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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:
http://www.mercurymadness.org
and go to the Mercury In Vaccines page.
It's an excellant 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.
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.
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.
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
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
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
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.
Julia a three year old US citizen has just won substantial compensation in the US Federal Court for autism caused by MMR vaccine – says her mother.
What is different about this case? They kept the “autism” word out of the case. Many parents in other US cases have been advised to do this:-
CBS News has found that since 1988, the vaccine court has awarded money judgments, often in the millions of dollars, to thirteen hundred and twenty two families whose children suffered brain damage from vaccines. In many … cases, the government paid out awards following a judicial finding that vaccine injury lead to the child’s autism spectrum disorder. In each of these cases, the plaintiffs’ attorneys made the same tactical decision made by Bailey Bank’s lawyer, electing to opt out of the highly charged Omnibus Autism Proceedings and argue their autism cases in the regular vaccine court. In many other successful cases, attorneys elected to steer clear of the hot button autism issue altogether and seek recovery instead for the underlying brain damage that caused their client’s autism.”: [Vaccine Court: Autism Debate Continues - Robert F. Kennedy, Jr. and David Kirby Huffington Post 24 Feb 2009]
Julia’s Mom emphasises Julia has no formal diagnosis of autism and says:-
after Julia’s last neuro appointment when her dr said she had signs of autism. I didn’t want that “word” in her records until Julia’s case was decided.
Julia’s diagnosis was “Encephalitis (inflammation of her brain) most likely attributed to the MMR-V (measles, mumps, reubella, chicken pox) vaccine she had received nine days previously.
I do not want this to be misunderstood. She was never formally diagnosed. Do I think that there is a link between vaccines and Autism, absolutely. Is Julia Autistic? I’m not sure.“
Data from formal peer refereed medical papers show vaccines caused autism in Japanese children: Japanese Data Show Vaccines Cause Autism. The number developing autism rose and fell in direct proportion to the number of children vaccinated each year. HERE is research showing Autistic Spectrum Conditions can result from brain injury caused by encephalopathy (a degenerative disease of the brain). Encephalopathies are normally caused by an infection (90% of the time), and most often we will expect a viral infection. MMR contains three live viruses. [See also Explaining Vaccines Autism & Mitochondrial Dysfunction/Disorder]
Julia’s Mom says she was:
accepting the loss of the world as i knew it before she got sick, before my divorce, before i lost my house.
This is such a huge, huge, huge help for Julia and my family”
If this is what compensation means for Julia’s Mom think of all the families and children who should never have got sick in the first place and will never get compensation just because they used the “autism” word.
Does it help to think your child is “just a little bit” autistic but still injured and in need of financial help with medical care for life? Autism Spectrum Conditions are a spectrum from very mild to incapacitating.
Not only does it not end like this for other families – some children die as this 2005 Federal Court decision in a case very similar to Julia’s shows [and which took 9 years to achieve a decision]:-
Eric Fernandez Cusati v Secretary for Health and Human Services
How many cases are like these ones? Who knows the exact number – the majority of decisions are never published – kept in secret. And then there are all the cases the US Secretary of Health and Human Services settles – also kept in secret. And how many cases are just not filed? No one publicly knows for sure.
Before drug companies came up with the triple MMR vaccine rubella vaccine was of no benefit to a child especially boys and especially compared to the risks. Mumps vaccine was expressly not recommended for children.
So why are we giving them? It is time all parents started asking the simple questions – like that one.
And who said so?
The British Medical Association, the Royal Pharmaceutical Society of Great Britain, the UK’s Joint Committee on Vaccination and Immunisation and the UK’s Ministry of Defence:
“Since mumps and its complications are very rarely serious there is little indication for the routine use of mumps vaccine”: British National Formulary (’BNF’) 1985 and 1986
The BNF is a joint publication of the BMA and RPSGB.
Freedom of Information documents show the UK’s Joint Committee on Vaccination and Immunisation and Ministry of Defence agreed as early as 1974 that:-
“there was no need to introduce routine vaccination against mumps” because “complications from the disease were rare” JCVI minutes 11 Dec 1974.
It is unethical to give a child unnecessary medical treatment and can be a criminal offence: Appleton v Garrett (1995) 34 BMLR 23.
And with 1 in 38 British boys with an autistic condition [and the problem is not just autism] the question must be asked – how many children who would otherwise have grown up healthy are going to continue to be sacrificed and claimed to be for the very few but in reality for drug company profits in their move to a new business model based on “vaccines for all”. [Autism Rates Rocket – 1 in 38 British Boys – Cambridge Study See also: Government Risks Male Sterility As Mumps Vaccine Fails]
Today it is your kid. Tomorrow it is you.
New Report Forecasts More Than Doubling of Vaccine Sales by 2013 – MarketWatch Jun 11, 2009 – Kalorama News Release
Kids’ vaccine market set to quadruple – Drug Researcher – By Anna Lewcock 20-Nov-2007
Julia’s Story
[by her Mom]
Julia was born a healthy baby on 12-28-05. She was a delight to her family and friends.
On January 5th, 2007, one week after her 1st birthday, our family’s lives changed forever. Julia (unknowingly to her family) had been seizing in her crib most of the night, was transported to the nearest ER for stabilization, and then airlifted to Miami Children’s hospital, where she stayed in PICU and the neurology ward for close to one month.
Her diagnosis? Encephalitis (inflammation of her brain) most likely attributed to the MMR-V (measles, mumps, reubella, chicken pox) vaccine she had received nine days previously. When Julia left the hospital, she was functioning at a two month level. She was (and in some respects still is) globally delayed and with significant left sided hemiplegia.
It has been over two years since her MMR-V induced encephalitis, and Julia has come a long way, but has a very long way to go. Julia lives with her brother, Jack who is six and so understanding of her. She also lives with her mom, Susan. Her father recently moved out of state following her parent’s divorce. Julia and her family are hanging in there and hope you enjoy her blog! Go Julia!
AMAZING DAY! A MIRACLE HAS HAPPENED!
[Posted by Julia's Mom - 12 June 2009]
JULIA WON HER LAWSUIT WITH THE VACCINE INJURY COMPENSATION PROGRAM! THE GOVERNMENT CONCEDED!
This means that they agreed that the MMR vaccine caused her encephalitis and resultant brain damage (I mean Marvelous Mind – right Howard!!).
This is such a huge, huge, huge help for Julia and my family. The government will reimburse all of her past medical expenses (to her, not to us, which I find a little odd, but OK!) and will pay for all future medical expenses that she incurs from her vaccine injury. I will update as I find out more.
Her attorney (Ron Homer and/or Kevin Conway) will be flying out here this summer to evaluate her and her needs with a “life planner” to try to determine what her needs will be. This is HUGE! HUGE! The VICP rarely concedes…..almost never……but they did for her! AMAZING!
Another funny thing to go along with this…..I had just the day before changed my ringtone on my phone to “Its the end of the world as we know it….and I feel fine” trying to find a positive ringtone – accepting the loss of the world as i knew it before she got sick, before my divorce, before i lost my house, and moving forward – and being fine with it….AND NOW – ITS THE END OF THE WORLD AS I KNOW IT – AND I REALLY FEEL FINE! SHE has HELP!!!!! Our struggle is going to be lessened!!!!
Source: Child Health Safety, 14th June 2009.
[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
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
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.
Universal newborn immunization with hepatitis
B vaccine 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.
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
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
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 coauthored 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.
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 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.
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
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
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
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.
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.
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.
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.
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.
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
http://www.springerlink.com/content/d751p01x01013627/fulltext.pdf
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.
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
In case the webpage diappears or you can't access it, here's the list of aluminium caused diseases:
These diseases are associated with Aluminum or at least one of its descendants. Each association is curated (M marker/mechanism and/or T therapeutic) and/or inferred (via a curated gene interaction).
