microM) further increased IL-6 release.
Conclusions
HgCl2 stimulates VEGF and IL-6 release from human mast cells. This phenomenon could disrupt the blood-brain-barrier and permit brain inflammation. As a result, the findings of the present study provide a biological mechanism for how low levels of mercury may contribute to ASD pathogenesis.
Source: Journal of Neuroinflammation 2010, 7:20doi:10.1186/1742-2094-7-20
Shocker: SV40 (from vaccines) and other Viruses Found in the Brains of Autistic People!
Autism is a highly heritable behavioral disorder. Yet, two decades of genetic investigation have unveiled extremely few cases that can be solely explained on the basis of de novo mutations or cytogenetic abnormalities. Vertical viral transmission represents a nongenetic mechanism of disease compatible with high parent-to-offspring transmission and with low rates of disease-specific genetic abnormalities. Vertically transmitted viruses should be found more frequently in the affected tissues of autistic individuals compared to controls. Our initial step was thus to assess by nested polymerase chain reaction (PCR) and DNA sequence analysis the presence of cytomegalovirus (CMV), Epstein-Barr virus (EBV), herpes simplex virus type 1 (HSV1), herpes simplex virus type 2 (HSV2), human herpes virus 6 (HHV6), BK virus (BKV), JC virus (JCV), and simian virus 40 (SV40) in genomic DNA extracted from postmortem temporocortical tissue (Brodmann areas 41/42) belonging to 15 autistic patients and 13 controls. BKV, JCV, and SV40 combined are significantly more frequent among autistic patients compared to controls (67% versus 23%, respectively; P <.05). The majority of positives yielded archetypal sequences, whereas six patients and two controls unveiled single–base pair changes in two or more sequenced clones. No association is present with the remaining viruses, which are found in relatively few individuals (N ≤ 3). Also polyviral infections tend to occur more frequently in the brains of autistic patients compared to controls (40% versus 7.7%, respectively; P =.08). Follow-up studies exploring vertical viral transmission as a possible pathogenetic mechanism in autistic disorder should focus on, but not be limited to, the role of polyomaviruses.
Source: http://informahealthcare.com/doi/abs/10.3109/13550281003685839
The severity of autism is associated with toxic metal body burden and red blood cell glutathione levels.
Abstract
This study investigated the relationship of children’s autism symptoms with their toxic metal body burden and red blood cell (RBC) glutathione levels. In children ages 3-8 years, the severity of autism was assessed using four tools: ADOS, PDD-BI, ATEC, and SAS. Toxic metal body burden was assessed by measuring urinary excretion of toxic metals, both before and after oral dimercaptosuccinic acid (DMSA). Multiple positive correlations were found between the severity of autism and the urinary excretion of toxic metals. Variations in the severity of autism measurements could be explained, in part, by regression analyses of urinary excretion of toxic metals before and after DMSA and the level of RBC glutathione (adjusted R(2) of 0.22-0.45, P < .005 in all cases). This study demonstrates a significant positive association between the severity of autism and the relative body burden of toxic metals.
Source: J Toxicol. 2009;2009:532640. Epub 2009 Aug 26.
Autism: a novel form of mercury poisoning.
Abstract
Autism is a syndrome characterized by impairments in social relatedness and communication, repetitive behaviors, abnormal movements, and sensory dysfunction. Recent epidemiological studies suggest that autism may affect 1 in 150 US children. Exposure to mercury can cause immune, sensory, neurological, motor, and behavioral dysfunctions similar to traits defining or associated with autism, and the similarities extend to neuroanatomy, neurotransmitters, and biochemistry. Thimerosal, a preservative added to many vaccines, has become a major source of mercury in children who, within their first two years, may have received a quantity of mercury that exceeds safety guidelines. A review of medical literature and US government data suggests that: (i) many cases of idiopathic autism are induced by early mercury exposure from thimerosal; (ii) this type of autism represents an unrecognized mercurial syndrome; and (iii) genetic and non-genetic factors establish a predisposition whereby thimerosal’s adverse effects occur only in some children.
Source: Med Hypotheses. 2001 Apr;56(4):462-71.
