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Some parents of children with autism spectrum disorders have attributed the disorders' onset to vaccines, often citing the mercury-based preservative thiomersal as the cause, and some have filed suit for compensation from vaccine makers. The medical and scientific communities nearly unanimously deny a link between routine childhood vaccines and autism, as no evidence has been found to support this.
originally posted by: Witness2008
a reply to: SkepticOverlord
I think a part one, part two, possibly a part three for such a meaty subject. There are states now attempting to circumvent personal medical freedoms based on uneducated hysterics, seems an important enough subject to provide a complete commentary.
originally posted by: SkepticOverlord
originally posted by: ElectricUniverse
So, why is it that the NLBS folk claim that Wakenfield is one of the main originators of the "anti-vaccine movement"?
Because that's what he did. Previous data did not result in a "movement." In the interest of a concise presentation, we started with the person credited (by many more than us, in fact, just about everyone) for starting the anti-vaccine movement.
What's the big deal?
originally posted by: roth1
Thanks. Sorry to say i am not to find of NLBS. But only to be aware of some things i may not have been. I will do my own research. NLBS seems biased. Sorry but i want to choose about a vaccine. I f you get yourself vaccinated. Why the hell should you care about others. You should be protected if it works so well. Same for the BS about Fluoride. Brush you freaking teeth, don't poison me. Who the hell does NLBS work for? Touting this BS and selling junk to people. Because at the end they seem to recommend it. Not just present cherry picked facts or comments.
originally posted by: Astyanax
a reply to: ElectricUniverse
You quoted the first paragraph of that Wikipedia page in your opening post. Here's the second.
Some parents of children with autism spectrum disorders have attributed the disorders' onset to vaccines, often citing the mercury-based preservative thiomersal as the cause, and some have filed suit for compensation from vaccine makers. The medical and scientific communities nearly unanimously deny a link between routine childhood vaccines and autism, as no evidence has been found to support this.
The article goes on to discuss the encounter between the autism/antivax lobby and the courts in some detail. Essentially, the vaccine courts were set up for a different reason, have made awards to many people who have proved injury (or even a substantial possibility of injury) by vaccines, but they have made only one award relating to an autism case. It was a very special case, described in the Wikipedia article.
Anticancer Res. 1999 May-Jun;19(3B):2173-80.
Cancer risk associated with simian virus 40 contaminated polio vaccine.
Fisher SG1, Weber L, Carbone M.
Author information
Abstract
BACKGROUND:
The presence of SV40 in monkey cell cultures used in the preparation of the polio vaccine from 1955 through 1961 is well documented. Investigations have consistently demonstrated the oncogenic behavior of SV40 in animal models. Early epidemiologic studies were inadequate in demonstrating an increase in cancer incidence associated with contaminated vaccine. Recently, investigators have provided persuasive evidence that SV40 is present in human ependymomas, choroid plexus tumors, bone tumors, and mesotheliomas, however, the etiologic role of the virus in tumorigenesis has not been established.
MATERIALS AND METHODS:
Using data from SEER, we analyzed the incidence of brain tumors, bone tumors, and mesotheliomas from 1973-1993 and the possible relationship of these tumors with the administration of the SV40 contaminated vaccine.
RESULTS:
Our analysis indicates increased rates of ependymomas (37%), osteogenic sarcomas (26%), other bone tumors (34%) and mesothelioma (90%) among those in the exposed as compared to the unexposed birth cohort.
CONCLUSIONS:
These data suggest that there may be an increased incidence of certain cancers among the 98 million persons exposed to contaminated polio vaccine in the U.S.; further investigations are clearly justified.
Fungal Meningitis Outbreak: 13,000 Tainted Shots
By Daniel J. DeNoon
WebMD Health News
Reviewed by Louise Chang, MD
WebMD News Archive
Oct. 9, 2012 – About 13,000 people in 23 states got the fungus-contaminated steroid pain shots in the ongoing outbreak of fungal meningitis.
So far, 119 people who got the shots have come down with fungal infections of the fluid surrounding their spinal cords and brains.
Eleven of those people have died. The case count rises daily, as symptoms of fungal infection can take up to a month to appear, and there's often a delay in case reporting.
...
FDA Warns GSK Over Flu Vaccine Contamination
By Jeff Overley
Law360, New York (June 24, 2014, 2:48 PM ET) -- GlaxoSmithKline PLC failed to take appropriate steps to prevent bacterial contamination of its widely used flu vaccine Flulaval, causing many product batches to become tainted, according to a U.S. Food and Drug Administration warning letter released Tuesday.
The FDA’s letter, which stems from inspections in March and April, describes quality control processes at a GSK plant in Canada that had several loopholes and were applied inconsistently, resulting in microbial contamination that forced drug lots to be discarded.
For example, GSK did not have comprehensive written policies to prevent contamination of purportedly sterile products, and to the extent that policies were in place, they weren’t always followed, the letter charged.
Separately, regulators criticized the performance of GSK’s water purification system, writing that it was found to have missed various types of bacteria, including organisms from a chicken egg hatchery involved in the vaccine’s production. There also is “no set schedule” for disinfecting the system, according to the letter, which said that such cleanings took place twice in 2011, five times in 2012, four times in 2013 and once to date in 2014.