Showing 1–240 of 240
Chemical Disease Direct Evidence Inference Network Inference Score References
1. Aluminum Multiple Sclerosis, Chronic Progressive M 1
2. Aluminum Multiple Sclerosis, Relapsing-Remitting M 1
3. Aluminum Alzheimer Disease M Via 7 genes: ACE; APP; IL1B; MAPT; MPO; TF; TNF 55.47 17
4. Aluminum Inflammation M Via 5 genes: LTF; NOS2; SCGB1A1; TFRC; TNF 40.16 5
5. Aluminum Lung Diseases M Via 3 genes: ACE; SCGB1A1; TNF 27.11 3
6. Aluminum Autistic Disorder Via 8 genes: CAT; GPX1; IL4; NOS2; PLA2G4A; PTGS2; TF; XDH 56.13 7
7. Aluminum Drug-Induced Liver Injury Via 6 genes: ALB; IL1B; LTF; MMP2; PTGS2; TF 45.79 6
8. Aluminum Liver Cirrhosis, Experimental Via 7 genes: ACHE; IL1B; MMP2; MMP9; NOS2; PTGS2; TNF 45.31 5
9. Aluminum Lung Neoplasms Via 6 genes: GPX1; MAPK3; MPO; NOS2; TFRC; TNF 40.60 6
10. Aluminum Asthma Via 5 genes: CAT; IL4; MMP9; SCGB1A1; TNF 38.80 8
11. Aluminum Breast Neoplasms Via 6 genes: GPX1; IL1B; NOS2; PTGS2; TFRC; TNF 36.53 8
12. Aluminum Oral Submucous Fibrosis Via 4 genes: MMP2; MMP9; PTGS2; TNF 34.83 1
13. Aluminum Metabolism, Inborn Errors Via 3 genes: KLK1; OGDH; PLA2G4A 30.94 3
14. Aluminum Carcinoma, Squamous Cell Via 4 genes: GPX1; HIF1A; MMP9; PTGS2 29.55 5
15. Aluminum Coronary Artery Disease Via 3 genes: ACE; GPX1; PTGS2 26.06 3
16. Aluminum Osteoporosis, Postmenopausal Via 3 genes: CAT; IL1B; TNF 25.47 2
17. Aluminum Myocardial Infarction Via 3 genes: ACE; KLK1; NOS2 25.39 4
18. Aluminum Cell Transformation, Neoplastic Via 3 genes: MMP9; NOS2; SLC2A1 25.26 2
19. Aluminum Sepsis Via 3 genes: MAPK3; MMP9; TNF 24.75 2
20. Aluminum Parkinson Disease Via 3 genes: DBH; GPX1; MAPT 24.67 4
21. Aluminum Prostatic Neoplasms Via 4 genes: ACE; HIF1A; MMP9; PTGS2 23.53 6
22. Aluminum Glioblastoma Via 3 genes: IL1B; MMP2; MMP9 23.18 2
23. Aluminum Skin Neoplasms Via 3 genes: HIF1A; MMP9; PTGS2 22.00 3
24. Aluminum Psoriasis Via 3 genes: IL4; NOS2; TNF 21.32 3
25. Aluminum Esophageal Neoplasms Via 3 genes: HIF1A; NOS2; PTGS2 20.94 6
26. Aluminum Enterocolitis, Necrotizing Via 2 genes: LTF; NOS2 20.90 2
27. Aluminum Pancreatic Neoplasms Via 3 genes: HIF1A; PTGS2; TNF 20.79 5
28. Aluminum Colonic Neoplasms Via 3 genes: IL1B; MMP9; SLC2A1 20.70 3
29. Aluminum Stomach Ulcer Via 3 genes: NOS2; PTGS2; TNF 20.58 3
30. Aluminum Arthritis, Rheumatoid Via 3 genes: MMP2; PTGS2; TNF 20.13 4
31. Aluminum Anemia, Iron-Deficiency Via 2 genes: TF; TFRC 19.96 4
32. Aluminum Skin Diseases Via 3 genes: IL1B; PTGS2; TNF 19.93 2
33. Aluminum Nephrotic Syndrome Via 2 genes: ALB; TF 18.85 1
34. Aluminum Bone Neoplasms Via 2 genes: MMP2; MMP9 18.56 1
35. Aluminum Osteoporosis Via 2 genes: LTF; PTH 18.53 4
36. Aluminum Respiratory Distress Syndrome, Adult Via 2 genes: ALB; PLA2G4A 18.48 2
37. Aluminum Myocardial Stunning Via 2 genes: NOS2; TNF 18.44 1
38. Aluminum Multiple Organ Failure Via 2 genes: MMP9; TNF 18.11 2
39. Aluminum PLASMODIUM FALCIPARUM BLOOD INFECTION LEVEL Via 2 genes: NOS2; TNF 17.93 1
40. Aluminum Berylliosis Via 2 genes: ACE; TNF 17.51 5
41. Aluminum Dermatomyositis Via 2 genes: IL1B; TNF 17.45 1
42. Aluminum Cholangiocarcinoma Via 2 genes: NOS2; PTGS2 16.84 1
43. Aluminum Stomach Neoplasms Via 3 genes: IL1B; PTGS2; TNF 16.78 4
44. Aluminum Diabetes Mellitus Via 2 genes: CAT; PTGS2 16.29 2
45. Aluminum Amyotrophic Lateral Sclerosis Via 2 genes: PLA2G4A; PTGS2 16.21 1
46. Aluminum Colitis, Ulcerative Via 2 genes: IL1B; LTF 16.01 2
47. Aluminum Hypersensitivity Via 2 genes: IL4; TNF 15.84 1
48. Aluminum Obesity Via 2 genes: GPX1; TFRC 15.76 2
49. Aluminum Head and Neck Neoplasms Via 2 genes: GPX1; MAPK3 15.67 2
50. Aluminum Hypertension Via 2 genes: KLK1; PTGS2 15.60 2
51. Aluminum Respiratory Hypersensitivity Via 2 genes: IL4; TNF 15.53 1
52. Aluminum Drug Hypersensitivity Via 2 genes: IL4; TNF 15.53 3
53. Aluminum Leukemia, Lymphocytic, Chronic, B-Cell Via 2 genes: PTGS2; TFRC 15.52 2
54. Aluminum Duodenal Ulcer Via 2 genes: NOS2; PTGS2 15.52 2
55. Aluminum Carcinoma, Renal Cell Via 2 genes: PTGS2; SLC2A1 15.48 2
56. Aluminum Neoplasm Metastasis Via 2 genes: MMP2; MMP9 15.44 1
57. Aluminum Craniofacial Abnormalities Via 2 genes: GNAQ; MMP2 15.27 3
58. Aluminum Fever Via 2 genes: IL1B; TNF 15.26 1
59. Aluminum Glioma Via 2 genes: PTGS2; TFRC 15.23 2
60. Aluminum Malaria Via 2 genes: NOS2; TNF 15.22 1
61. Aluminum Urinary Bladder Neoplasms Via 2 genes: PTGS2; TFRC 14.60 4
62. Aluminum Leiomyomatosis and renal cell cancer, hereditary Via 1 gene: FH 13.78 1
63. Aluminum LEIOMYOMA, HEREDITARY MULTIPLE, OF SKIN Via 1 gene: FH 13.78 1
64. Aluminum FUMARASE DEFICIENCY Via 1 gene: FH 13.78 1
65. Aluminum Machado-Joseph Disease Via 1 gene: ATXN3 13.26 1
66. Aluminum Colorectal Neoplasms Via 2 genes: PTGS2; TFRC 13.23 4
67. Aluminum Pulmonary Fibrosis Via 2 genes: IL1B; TNF 13.15 3
68. Aluminum Carcinoma, Hepatocellular Via 2 genes: PTGS2; SLC2A1 13.13 2
69. Aluminum CHARCOT-MARIE-TOOTH DISEASE, DEMYELINATING, TYPE 1C Via 1 gene: LITAF 13.10 1
70. Aluminum ERYTHROCYTOSIS, FAMILIAL, 1 Via 1 gene: EPOR 13.10 1
71. Aluminum HEMOLYTIC ANEMIA, NONSPHEROCYTIC, DUE TO HEXOKINASE DEFICIENCY Via 1 gene: HK1 13.06 1
72. Aluminum MYASTHENIC SYNDROME, CONGENITAL, ASSOCIATED WITH EPISODIC APNEA Via 1 gene: CHAT 12.93 1
73. Aluminum Arsenic Poisoning Via 2 genes: IL1B; TNF 12.86 1
74. fluoroaluminum Silver-Russell Syndrome Via 1 gene: IGF2 12.67 1
75. Aluminum Liver Diseases Via 2 genes: MMP9; NOS2 12.67 1
76. Aluminum DOPAMINE BETA-HYDROXYLASE DEFICIENCY, CONGENITAL Via 1 gene: DBH 12.51 1
77. Aluminum ADENOSINE TRIPHOSPHATE, ELEVATED, OF ERYTHROCYTES Via 1 gene: PKLR 12.46 1