Mercury and autism: accelerating evidence?
Abstract
The causes of autism and neurodevelopmental disorders are unknown. Genetic and environmental risk factors seem to be involved. Because of an observed increase in autism in the last decades, which parallels cumulative mercury exposure, it was proposed that autism may be in part caused by mercury. We review the evidence for this proposal. Several epidemiological studies failed to find a correlation between mercury exposure through thimerosal, a preservative used in vaccines, and the risk of autism. Recently, it was found that autistic children had a higher mercury exposure during pregnancy due to maternal dental amalgam and thimerosal-containing immunoglobulin shots. It was hypothesized that children with autism have a decreased detoxification capacity due to genetic polymorphism. In vitro, mercury and thimerosal in levels found several days after vaccination inhibit methionine synthetase (MS) by 50%. Normal function of MS is crucial in biochemical steps necessary for brain development, attention and production of glutathione, an important antioxidative and detoxifying agent. Repetitive doses of thimerosal leads to neurobehavioral deteriorations in autoimmune susceptible mice, increased oxidative stress and decreased intracellular levels of glutathione in vitro. Subsequently, autistic children have significantly decreased level of reduced glutathione. Promising treatments of autism involve detoxification of mercury, and supplementation of deficient metabolites.
Source: Neuro Endocrinol Lett. 2005 Oct;26(5):439-46.
Reduced levels of mercury in first baby haircuts of autistic children.
Abstract
Reported rates of autism have increased sharply in the United States and the United Kingdom. One possible factor underlying these increases is increased exposure to mercury through thimerosal-containing vaccines, but vaccine exposures need to be evaluated in the context of cumulative exposures during gestation and early infancy. Differential rates of postnatal mercury elimination may explain why similar gestational and infant exposures produce variable neurological effects. First baby haircut samples were obtained from 94 children diagnosed with autism using Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM IV) criteria and 45 age- and gender-matched controls. Information on diet, dental amalgam fillings, vaccine history, Rho D immunoglobulin administration, and autism symptom severity was collected through a maternal survey questionnaire and clinical observation. Hair mercury levels in the autistic group were 0.47 ppm versus 3.63 ppm in controls, a significant difference. The mothers in the autistic group had significantly higher levels of mercury exposure through Rho D immunoglobulin injections and amalgam fillings than control mothers. Within the autistic group, hair mercury levels varied significantly across mildly, moderately, and severely autistic children, with mean group levels of 0.79, 0.46, and 0.21 ppm, respectively. Hair mercury levels among controls were significantly correlated with the number of the mothers’ amalgam fillings and their fish consumption as well as exposure to mercury through childhood vaccines, correlations that were absent in the autistic group. Hair excretion patterns among autistic infants were significantly reduced relative to control. These data cast doubt on the efficacy of traditional hair analysis as a measure of total mercury exposure in a subset of the population. In light of the biological plausibility of mercury’s role in neurodevelopmental disorders, the present study provides further insight into one possible mechanism by which early mercury exposures could increase the risk of autism.
Source: Int J Toxicol. 2003 Jul-Aug;22(4):277-85.
Mercury, lead, and zinc in baby teeth of children with autism versus controls – How Antibiotics Stop the Body’s Ability to Excrete Mercury From Vaccines and other Sources
Abstract
This study determined the level of mercury, lead, and zinc in baby teeth of children with autism spectrum disorder (n = 15, age 6.1 +/- 2.2 yr) and typically developing children (n = 11, age = 7 +/- 1.7 yr). Children with autism had significantly (2.1-fold) higher levels of mercury but similar levels of lead and similar levels of zinc. Children with autism also had significantly higher usage of oral antibiotics during their first 12 mo of life, and possibly higher usage of oral antibiotics during their first 36 mo of life. Baby teeth are a good measure of cumulative exposure to toxic metals during fetal development and early infancy, so this study suggests that children with autism had a higher body burden of mercury during fetal/infant development. Antibiotic use is known to almost completely inhibit excretion of mercury in rats due to alteration of gut flora. Thus, higher use of oral antibiotics in the children with autism may have reduced their ability to excrete mercury, and hence may partially explain the higher level in baby teeth. Higher usage of oral antibiotics in infancy may also partially explain the high incidence of chronic gastrointestinal problems in individuals with autism.