Further, the FDA asserted that manufacturing lapses persisted even after attempts to address them, writing that the production process “continued to generate out-of-specification results for [bacteria] even after several corrective and preventive actions were implemented.”
To rectify the matter, GSK is expected to undertake a “comprehensive and global assessment of all of its manufacturing operations to ensure that all products conform to FDA requirements,” the warning letter said.
...
Fever Plus Mitochondrial Disease Could Be Risk Factors for Autistic Regression
John Shoffner, MD
Medical Neurogenetics, LLC, Atlanta, Georgia, [email protected], Georgia State University, Atlanta, Georgia
Lauren Hyams, PhD
Medical Neurogenetics, LLC, Atlanta, Georgia
Genevieve Niedziela Langley, BS
Medical Neurogenetics, LLC, Atlanta, Georgia
Stephanie Cossette, BS
Medical Neurogenetics, LLC, Atlanta, Georgia
Lauren Mylacraine, BS
Medical Neurogenetics, LLC, Atlanta, Georgia
Jeffrey Dale, BS
Medical Neurogenetics, LLC, Atlanta, Georgia
Lisa Ollis, BS
Medical Neurogenetics, LLC, Atlanta, Georgia
Sara Kuoch, BS
Medical Neurogenetics, LLC, Atlanta, Georgia
Kevin Bennett, HT
Medical Neurogenetics, LLC, Atlanta, Georgia
Audra Aliberti, BS
Medical Neurogenetics, LLC, Atlanta, Georgia
Keith Hyland, PhD
Medical Neurogenetics, LLC, Atlanta, Georgia
Abstract
Autistic spectrum disorders encompass etiologically heterogeneous persons, with many genetic causes. A subgroup of these individuals has mitochondrial disease. Because a variety of metabolic disorders, including mitochondrial disease show regression with fever, a retrospective chart review was performed and identified 28 patients who met diagnostic criteria for autistic spectrum disorders and mitochondrial disease. Autistic regression occurred in 60.7% (17 of 28), a statistically significant increase over the general autistic spectrum disorder population (P < .0001). Of the 17 individuals with autistic regression, 70.6% (12 of 17) regressed with fever and 29.4% (5 of 17) regressed without identifiable linkage to fever or vaccinations.None showed regression with vaccination unless a febrile response was present. Although the study is small, a subgroup of patients with mitochondrial disease may be at risk of autistic regression with fever. Although recommended vaccinations schedules are appropriate in mitochondrial disease, fever management appears important for decreasing regression risk.
Thimerosal-Derived Ethylmercury Is a Mitochondrial Toxin in Human Astrocytes: Possible Role of Fenton Chemistry in the Oxidation and Breakage of mtDNA
Martyn A. Sharpe, * Andrew D. Livingston, and David S. Baskin
Department of Neurosurgery, The Methodist Hospital, 6565 Fannin Street, Houston, TX 77030, USA
*Martyn A. Sharpe: Email: gro.shmt@eprahsam
Academic Editor: Y. James Kang
Abstract
Thimerosal generates ethylmercury in aqueous solution and is widely used as preservative. We have investigated the toxicology of Thimerosal in normal human astrocytes, paying particular attention to mitochondrial function and the generation of specific oxidants. We find that ethylmercury not only inhibits mitochondrial respiration leading to a drop in the steady state membrane potential, but also concurrent with these phenomena increases the formation of superoxide, hydrogen peroxide, and Fenton/Haber-Weiss generated hydroxyl radical. These oxidants increase the levels of cellular aldehyde/ketones. Additionally, we find a five-fold increase in the levels of oxidant damaged mitochondrial DNA bases and increases in the levels of mtDNA nicks and blunt-ended breaks. Highly damaged mitochondria are characterized by having very low membrane potentials, increased superoxide/hydrogen peroxide production, and extensively damaged mtDNA and proteins. These mitochondria appear to have undergone a permeability transition, an observation supported by the five-fold increase in Caspase-3 activity observed after Thimerosal treatment.
...
Oxidative stress precedes mitochondrial dysfunction in gerbil brain after aluminum ingestion
Svetlana Vučetić-Arsića,
Nevena V. Radonjićb,
Marina Jovanovićc,
Vesna Selakovićc,
Tatjana Nikolićb,
Milica Velimirovićb,
Tihomir Stojkovićb,
Andjela Milovanovićd,
Jovica Milovanoviće,
Nataša D. Petronijevićb, , ,
a Special Hospital for Addictions, Teodora Drajzera 44, Belgrade, Serbia
b Institute of Clinical and Medical Biochemistry, School of Medicine, University of Belgrade, Pasterova 2, Belgrade, Serbia
c Military Medical Academy, Crnotravska 1, Belgrade, Serbia
d School of Medicine, University of Belgrade, Clinic for Physical Medicine and Rehabilitation, Clinical Center of Serbia, Visegradska 26, 11000 Belgrade, Serbia
e School of Medicine, University of Belgrade, Institute of Otorhinolaryngology and Maxillofacial Surgery, Clinical Center of Serbia, Visegradska 26, 11000 Belgrade, Serbia
Received 11 October 2012, Revised 10 October 2013, Accepted 12 October 2013, Available online 23 October 2013
Abstract
Several studies suggest that aluminum (Al) intake might increase an individual's risk of developing Alzheimer disease.