78. Aluminum PYRUVATE KINASE DEFICIENCY OF RED CELLS Via 1 gene: PKLR 12.46 1
79. Aluminum Candidiasis, Oral Via 1 gene: LTF 12.30 1
80. Aluminum Joint Diseases Via 1 gene: LTF 12.30 1
81. Aluminum XANTHINURIA, TYPE I Via 1 gene: XDH 12.16 1
82. Aluminum Hypobetalipoproteinemias Via 1 gene: APOB 12.15 1
83. Aluminum ATRANSFERRINEMIA Via 1 gene: TF 12.12 1
84. Aluminum Hemophilia A Via 1 gene: F8 12.05 3
85. Aluminum Arenaviridae Infections Via 1 gene: TFRC 12.00 1
86. Aluminum Death, Sudden Via 1 gene: ACE 11.99 1
87. Aluminum MICROVASCULAR COMPLICATIONS OF DIABETES, SUSCEPTIBILITY TO, 3 Via 1 gene: ACE 11.99 1
88. Aluminum Anuria Via 1 gene: ACE 11.99 1
89. Aluminum Bone Diseases, Endocrine Via 1 gene: PTH 11.98 1
90. Aluminum Rickets Via 1 gene: PTH 11.98 1
91. Aluminum Glucosephosphate Dehydrogenase Deficiency Via 1 gene: G6PD 11.88 1
92. Aluminum PARKINSON-DEMENTIA SYNDROME Via 1 gene: MAPT 11.86 1
93. Aluminum GLUT1 DEFICIENCY SYNDROME 1 Via 1 gene: SLC2A1 11.82 2
94. Aluminum Schizophrenia Via 2 genes: IL1B; TNF 11.66 2
95. fluoroaluminum Growth Disorders Via 1 gene: IGF2 11.63 1
96. Aluminum Alexander Disease Via 1 gene: GFAP 11.61 1
97. Aluminum HYPOPARATHYROIDISM, FAMILIAL ISOLATED Via 1 gene: PTH 11.57 1
98. Aluminum MYELOPEROXIDASE DEFICIENCY Via 1 gene: MPO 11.34 1
99. Aluminum Blood Platelet Disorders Via 1 gene: PLA2G4A 11.22 1
100. Aluminum CEREBRAL AMYLOID ANGIOPATHY, APP-RELATED Via 1 gene: APP 11.21 1
101. Aluminum Premature Birth Via 1 gene: LTF 11.20 1
102. Aluminum Candidiasis, Vulvovaginal Via 1 gene: LTF 11.20 1
103. Aluminum Diarrhea Via 1 gene: LTF 11.20 1
104. Aluminum Melanoma Via 2 genes: PTGS2; TNF 11.20 3
105. Aluminum Frontotemporal Dementia Via 1 gene: MAPT 11.16 1
106. Aluminum TORG-WINCHESTER SYNDROME Via 1 gene: MMP2 11.16 2
107. Aluminum Tuberculosis, Bovine Via 1 gene: IL4 10.99 1
108. Aluminum Venous Thrombosis Via 1 gene: F8 10.96 1
109. Aluminum METAPHYSEAL ANADYSPLASIA 2 Via 1 gene: MMP9 10.96 1
110. Aluminum MICROVASCULAR COMPLICATIONS OF DIABETES, SUSCEPTIBILITY TO, 1 Via 1 gene: ACE 10.89 1
111. Aluminum ZINC, ELEVATED PLASMA Via 1 gene: ALB 10.89 1
112. fluoroaluminum Skin Neoplasms Via 1 gene: PTK2B 10.77 1
113. Aluminum Supranuclear Palsy, Progressive Via 1 gene: MAPT 10.76 2
114. Aluminum Pick Disease of the Brain Via 1 gene: MAPT 10.76 2
115. Aluminum Nervous System Diseases Via 1 gene: OGDH 10.72 1
116. Aluminum Acatalasia Via 1 gene: CAT 10.66 1
117. Aluminum RENAL TUBULAR DYSGENESIS Via 1 gene: ACE 10.61 1
118. Aluminum Gaucher Disease Via 1 gene: ACE 10.61 1
119. fluoroaluminum Hernia, Diaphragmatic Via 1 gene: IGF2 10.54 1
120. Aluminum Ulcer Via 1 gene: PLA2G4A 10.53 1
121. Aluminum Cerebral Amyloid Angiopathy Via 1 gene: APP 10.52 1
122. Aluminum Osteonecrosis Via 1 gene: MMP2 10.47 1
123. Aluminum Maxillary Diseases Via 1 gene: MMP2 10.47 1
124. Aluminum Bone Diseases Via 1 gene: MMP2 10.47 1
125. Aluminum Urinary Tract Infections Via 1 gene: NOS2 10.37 1
126. Aluminum Mandibuloacral dysplasia with type A lipodystrophy Via 1 gene: MMP9 10.26 1
127. Aluminum Iron Metabolism Disorders Via 1 gene: TFRC 10.22 2
128. Aluminum Central Nervous System Diseases Via 1 gene: ACE 10.21 1
129. Aluminum Hyperthyroxinemia Via 1 gene: ALB 10.20 1
130. Aluminum Nose Neoplasms Via 1 gene: MMP2 10.07 1
131. Aluminum Bone Diseases, Metabolic Via 1 gene: MMP2 10.07 1
132. Aluminum Mandibular Diseases Via 1 gene: MMP2 10.07 1
133. fluoroaluminum Melanoma Via 1 gene: PTK2B 10.04 1
134. Aluminum Heart Defects, Congenital Via 1 gene: GNAQ 9.99 1
135. Aluminum Dermatitis Via 1 gene: PLA2G4A 9.98 1
136. Aluminum Hypertriglyceridemia Via 1 gene: APOB 9.96 1
137. Aluminum beta-Thalassemia Via 1 gene: TFRC 9.93 1
138. Aluminum Tauopathies Via 1 gene: MAPT 9.92 1
139. Aluminum Respiratory Insufficiency Via 1 gene: MAPT 9.92 1
140. Aluminum Peripheral Nervous System Diseases Via 1 gene: GFAP 9.92 1
141. Aluminum Bone Resorption Via 1 gene: PTH 9.92 1
142. Aluminum Dystonia Via 1 gene: SLC2A1 9.89 1
143. Aluminum Listeriosis Via 1 gene: TNF 9.84 1
144. Aluminum Glomerulonephritis, IGA Via 1 gene: ACE 9.80 1
145. Aluminum HIV Seropositivity Via 1 gene: ALB 9.80 1
146. fluoroaluminum Arthritis, Experimental Via 1 gene: ABCB1 9.77 1
147. Aluminum Carbon Tetrachloride Poisoning Via 1 gene: LTF 9.75 1
148. Aluminum Helicobacter Infections Via 1 gene: TFRC 9.71 2
149. fluoroaluminum Colonic Neoplasms Via 1 gene: IGF2 9.67 1
150. Aluminum Restless Legs Syndrome Via 1 gene: TF 9.65 1
151. Aluminum Hyperlipoproteinemia Type II Via 1 gene: APOB 9.60 1
152. Aluminum Aortic Aneurysm Via 1 gene: MMP9 9.57 1
153. Aluminum Lead Poisoning Via 1 gene: MMP9 9.57 1
154. fluoroaluminum Carcinoma, Hepatocellular Via 1 gene: PTK2 9.57 1
155. Aluminum Carcinoma in Situ Via 1 gene: PTGS2 9.56 2
156. Aluminum Leiomyosarcoma Via 1 gene: PTGS2 9.56 1
157. Aluminum Wounds and Injuries Via 1 gene: LTF 9.55 1
158. Aluminum Bipolar Disorder Via 1 gene: S100B 9.44 1
159. Aluminum Dementia Via 1 gene: MAPT 9.39 1
160. fluoroaluminum Inflammatory Bowel Diseases Via 1 gene: ABCB1 9.38 1
161. fluoroaluminum Epilepsy Via 1 gene: ABCB1 9.38 2
162. Aluminum Atrial Fibrillation Via 1 gene: ACE 9.37 1
163. Aluminum Infarction, Middle Cerebral Artery Via 1 gene: MMP9 9.35 1
164. Aluminum Cerebral Hemorrhage Via 1 gene: MMP9 9.35 1
165. Aluminum Pre-Eclampsia Via 1 gene: ACE 9.30 1
166. Aluminum Hypercholesterolemia Via 1 gene: APOB 9.28 1
167. Aluminum Arrhythmias, Cardiac Via 1 gene: ACE 9.24 1