Source: J Toxicol Environ Health A. 2007 Jun;70(12):1046-51.
Brain Damage in Monkeys After Full US Childhood Vaccine Schedule
This longitudinal, case-control pilot study examined amygdala growth in rhesus macaque infants receiving the complete US childhood vaccine schedule (1994-1999). Longitudinal structural and functional neuroimaging was undertaken to examine central effects of the vaccine regimen on the developing brain. Vaccine-exposed and saline-injected control infants underwent MRI and PET imaging at approximately 4 and 6 months of age, representing two specific timeframes within the vaccination schedule. Volumetric analyses showed that exposed animals did not undergo the maturational changes over time in amygdala volume that was observed in unexposed animals. After controlling for left amygdala volume, the binding of the opioid antagonist [11C]diprenorphine (DPN) in exposed animals remained relatively constant over time, compared with unexposed animals, in which a significant decrease in [11C]DPN binding occurred. These results suggest that maturational changes in amygdala volume and the binding capacity of [11C]DPN in the amygdala was significantly altered in infant macaques receiving the vaccine schedule. The macaque infant is a relevant animal model in which to investigate specific environmental exposures and structural/functional neuroimaging during neurodevelopment.
Source: Acta Neurobiol Exp 2010, 70: 147–164
Thimerosal Damages Rat Brains
http://www.springerlink.com/content/d751p01x01013627/fulltext.pdf
Infants’ exposure to aluminum from vaccines and breast milk during the first 6 months.
Abstract
The success of vaccination programs in reducing and eliminating infectious diseases has contributed to an ever-increasing number of vaccines given at earlier ages (newborns and infants). Exposure to low levels of environmental toxic substances (including metals) at an early age raises plausible concerns over increasingly lower neuro-cognitive rates. Current immunization schedules with vaccines containing aluminum (as adjuvant) are given to infants, but thimerosal (as preservative) is found mostly in vaccines used in non-industrialized countries. Exclusively, breastfed infants (in Brazil) receiving a full recommended schedule of immunizations showed an exceedingly high exposure of Al (225 to 1750 μg per dose) when compared with estimated levels absorbed from breast milk (2.0 μg). This study does not dispute the safety of vaccines but reinforces the need to study long-term effects of early exposure to neuro-toxic substances on the developing brain. Pragmatic vaccine safety needs to embrace conventional toxicology, addressing especial characteristics of unborn fetuses, neonates and infants exposed to low levels of aluminum, and ethylmercury traditionally considered innocuous to the central nervous system.
Source: J Expo Sci Environ Epidemiol. 2010 Nov;20(7):598-601. Epub 2009 Dec 16.
VAN UK’s Comment: They know that giving multiple vaccines at very young ages declines neuro-cognitive function yet they won’t say they’re unsafe, probably because they’d lose their grant money and income from vaccines!
Lasting neuropathological changes in rat brain after intermittent neonatal administration of thimerosal
Abstract
Thimerosal, an organomercurial added as a preservative to some vaccines, is a suspected iatrogenic factor, possibly contributing to paediatric neurodevelopmental disorders including autism. We examined the effects of early postnatal administration of thimerosal (four i.m. injections, 12 or 240 g THIM-Hg/kg, on postnatal days 7, 9, 11 and 15) on brain pathology in Wistar rats. Numerous neuropathological changes were observed in young adult rats which were treated postnatally with thimerosal. They included: ischaemic degeneration of neurons and “dark” neurons in the prefrontal and temporal cortex, the hippocampus and the cerebellum, pathological changes of the blood vessels in the temporal cortex, diminished synaptophysin reaction in the hippocampus, atrophy of astroglia in the hippocampus and cerebellum, and positive caspase-3 reaction in Bergmann astroglia. These findings document neurotoxic effects of thimerosal, at doses equivalent to those used in infant vaccines or higher, in developing rat brain, suggesting likely involvement of this mercurial in neurodevelopmental disorders.
Source: Folia Neuropathol. 2010;48(4):258-69