The dynamic of changes in acetylcholinesterase (AChE), cytochrome c oxidase (COX), Complex I, superoxide dismutase (SOD) and catalase (CAT) activities, and the lipid peroxide (MDA), superoxide anion (O2−) and thiol (SH) group levels in gerbil's brain after aluminum ingestion were analyzed.
Gerbils that orally received aluminum chloride (LD25 or LD50) were sacrificed 2, 6 or 24 h later. Another group was subacutely treated (21 days; LD10). Controls received saline. Biochemical parameters were measured in cortex, hippocampus, thalamus and nucleus caudatus.
Two hours after acute Al exposure AChE activity and SH group content were decreased and MDA and O2− levels were elevated in all investigated brain structures. The changes of COX and CAT were structure specific. SOD was increased after 6 h. Changes of investigated parameters were also seen after subacute Al treatment.
These results might suggest the presence of additional source of free radicals in early phase of Al poisoning.
Keywords
Aluminum; Oxidative stress; Alzheimer's disease; Cytochrome c oxidase; Gerbils
Wei Sheng Yan Jiu. 2005 Nov;34(6):674-7.
[Effect of aluminum on neuronal mitochondria of rats].
[Article in Chinese]
Zhang QL1, Niu PY, Niu Q, Wang LP.
Author information
Abstract
OBJECTIVE:
To observe and explore the effect of aluminum on mitochondria in nerve cells of rats.
METHODS:
Nerve cells of new born rats (1-3 days) were cultured. Ultrastructure of mitochondria, cell death rate (CDR), reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and MTF were performed to investigate the alteration of mitochondrial structure and functions in cultured nerve cells.
RESULTS:
Aluminum can impair the ultrastructure of cultured nerve cells of rats. Increased CDR, enhanced ROS, decreased MMP, and decreased activity of enzyme in mitochondria were investigated in the group of Al3+ 100 micromol/L and Al3+ 500 micromol/L.
CONCLUSION:
The present study shows that the alteration of mitochondrial structure and functions have played important roles in neurotoxic mechanism induced by aluminum.
Susceptibility of mitochondrial superoxide dismutase to aluminium induced oxidative damage
Vijay Kumara,
Amanjit Balb,
Kiran Dip Gilla, ,
a Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh 160012, India
b Department of Histopathology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
Received 8 September 2008, Revised 1 October 2008, Accepted 1 October 2008, Available online 1 November 2008
Abstract
Aluminium has been implicated in various neurodegenerative diseases but exact mechanism of action is still not known. Mitochondria being a major site of reactive oxygen species production are considered to be target of oxidative stress and it seems that the oxidative damage to mitochondrial proteins may underlie the pathogenesis of aluminium induced neurodegeneration. Thus, the present study was undertaken to reveal the effects of chronic aluminium exposure (10 mg/kg b.wt, intragastrically for 12 weeks) on the oxidative damage to mitochondrial proteins in male albino Wistar rats. Chronic aluminium exposure resulted in decrease in the activity of mitochondrial superoxide dismutase (MnSOD) and aconitase in different regions of rat brain suggesting increased oxidative stress. This decrease in MnSOD activity in turn might be responsible for the increased protein oxidation as observed in our study. All these processes taken together may cause increased oxidative damage to mitochondrial proteins in general. By taking the advantage of recent immunochemical probe for oxidatively modified proteins, we identified MnSOD to be susceptible to oxidative damage in aluminium treated animals. The quantitative RT-PCR analysis for Lon protease, a protease involved in the removal of oxidatively modified proteins from mitochondria, showed decreased mRNA expression suggesting increased oxidative damage and decreased removal of mitochondrial proteins. The identification of specific proteins as targets of oxidative damage may provide new therapeutic measures to reverse the effects of aluminium induced neurodegeneration.
Let's take a look at an earlier study which found cases in which some children developed acute cerebral symptoms within a period of hours after the administration of pertussis vaccine.
As you can see from the abstract above the link between vaccines and autism is far older than the research that Wakefield published.
Science loses ground to pseudo-science because the latter seems to offer more comfort.
There’s another reason I think popularizing science is important, why I try to do it. It’s a foreboding I have — maybe ill-placed — of an America in my children’s generation, or my grandchildren’s generation, when all the manufacturing industries have slipped away to other countries; when we’re a service and information-processing economy; when awesome technological powers are in the hands of a very few, and no one representing the public interest even grasps the issues; when the people (by “the people” I mean the broad population in a democracy) have lost the ability to set their own agendas, or even to knowledgeably question those who do set the agendas; when there is no practice in questioning those in authority; when, clutching our crystals and religiously consulting our horoscopes, our critical faculties in steep decline, unable to distinguish between what’s true and what feels good, we slide, almost without noticing, into superstition and darkness…