168. Aluminum Heart Failure Via 1 gene: PTH 9.22 1
169. Aluminum Hypersensitivity, Immediate Via 1 gene: IL4 9.20 1
170. Aluminum Bronchopulmonary Dysplasia Via 1 gene: IL1B 9.20 1
171. Aluminum Diabetic Nephropathies Via 1 gene: ACE 9.18 1
172. Aluminum Infection Via 1 gene: TNF 9.15 1
173. Aluminum Atrophy Via 1 gene: MAPK3 9.11 1
174. Aluminum Occupational Diseases Via 1 gene: MPO 9.05 1
175. Aluminum Intervertebral disc disease Via 1 gene: MMP9 9.02 1
176. Aluminum Parkinsonian Disorders Via 1 gene: MAPT 8.99 1
177. Aluminum Asbestosis Via 1 gene: NOS2 8.99 1
178. Aluminum Schistosomiasis mansoni Via 1 gene: NOS2 8.99 1
179. Aluminum Nasopharyngeal Neoplasms Via 1 gene: MMP2 8.98 1
180. Aluminum Hyperinsulinism Via 1 gene: GPX1 8.96 2
181. Aluminum Anemia, Hemolytic Via 1 gene: GPX1 8.96 1
182. Aluminum Lymphoma, Non-Hodgkin Via 1 gene: TFRC 8.94 1
183. Aluminum Stroke Via 1 gene: ACE 8.93 1
184. fluoroaluminum Autistic Disorder Via 1 gene: IGF2 8.84 1
185. Aluminum Stevens-Johnson Syndrome Via 1 gene: ALB 8.82 1
186. Aluminum Hypertension, Pulmonary Via 1 gene: ACE 8.81 1
187. Aluminum Hypothermia Via 1 gene: TNF 8.74 1
188. Aluminum Bronchiectasis Via 1 gene: TNF 8.74 1
189. Aluminum Hyperglycemia Via 1 gene: GPX1 8.66 1
190. Aluminum Arthritis, Psoriatic Via 1 gene: NOS2 8.43 1
191. Aluminum Cardiovascular Diseases Via 1 gene: ACE 8.41 1
192. Aluminum Entamoebiasis Via 1 gene: IL1B 8.36 1
193. Aluminum Intestinal Polyps Via 1 gene: PTGS2 8.31 3
194. Aluminum Infertility, Male Via 1 gene: ACE 8.29 1
195. Aluminum Kidney Failure, Chronic Via 1 gene: CAT 8.28 1
196. Aluminum Leukemia, Myeloid, Acute Via 1 gene: ENO2 8.23 1
197. Aluminum Kidney Diseases Via 1 gene: ACE 8.08 1
198. Aluminum Soft Tissue Neoplasms Via 1 gene: TNF 8.06 2
199. Aluminum Poisoning Via 1 gene: ACHE 8.03 1
200. Aluminum ALLERGIC RHINITIS Via 1 gene: PTGS2 7.96 1
201. Aluminum Coronary Restenosis Via 1 gene: TNF 7.90 1
202. Aluminum Lymphoma, B-Cell Via 1 gene: PTGS2 7.86 1
203. Aluminum Carcinoma, Transitional Cell Via 1 gene: PTGS2 7.86 3
204. Aluminum Neoplasms Via 1 gene: LTF 7.84 1
205. Aluminum Asthma, Aspirin-Induced Via 1 gene: PTGS2 7.78 1
206. Aluminum Tongue Neoplasms Via 1 gene: PTGS2 7.78 1
207. Aluminum Intestinal Diseases Via 1 gene: NOS2 7.75 1
208. Aluminum Arthritis, Experimental Via 1 gene: IL4 7.73 1
209. Aluminum Epilepsy Via 1 gene: GPX1 7.71 1
210. fluoroaluminum Liver Cirrhosis, Experimental Via 1 gene: ABCB1 7.64 1
211. Aluminum Dermatitis, Allergic Contact Via 1 gene: IL4 7.63 1
212. Aluminum Adenomatous Polyposis Coli Via 1 gene: PTGS2 7.63 1
213. Aluminum Liver Cirrhosis Via 1 gene: MMP2 7.60 1
214. Aluminum Cardiomyopathy, Dilated Via 1 gene: GPX1 7.52 1
215. Aluminum Myocardial Reperfusion Injury Via 1 gene: NOS2 7.50 1
216. Aluminum HYPERTENSION, ESSENTIAL Via 1 gene: NOS2 7.50 1
217. Aluminum Depressive Disorder Via 1 gene: ALB 7.47 1
218. Aluminum Weight Gain Via 1 gene: TNF 7.46 1
219. Aluminum Carcinoma Via 1 gene: PTGS2 7.38 1
220. Aluminum Hemochromatosis Via 1 gene: TNF 7.29 1
221. Aluminum Anemia Via 1 gene: TNF 7.15 1
222. Aluminum Hyperhomocysteinemia Via 1 gene: TNF 7.09 1
223. Aluminum Sarcoma Via 1 gene: TNF 7.09 3
224. Aluminum HIV Infections Via 1 gene: ALB 7.05 1
225. Aluminum Cardiomyopathies Via 1 gene: PTGS2 7.03 1
226. Aluminum Kidney Neoplasms Via 1 gene: PTGS2 6.95 1
227. Aluminum Lupus Erythematosus, Systemic Via 1 gene: IL4 6.95 1
228. Aluminum Urticaria Via 1 gene: TNF 6.78 1
229. Aluminum Diabetes Mellitus, Type 1 Via 1 gene: CAT 6.71 1
230. Aluminum Acute Kidney Injury Via 1 gene: TNF 6.70 1
231. Aluminum Diabetes Mellitus, Experimental Via 1 gene: TNF 6.66 1
232. Aluminum Hyperalgesia Via 1 gene: TNF 6.58 3
233. Aluminum Crohn Disease Via 1 gene: TNF 6.51 1
234. Aluminum Diabetes Mellitus, Type 2 Via 1 gene: CAT 6.31 1
235. Aluminum Migraine Disorders Via 1 gene: TNF 6.31 1
236. Aluminum Reperfusion Injury Via 1 gene: TNF 6.26 2
237. Aluminum Adenocarcinoma Via 1 gene: PTGS2 6.01 3
238. Aluminum Pain Via 1 gene: TNF 5.98 1
239. Aluminum Hernia, Diaphragmatic Via 1 gene: TNF 5.98 1
240. Aluminum Ovarian Neoplasms Via 1 gene: MAPK3 5.95 1
Abstract
OBJECTIVE: To compare epidemiological studies dealing with neurological issues (compatible with Hg toxicity) linked to exposing newborns and infants to intramuscular doses of preservative-Hg resulting from vaccination with thimerosal-containing vaccines (TCV).
METHODS: Major databases were searched for studies that addressed neurodevelopment outcomes other than autism. Eight studies were identified and compared.
RESULTS: Information extracted from the studies done in the USA, the UK, and Italy is important in understanding the complex interplay of variables but insufficient to establish non-toxicity for infants and young children still receiving TCV: a) there is ambiguity in some studies reporting neurodevelopment outcomes that seem to depend on confounding variables; b) the risk of neurotoxicity due to low doses of thimerosal is plausible at least for susceptible infants; c) there is a need to address these issues in less developed countries still using TCV in pregnant mothers, newborns, and young children.
CONCLUSIONS: Since the use of TCV is still inevitable in many countries, this increases the need to protect vulnerable infants and promote actions that strengthen neurodevelopment. Developing countries should intensify campaigns that include breastfeeding among efforts to help prime the central nervous system to tolerate exposure to neurotoxic substances, especially thimerosal-Hg.
Source: Clin Chim Acta. 2010 Nov 11;411(21-22):1580-6. Epub 2010 Jul 16
The reason for the rapid rise of autism in the United States that began in the 1990s is a mystery. Although individuals probably have a genetic predisposition to develop autism, researchers suspect that one or more environmental triggers are also needed. One of those triggers might be the battery of vaccinations that young children receive. Using regression analysis and controlling for family income and ethnicity, the relationship between the proportion of children who received the recommended vaccines by age 2 years and the prevalence of autism (AUT) or speech or language impairment (SLI) in each U.S. state from 2001 and 2007 was determined. A positive and statistically significant relationship was found: The higher the proportion of children receiving recommended vaccinations, the higher was the prevalence of AUT or SLI. A 1% increase in vaccination was associated with an additional 680 children having AUT or SLI. Neither parental behavior nor access to care affected the results, since vaccination proportions were not significantly related (statistically) to any other disability or to the number of pediatricians in a U.S. state. The results suggest that although mercury has been removed from many vaccines, other culprits may link vaccines to autism. Further study into the relationship between vaccines and autism is warranted.
Source: J Toxicol Environ Health A. 2011 Jan;74(14):903-16.
http://www.ncbi.nlm.nih.gov/pubmed/21623535
Aluminum-based adjuvants (aluminum salts or alum) are widely used in human vaccination, although their mechanisms of action are poorly understood. Here we report that, in mice, alum causes cell death and the subsequent release of host cell DNA, which acts as a potent endogenous immunostimulatory signal mediating alum adjuvant activity. Furthermore, we propose that host DNA signaling differentially regulates IgE and IgG1 production after alum-adjuvanted immunization. We suggest that, on the one hand, host DNA induces primary B cell responses, including IgG1 production, through interferon response factor 3 (Irf3)-independent mechanisms. On the other hand, we suggest that host DNA also stimulates 'canonical' T helper type 2 (TH2) responses, associated with IgE isotype switching and peripheral effector responses, through Irf3-dependent mechanisms. The finding that host DNA released from dying cells acts as a damage-associated molecular pattern that mediates alum adjuvant activity may increase our understanding of the mechanisms of action of current vaccines and help in the design of new adjuvants.
Source: http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.2403.html
"In addition to the multidose vaccines containing thimerosal discussed above, some companies offer a 0.5 mg/L single dose, pre-filled syringe vaccine. Some of these products are labeled “preservative- or thimerosal-free”. Preservative-free products may contain trace amounts (less than or equal to 1 microgram/0.5 mL dose) because thimerosal was used during the manufacturing process. The term preservative- or thimerosal-free can be utilized if the manufacturer further purified the product, leaving only trace amounts (less than or equal to 1 microgram/0.5 mL) per dose. Even at this level, calculations indicate mercury would exceed the TCLP standard; therefore these vaccines, if deemed unusable, should be managed as hazardous waste as well."
Source: South Dakota Waste Management Guidelines - http://www.iaomt.org/news/files/files372/Thimerosal%20-%20South%20Dakota%20Waste%20Mgmt%20Guidelines.pdf
Pink disease (infantile acrodynia) was especially prevalent in the first half of the 20th century. Primarily attributed to exposure to mercury (Hg) commonly found in teething powders, the condition was developed by approximately 1 in 500 exposed children. The differential risk factor was identified as an idiosyncratic sensitivity to Hg. Autism spectrum disorders (ASD) have also been postulated to be produced by Hg. Analogous to the pink disease experience, Hg exposure is widespread yet only a fraction of exposed children develop an ASD, suggesting sensitivity to Hg may also be present in children with an ASD. The objective of this study was to test the hypothesis that individuals with a known hypersensitivity to Hg (pink disease survivors) may be more likely to have descendants with an ASD. Five hundred and twenty-two participants who had previously been diagnosed with pink disease completed a survey on the health outcomes of their descendants. The prevalence rates of ASD and a variety of other clinical conditions diagnosed in childhood (attention deficit hyperactivity disorder, epilepsy, Fragile X syndrome, and Down syndrome) were compared to well-established general population prevalence rates. The results showed the prevalence rate of ASD among the grandchildren of pink disease survivors (1 in 25) to be significantly higher than the comparable general population prevalence rate (1 in 160). The results support the hypothesis that Hg sensitivity may be a heritable/genetic risk factor for ASD.
Source: Journal of Toxicology and Environmental Health, Part A
Volume 74, Issue 18, 2011
Autism spectrum disorders (ASD) are serious multisystem developmental disorders and an urgent global public health concern. Dysfunctional immunity and impaired brain function are core deficits in ASD. Aluminum (Al), the most commonly used vaccine adjuvant, is a demonstrated neurotoxin and a strong immune stimulator. Hence, adjuvant Al has the potential to induce neuroimmune disorders. When assessing adjuvant toxicity in children, two key points ought to be considered: (i) children should not be viewed as “small adults” as their unique physiology makes them much more vulnerable to toxic insults; and (ii) if exposure to Al from only few vaccines can lead to cognitive impairment and autoimmunity in adults, is it unreasonable to question whether the current pediatric schedules, often containing 18 Al adjuvanted vaccines, are safe for children? By applying Hill's criteria for establishing causality between exposure and outcome we investigated whether exposure to Al from vaccines could be contributing to the rise in ASD prevalence in the Western world. Our results show that: (i) children from countries with the highest ASD prevalence appear to have the highest exposure to Al from vaccines; (ii) the increase in exposure to Al adjuvants significantly correlates with the increase in ASD prevalence in the United States observed over the last two decades (Pearson r = 0.92, p < 0.0001); and (iii) a significant correlation exists between the amounts of Al administered to preschool children and the current prevalence of ASD in seven Western countries, particularly at 3–4 months of age (Pearson r = 0.89–0.94, p = 0.0018–0.0248). The application of the Hill's criteria to these data indicates that the correlation between Al in vaccines and ASD may be causal. Because children represent a fraction of the population most at risk for complications following exposure to Al, a more rigorous evaluation of Al adjuvant safety seems warranted.
Source: Journal of Inorganic Biochemistry, doi:10.1016/j.jinorgbio.2011.08.008 http://www.sciencedirect.com/science/article/pii/S0162013411002212
This review covers the occurrence of aluminium in soil, air, water and food. In addition, aluminium levels in body tissues and its movement within the body have been considered. The adverse effects of aluminium that have been reported in recent years include Alzheimer's disease, dementia and hyperactivity and learning disorders in children.
Source: J R Soc Health. 1991 Oct;111(5):163-8
Immune challenges during early development, including those vaccine-induced, can lead to permanent detrimental alterations of the brain and immune function. Experimental evidence also shows that simultaneous administration of as little as two to three immune adjuvants can overcome genetic resistance to autoimmunity. In some developed countries, by the time children are 4 to 6 years old, they will have received a total of 126 antigenic compounds along with high amounts of aluminum (Al) adjuvants through routine vaccinations. According to the US Food and Drug Administration, safety assessments for vaccines have often not included appropriate toxicity studies because vaccines have not been viewed as inherently toxic. Taken together, these observations raise plausible concerns about the overall safety of current childhood vaccination programs. When assessing adjuvant toxicity in children, several key points ought to be considered: (i) infants and children should not be viewed as "small adults" with regard to toxicological risk as their unique physiology makes them much more vulnerable to toxic insults; (ii) in adult humans Al vaccine adjuvants have been linked to a variety of serious autoimmune and inflammatory conditions (i.e., "ASIA"), yet children are regularly exposed to much higher amounts of Al from vaccines than adults; (iii) it is often assumed that peripheral immune responses do not affect brain function. However, it is now clearly established that there is a bidirectional neuro-immune cross-talk that plays crucial roles in immunoregulation as well as brain function. In turn, perturbations of the neuro-immune axis have been demonstrated in many autoimmune diseases encompassed in "ASIA" and are thought to be driven by a hyperactive immune response; and (iv) the same components of the neuro-immune axis that play key roles in brain development and immune function are heavily targeted by Al adjuvants. In summary, research evidence shows that increasing concerns about current vaccination practices may indeed be warranted. Because children may be most at risk of vaccine-induced complications, a rigorous evaluation of the vaccine-related adverse health impacts in the pediatric population is urgently needed.
Source: Lupus. 2012;21(2):223-30. http://www.ncbi.nlm.nih.gov/pubmed/22235057
The first conjugate vaccine was approved for use in the US in 1988 to protect infants and young children against the capsular bacteria Haemophilus influenzae type b (Hib). Since its introduction in the US, this vaccine has been approved in most developed countries, including Denmark and Israel where the vaccine was added to their national vaccine programs in 1993 and 1994, respectively. There have been marked increases in the reported prevalence of autism spectrum disorders (ASDs) among children in the US beginning with birth cohorts in the late 1980s and in Denmark and Israel starting approximately 4-5 years later. Although these increases may partly reflect ascertainment biases, an exogenous trigger could explain a significant portion of the reported increases in ASDs. It is hypothesized here that the introduction of the Hib conjugate vaccine in the US in 1988 and its subsequent introduction in Denmark and Israel could explain a substantial portion of the initial increases in ASDs in those countries. The continuation of the trend toward increased rates of ASDs could be further explained by increased usage of the vaccine, a change in 1990 in the recommended age of vaccination in the US from 15 to 2 months, increased immunogenicity of the vaccine through changes in its carrier protein, and the subsequent introduction of the conjugate vaccine for Streptococcus pneumoniae. Although conjugate vaccines have been highly effective in protecting infants and young children from the significant morbidity and mortality caused by Hib and S. pneumoniae, the potential effects of conjugate vaccines on neural development merit close examination. Conjugate vaccines fundamentally change the manner in which the immune systems of infants and young children function by deviating their immune responses to the targeted carbohydrate antigens from a state of hypo-responsiveness to a robust B2 B cell mediated response. This period of hypo-responsiveness to carbohydrate antigens coincides with the intense myelination process in infants and young children, and conjugate vaccines may have disrupted evolutionary forces that favored early brain development over the need to protect infants and young children from capsular bacteria.
Source: Med Hypotheses. 2011 Dec;77(6):940-7. http://www.ncbi.nlm.nih.gov/pubmed/21993250#
Watch this video done by a university of mercury destroying brain cells:
http://www.youtube.com/watch?v=IHqVDMr9ivo
Donald Trump chose the fifth annual World Autism Awareness Day to reveal on Fox News that he strongly believes that autism is linked to childhood vaccines (video below).
In a Monday interview on Fox News, Trump said: “I’ve seen people where they have a perfectly healthy child, and they go for the vaccinations and a month later the child is no longer healthy. It happened to somebody that worked for me recently. I mean, they had this beautiful child, not a problem in the world, and all of the sudden they go in and they get this monster shot."
"You ever see the size of it? It’s like they’re pumping in — you know, it’s terrible, the amount. And they pump this in to this little body and then all of the sudden the child is different a month later. I strongly believe that’s it.”
Source: Opposing Views, 2nd April 2012. http://www.opposingviews.com/i/health/autism/video-donald-trump-claims-autism-caused-vaccines?page=2
Basic google translation from Italian:
This judgment No. 2010/148, part No. 2010/0474, journal.n ° 2012/886, gave the appeal lodged by parents against the Department of Health, who demanded the payment of compensation for irreversible complications caused by a vaccine.
Le vaccin en question est le ROR . The vaccine is MMR. Selon les parents, en fait, les symptômes de l'autisme de leur fils sont vraiment apparus à la suite de l'inoculation. According to parents, in fact, symptoms of autism in their son did appear after inoculation.
Et vraiment le jour même, comme lu dans le jugement . And really the same day, as read in the judgment . Au retour du dispensaire de Riccione, le 26 mars 2004, l'enfant a commencé à manifester des symptômes préoccupants (diarrhée et nervosité) puis entre 2004 et 2005 sont survenus des signes de grave détresse psycho-physique jusqu'à la reconnaissance, le 7 août 2007, de l'invalidité totale et permanente à 100%. Return to the clinic in Riccione, March 26, 2004, the child began to show troubling symptoms (diarrhea and nervousness) and then between 2004 and 2005 occurred signs of severe psychological distress to physical recognition, 7 August 2007, the total and permanent disability to 100%.
That it was told the vaccination, the specialist Niglio had already stated in June 2008 and the confirmation came a year later by the specialist Montanari. Le lien, selon le jugement est donc « établi ». Jusqu'à condamner le ministère de la Santé à payer une indemnité . The link, in the judgment is "established." Up condemn the Ministry of Health to pay compensation.
Le jugement a provoqué une « grande confusion » entre les experts du Conseil Scientifique du Calendrier Vaccinal pour la Vie, qui rassemble des personnalités de hauts rangs de l'Hygiène et de la Santé Publique, de la Médecine Générale, de la Pédiatrie régionale-hospitalière et universitaire chapeautant la Société Italienne de l'Hygiène, de la Médecine Préventive et de la Santé Publique (SItI), la Fédération Italienne des Médecins de Médecine Générale (Fimmg), la Fédération Italienne des Médecins Pédiatres (Fimp) et la Société Italienne de Pédiatrie (Sip). The judgment has caused "great confusion" between the experts of the Scientific Council of the immunization schedule for Life, which brings together people with high ranks of Hygiene and Public Health, General Practice, the Regional Pediatric Hospital- university umbrella and the Italian Society of Hygiene, Preventive Medicine and Public Health (ITIS), the Italian Federation of General Practice Doctors (Fimmg), the Italian Federation of Paediatricians Doctors (FIMP) and the Italian Society of Pediatrics (Sip)..........
Finally, to prevent this negative judgment set a precedent on professional dynamics, the Council hopes that the Ministry of Health, as an advocate in the case which led to the controversial judgment of first instance, will appeal to the Court of Bologna. A cette fin, les membres du Conseil se rendent « disponibles à aider le bureau du Procureur Général à fournir conseils et littératures scientifiques valables pour souligner en particulier l'incapacité de cette vaccination spécifique à créer des antécédents provocant l'autisme». To this end, Council members will make "available to assist the Attorney General's office to provide advice and valid scientific literature to highlight in particular the failure of this specific vaccination to create provocative history of autism."
Source: http://translate.googleusercontent.com/translate_c?hl=en&prev=/search%3Fq%3DCas%2Bd%2527autisme:%2Bpour%2Ble%2Btribunal%2Bde%2BRimini,%2B%2527c%2527est%2Bla%2Bfaute%2Bdu%2Bvaccin%2527%26hl%3Den%26biw%3D1173%26bih%3D647%26prmd%3Dimvns&rurl=translate.google.com&sl=fr&u=http://www.initiativecitoyenne.be/article-cas-d-autisme-pour-le-tribunal-de-rimini-c-est-la-faute-du-vaccin-104129856.html&usg=ALkJrhjs2U-ZQiHqQPXw1J3uvvNLWphQOQ
Aluminum is an experimentally demonstrated neurotoxin and the most commonly used vaccine adjuvant. Despite almost 90 years of widespread use of aluminum adjuvants, medical science's understanding about their mechanisms of action is still remarkably poor. There is also a concerning scarcity of data on toxicology and pharmacokinetics of these compounds. In spite of this, the notion that aluminum in vaccines is safe appears to be widely accepted. Experimental research, however, clearly shows that aluminum adjuvants have a potential to induce serious immunological disorders in humans. In particular, aluminum in adjuvant form carries a risk for autoimmunity, long-term brain inflammation and associated neurological complications and may thus have profound and widespread adverse health consequences. In our opinion, the possibility that vaccine benefits may have been overrated and the risk of potential adverse effects underestimated, has not been rigorously evaluated in the medical and scientific community. We hope that the present paper will provide a framework for a much needed and long overdue assessment of this highly contentious medical issue.
Source: Curr Med Chem. 2011;18(17):2630-7. http://www.ncbi.nlm.nih.gov/pubmed/21568886
Autoimmunity to the central nervous system (CNS), especially to myelin basic protein (MBP), may play a causal role in autism, a neurodevelopmental disorder. Because many autistic children harbor elevated levels of measles antibodies, we conducted a serological study of measles-mumps-rubella (MMR) and MBP autoantibodies. Using serum samples of 125 autistic children and 92 control children, antibodies were assayed by ELISA or immunoblotting methods. ELISA analysis showed a significant increase in the level of MMR antibodies in autistic children. Immunoblotting analysis revealed the presence of an unusual MMR antibody in 75 of 125 (60%) autistic sera but not in control sera. This antibody specifically detected a protein of 73-75 kD of MMR. This protein band, as analyzed with monoclonal antibodies, was immunopositive for measles hemagglutinin (HA) protein but not for measles nucleoprotein and rubella or mumps viral proteins. Thus the MMR antibody in autistic sera detected measles HA protein, which is unique to the measles subunit of the vaccine. Furthermore, over 90% of MMR antibody-positive autistic sera were also positive for MBP autoantibodies, suggesting a strong association between MMR and CNS autoimmunity in autism. Stemming from this evidence, we suggest that an inappropriate antibody response to MMR, specifically the measles component thereof, might be related to pathogenesis of autism.
Source: J Biomed Sci. 2002 Jul-Aug;9(4):359-64. http://www.ncbi.nlm.nih.gov/pubmed/12145534
Considering an autoimmunity and autism connection, brain autoantibodies to myelin basic protein (anti-MBP) and neuron-axon filament protein (anti-NAFP) have been found in autistic children. In this current study, we examined associations between virus serology and autoantibody by simultaneous analysis of measles virus antibody (measles-IgG), human herpesvirus-6 antibody (HHV-6-IgG), anti-MBP, and anti-NAFP. We found that measles-IgG and HHV-6-IgG titers were moderately higher in autistic children but they did not significantly differ from normal controls. Moreover, we found that a vast majority of virus serology-positive autistic sera was also positive for brain autoantibody: (i) 90% of measles-IgG-positive autistic sera was also positive for anti-MBP; (ii) 73% of measles-IgG-positive autistic sera was also positive for anti-NAFP; (iii) 84% of HHV-6-IgG-positive autistic sera was also positive for anti-MBP; and (iv) 72% of HHV-6-IgG-positive autistic sera was also positive for anti-NAFP. This study is the first to report an association between virus serology and brain autoantibody in autism; it supports the hypothesis that a virus-induced autoimmune response may play a causal role in autism.
Source: Clin Immunol Immunopathol. 1998 Oct;89(1):105-8. http://www.ncbi.nlm.nih.gov/pubmed/9756729
There is a need to interpret neurotoxic studies to help deal with uncertainties surrounding pregnant mothers, newborns and young children who must receive repeated doses of Thimerosal-containing vaccines (TCVs). This review integrates information derived from emerging experimental studies (in vitro and in vivo) of low-dose Thimerosal (sodium ethyl mercury thiosalicylate). Major databases (PubMed and Web-of-science) were searched for in vitro and in vivo experimental studies that addressed the effects of low-dose Thimerosal (or ethylmercury) on neural tissues and animal behaviour. Information extracted from studies indicates that: (a) activity of low doses of Thimerosal against isolated human and animal brain cells was found in all studies and is consistent with Hg neurotoxicity; (b) the neurotoxic effect of ethylmercury has not been studied with co-occurring adjuvant-Al in TCVs; (c) animal studies have shown that exposure to Thimerosal-Hg can lead to accumulation of inorganic Hg in brain, and that (d) doses relevant to TCV exposure possess the potential to affect human neuro-development. Thimerosal at concentrations relevant for infants' exposure (in vaccines) is toxic to cultured human-brain cells and to laboratory animals. The persisting use of TCV (in developing countries) is counterintuitive to global efforts to lower Hg exposure and to ban Hg in medical products; its continued use in TCV requires evaluation of a sufficiently nontoxic level of ethylmercury compatible with repeated exposure (co-occurring with adjuvant-Al) during early life.
Source: Neurochem Res. 2011 Jun;36(6):927-38 - http://www.ncbi.nlm.nih.gov/pubmed/21350943
The authors previously published the first epidemiological study from the United States associating thimerosal from childhood vaccines with neurodevelopmental disorders (NDs) based upon assessment of the Vaccine Adverse Event Reporting System (VAERS). A number of years have gone by since their previous analysis of the VAERS. The present study was undertaken to determine whether the previously observed effect between thimerosal-containing childhood vaccines and NDs are still apparent in the VAERS as children have had a chance to further mature and potentially be diagnosed with additional NDs. In the present study, a cohort of children receiving thimerosal-containing diphtheria-tetanus-acellular pertussis (DTaP) vaccines in comparison to a cohort of children receiving thimerosal-free DTaP vaccines administered from 1997 through 2000 based upon an assessment of adverse events reported to the VAERS were evaluated. It was determined that there were significantly increased odds ratios (ORs) for autism (OR = 1.8, p < .05), mental retardation (OR = 2.6, p < .002), speech disorder (OR = 2.1, p < .02), personality disorders (OR = 2.6, p < .01), and thinking abnormality (OR = 8.2, p < .01) adverse events reported to the VAERS following thimerosal-containing DTaP vaccines in comparison to thimerosal-free DTaP vaccines. Potential confounders and reporting biases were found to be minimal in this assessment of the VAERS. It was observed, even though the media has reported a potential association between autism and thimerosal exposure, that the other NDs analyzed in this assessment of the VAERS had significantly higher ORs than autism following thimerosal-containing DTaP vaccines in comparison to thimerosal-free DTaP vaccines. The present study provides additional epidemiological evidence supporting previous epidemiological, clinical and experimental evidence that administration of thimerosal-containing vaccines in the United States resulted in a significant number of children developing NDs.
Source: Int J Toxicol. 2004 Nov-Dec;23(6):369-76 - http://www.ncbi.nlm.nih.gov/pubmed/15764492
Methylmercury (Met-Hg) and ethylmercury (Et-Hg) are powerful toxicants with a range of harmful neurological effects in humans and animals. While Met-Hg is a recognized trigger of oxidative stress and an endocrine disruptor impacting neurodevelopment, the developmental neurotoxicity of Et-Hg, a metabolite of thimerosal (TM), has not been explored. We hypothesized that TM exposure during the perinatal period impairs central nervous system development, and specifically the cerebellum, by the mechanism involving oxidative stress. To test this, spontaneously hypertensive rats (SHR) or Sprague-Dawley (SD) rat dams were exposed to TM (200 μg/kg body weight) during pregnancy (G10-G15) and lactation (P5-P10). Male and female neonates were evaluated for auditory and motor function; cerebella were analyzed for oxidative stress and thyroid metabolism. TM exposure resulted in a delayed startle response in SD neonates and decreased motor learning in SHR male (22.6%), in SD male (29.8%), and in SD female (55.0%) neonates. TM exposure also resulted in a significant increase in cerebellar levels of the oxidative stress marker 3-nitrotyrosine in SHR female (35.1%) and SD male (14.0%) neonates. The activity of cerebellar type 2 deiodinase, responsible for local intra-brain conversion of thyroxine to the active hormone, 3',3,5-triiodothyronine (T3), was significantly decreased in TM-exposed SHR male (60.9%) pups. This coincided with an increased (47.0%) expression of a gene negatively regulated by T3, Odf4 suggesting local intracerebellar T3 deficiency. Our data thus demonstrate a negative neurodevelopmental impact of perinatal TM exposure which appears to be both strain- and sex-dependent.
Source: Cerebellum. 2012 Jun;11(2):575-86 - http://www.ncbi.nlm.nih.gov/pubmed/22015705
Thimerosal, a mercury-containing vaccine preservative, is a suspected factor in the etiology of neurodevelopmental disorders. We previously showed that its administration to infant rats causes behavioral, neurochemical and neuropathological abnormalities similar to those present in autism. Here we examined, using microdialysis, the effect of thimerosal on extracellular levels of neuroactive amino acids in the rat prefrontal cortex (PFC). Thimerosal administration (4 injections, i.m., 240 μg Hg/kg on postnatal days 7, 9, 11, 15) induced lasting changes in amino acid overflow: an increase of glutamate and aspartate accompanied by a decrease of glycine and alanine; measured 10-14 weeks after the injections. Four injections of thimerosal at a dose of 12.5 μg Hg/kg did not alter glutamate and aspartate concentrations at microdialysis time (but based on thimerosal pharmacokinetics, could have been effective soon after its injection). Application of thimerosal to the PFC in perfusion fluid evoked a rapid increase of glutamate overflow. Coadministration of the neurosteroid, dehydroepiandrosterone sulfate (DHEAS; 80 mg/kg; i.p.) prevented the thimerosal effect on glutamate and aspartate; the steroid alone had no influence on these amino acids. Coapplication of DHEAS with thimerosal in perfusion fluid also blocked the acute action of thimerosal on glutamate. In contrast, DHEAS alone reduced overflow of glycine and alanine, somewhat potentiating the thimerosal effect on these amino acids. Since excessive accumulation of extracellular glutamate is linked with excitotoxicity, our data imply that neonatal exposure to thimerosal-containing vaccines might induce excitotoxic brain injuries, leading to neurodevelopmental disorders. DHEAS may partially protect against mercurials-induced neurotoxicity.
Source: Neurochem Res. 2012 Feb;37(2):436-4 - http://www.ncbi.nlm.nih.gov/pubmed/22015977
Thimerosal, an organomercury compound, has been widely used as a preservative. Therefore, concerns have been raised about its neurotoxicity. We recently demonstrated perturbation of early serotonergic development by prenatal exposure to thimerosal (Ida-Eto et al. (2011) [11]). Here, we investigated whether prenatal thimerosal exposure causes persistent impairment after birth. Analysis on postnatal day 50 showed significant increase in hippocampal serotonin following thimerosal administration on embryonic day 9. Furthermore, not only serotonin, striatal dopamine was significantly increased. These results indicate that embryonic exposure to thimerosal produces lasting impairment of brain monoaminergic system, and thus every effort should be made to avoid the use of thimerosal.
Source: Brain Dev. 2012 May 31 - http://www.ncbi.nlm.nih.gov/pubmed/22658806
Even though neuronal toxicity due to organomercury compounds is well known, thimerosal, an organomercury compound, is widely used in pediatric vaccine preservation. In the present study, we examined whether embryonic exposure to thimerosal affects early development of serotonergic neurons. Thimerosal (1mg Hg/kg) was intramuscularly administered to pregnant rats on gestational day 9 (susceptible time window for development of fetal serotonergic system), and fetal serotonergic neurons were assessed at embryonic day 15 using anti-serotonin antibodies. A dramatic increase in the number of serotonergic neurons localized to the lateral portion of the caudal raphe was observed in thimerosal group (1.9-fold increase, p<0.01 compared to control). These results indicate that embryonic exposure to thimerosal affects early development of serotonergic neurons.
Source: Neurosci Lett. 2011 Nov 14;505(2):61-4 - http://www.ncbi.nlm.nih.gov/pubmed/21669256
Mercury (Hg) exposure is ubiquitous in modern society via vaccines, fish/crustacea, dental amalgam, food, water, and the atmosphere. This article examines Hg exposure in the context of primary exposure to pregnant women and secondary exposure experienced by their unborn babies. Babies in utero are particularly at risk of higher Hg exposure than adults (on a dose/weight basis through maternal Hg transfer via the placenta), and are more susceptible to adverse effects from mercury and its biologically active compounds. It is, therefore, critical that regulatory advisories around maximum safe Hg exposures account for pregnant women and secondary exposure that children in utero experience. This study focused on standardized embryonic and fetal Hg exposures via primary exposure to the pregnant mother of two common Hg sources (dietary fish and parenteral vaccines). Data demonstrated that Hg exposures, particularly during the first trimester of pregnancy, at well-established dose/weight ratios produced severe damage to humans including death. In light of research suggestive of a mercuric risk factor for childhood conditions such as tic disorders, cerebral palsy, and autism, it is essential that Hg advisories account for secondary prenatal human exposures.
Source: Toxicological and Environmental Chemistry,
Low-level prenatal mercury exposure is associated with a greater risk for attention-deficit/hyperactivity disorder-related behaviors, whereas fish consumption during pregnancy was reportedly protective of these behaviors, according to recent study results published in Archives of Pediatrics and Adolescent Medicine.
Non-occupational methylmercury exposure comes primarily from consuming fish, and the FDA has recommended that pregnant women limit their total fish intake to no more than two 6-oz servings per week. However, as a recognized source of omega-3 fatty acids, fish may also benefit brain development, potentially confounding mercury-related risk estimates.
To examine the association of prenatal mercury exposure and fish intake with ADHD-associated behavior, Sharon K. Sagiv, PhD, MPH, of the Boston University School of Public Health, and colleagues analyzed data from the New Bedford birth cohort, a group of infants born between 1993 and 1998.
The researchers analyzed data for children examined at aged 8 years with peripartum maternal hair mercury measures (n=421) or maternal report of fish consumption during pregnancy (n=515). Inattentive and impulsive/hyperactive behaviors were assessed using a teacher rating scale and neuropsychological testing.
According to study results, the median maternal hair mercury level was 0.45 mcg/g (range, 0.03-5.14 mcg/g), and 52% of mothers consumed more than two fish servings weekly.
“In this population-based prospective cohort study, hair mercury levels were consistently associated with ADHD-related behaviors, including inattention and hyperactivity/impulsivity,” Sagiv and colleagues said in a press release. “We also found that higher prenatal fish consumption was protective for these behaviors.”
In multivariable regression models, mercury exposure was associated with inattention and impulsivity/hyperactivity; some outcomes had an apparent threshold with associations at 1 mcg/g or greater of mercury. For instance, at 1 mcg/g or greater, the adjusted risk ratios for mild/markedly atypical inattentive and impulsive/hyperactive behaviors were 1.4 (95% CI, 1.0-1.8) and 1.7 (95% CI, 1.2-2.4), respectively, for an interquartile range (0.5 mcg/g) mercury increase; there was no confounding by fish consumption.
For neuropsychological assessments, mercury and behavior associations were detected primarily for boys. There was a protective association for fish consumption (more than two servings per week) with ADHD-related behaviors, particularly impulsive/hyperactive behaviors (RR=0.4; 95% CI, 0.2-0.6).
“These results suggest that prenatal mercury exposure is associated with a higher risk of ADHD-related behaviors, and fish consumption during pregnancy is associated with a lower risk of these behaviors,” Sagiv and colleagues wrote. “Although a single estimate combining these beneficial vs. detrimental effects vis-à-vis fish intake is not possible with these data, these findings are consistent with a growing literature showing risk of mercury exposure and benefits of maternal consumption of fish on fetal brain development and are important for informing dietary recommendations for pregnant women.”
Source: Infectious Diseases of Children, 1st November 2012.
http://www.healio.com/pediatrics/add-adhd/news/online/%7B7EEB721F-166C-4DB8-B872-523CCB05ED2D%7D/Prenatal-mercury-exposure-elevated-risk-for-ADHD-related-behavior
In a recently published study in the journal Biological Trace Element Research, Arizona State University researchers report that children with autism had higher levels of several toxic metals in their blood and urine compared to typical children. The study involved 55 children with autism ages 5–16 years compared to 44 controls of similar age and gender.
The autism group had significantly higher levels of lead in their red blood cells (+41 percent) and significantly higher urinary levels of lead (+74 percent), thallium (+77 percent), tin (+115 percent), and tungsten (+44 percent). Lead, thallium, tin, and tungsten are toxic metals that can impair brain development and function, and also interfere with the normal functioning of other body organs and systems.
A statistical analysis was conducted to determine if the levels of toxic metals were associated with autism severity, using three different scales of autism severity. It was found that 38-47 percent of the variation of autism severity was associated with the level of several toxic metals, with cadmium and mercury being the most strongly associated.
In the paper about the study, the authors state “We hypothesize that reducing early exposure to toxic metals may help ameliorate symptoms of autism, and treatment to remove toxic metals may reduce symptoms of autism; these hypotheses need further exploration, as there is a growing body of research to support it.”
The study was led by James Adams, a President’s Professor in the School for Engineering of Matter, Transport and Energy, one of ASU’s Ira A. Fulton Schools of Engineering. He directs the ASU Autism/Asperger’s Research Program.
Adams previously published a study on the use of DMSA, an FDA-approved medication for removing toxic metals. The open-label study found that DMSA was generally safe and effective at removing some toxic metals. It also found that DMSA therapy improved some symptoms of autism. The biggest improvement was for children with the highest levels of toxic metals in their urine.
Overall, children with autism have higher average levels of several toxic metals, and levels of several toxic metals are strongly associated with variations in the severity of autism for all three of the autism severity scales investigated.
The study was funded by the Autism Research Institute and the Legacy Foundation.
Source: Full Circle, 25th February 2013 - http://fullcircle.asu.edu/2013/02/study-finds-higher-levels-of-several-toxic-metals-in-children-with-autism/
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