From Gary Kohls
http://healthimpactnews.com/
Study: Vaccinated Children Have 2 to 5 Times More Diseases and Disorders Than Unvaccinated Children
A German study released in September 2011 of about 8000 UNVACCINATED children, newborn to 19 years, show vaccinated children have at least 2 to 5 times more diseases and disorders than unvaccinated children.
The results are presented in the bar chart below; the complete data and study results are here. The data is compared to the national German KIGGS health study of the children in the general population. Most of the respondents to the survey were from the U.S.
The results are presented in the bar chart below; the complete data and study results are here. The data is compared to the national German KIGGS health study of the children in the general population. Most of the respondents to the survey were from the U.S.
The data was collected from parents with vaccine-free children via an internet questionnaire by vaccineinjury.info and Andreas Bachmair, a German classical homeopathic practitioner. The website is not a pretty one (including Google ads for vaccines) but the actual data is what counts. The independent study is self-funded and is not sponsored by a large “credible” non-profit or government health organization with political and financial conflicts of interest. Each one of the 8000 cases are actual cases with medical documentation. Three other studies had similar results according to Bachmair and are reported below.
No study of health outcomes of vaccinated people versus unvaccinated has ever been conducted in the U.S. by CDC or any other agency in the 50 years or more of an accelerating schedule of vaccinations (now over 50 doses of 14 vaccines given before kindergarten, 26 doses in the first year). Most data collected by CDC is contained in the Vaccine Adverse Event Reporting System (VAERS) database. The VAERS is generally thought to contain only 3 to 5 percent of reportable incidents. This is simply because only some immediate reactions are reported by doctors; but many are not admitted to be reactions to the vaccine. Most importantly, the VAERS numbers are only immediate reactions, which I would place with a few hours to a few weeks. Long-term vaccine-induced diseases and disorders are not recognized by parents or doctors when these conditions develop perhaps a few months to five years or more and would never be realized to come from multiple vaccinations. In other words, many children and adults have diseases and disorders that are vaccine induced and they never suspect they are from the vaccines, as this study indicates.
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Increased Susceptibility to Thimerosal-Induced Mitochondrial Dysfunction in a Subset of Autism Lymphoblastoid Cell Lines
(Mitochondria Protected by Pre-treatment with the Glutathione Precursor, N-Acetyl Cysteine)
Journal of Toxicology
Volume 2015 (2015), Article ID 573701, 13 pages
http://dx.doi.org/10.1155/
Volume 2015 (2015), Article ID 573701, 13 pages
http://dx.doi.org/10.1155/
Research Article
Department of Pediatrics, University of Arkansas for Medical Sciences, Arkansas Children’s Hospital Research Institute, 13 Children’s Way, Slot 512-41B, Little Rock, AR 72202, USA
Accepted 13 December 2014
Academic Editor: Maria Teresa Colomina
Copyright © 2015 Shannon Rose et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
The association of autism spectrum disorders with oxidative stress, redox imbalance, and mitochondrial dysfunction has become increasingly recognized. In this study, extracellular flux analysis was used to compare mitochondrial respiration in lymphoblastoid cell lines (LCLs) from individuals with autism and unaffected controls exposed to ethylmercury, an environmental toxin known to deplete glutathione and induce oxidative stress and mitochondrial dysfunction. We also tested whether pretreating the autism LCLs with N-acetyl cysteine (NAC) to increase glutathione concentrations conferred protection from ethylmercury. Examination of 16 autism/control LCL pairs revealed that a subgroup (31%) of autism LCLs exhibited a greater reduction in ATP-linked respiration, maximal respiratory capacity, and reserve capacity when exposed to ethylmercury, compared to control LCLs. These respiratory parameters were significantly elevated at baseline in the ethylmercury-sensitive autism subgroup as compared to control LCLs. NAC pretreatment of the sensitive subgroup reduced (normalized) baseline respiratory parameters and blunted the exaggerated ethylmercury-induced reserve capacity depletion. These findings suggest that the epidemiological link between environmental mercury exposure and an increased risk of developing autism may be mediated through mitochondrial dysfunction and support the notion that a subset of individuals with autism may be vulnerable to environmental influences with detrimental effects on development through mitochondrial dysfunction.
1. Introduction
Autism spectrum disorders (ASD) are defined as a heterogeneous group of neurodevelopmental disorders characterized by impairments in communication and social interactions along with restrictive and repetitive behaviors [1]. The incidence of ASD in the United States is currently estimated to be 1 in 68 individuals, and it continues to rise [2]. While the etiology of ASD remains unknown, multiple interacting genetic and environmental factors are thought to contribute to the development of ASD. In addition to behavioral impairments, recent studies indicate that many children with ASD also exhibit impairments in energy production and redox homeostasis [3–5].
Multiple studies have demonstrated the presence of glutathione-mediated redox imbalance and oxidative stress in individuals with ASD [5–11]. Our group has consistently reported decreased concentrations of glutathione (GSH) and several of its metabolic precursors as well as increased oxidized glutathione disulfide (GSSG) and a decreased glutathione redox ratio (GSH/GSSG) in plasma, immune cells, and postmortem brain from children with ASD [4, 5, 11–13]. Oxidative stress and damage have been documented in blood and brain of individuals with ASD including reports of decreased levels and activities of antioxidant enzymes and elevated levels of oxidized lipids, proteins, and DNA [4, 7, 8, 11, 14, 15]. In primary lymphocytes and in lymphoblastoid cell lines (LCLs) derived from children with autistic disorder (AD), we have found that the production of reactive oxygen species (ROS) is elevated as compared to controls [12, 13, 16]. The imbalance between glutathione-mediated antioxidant capacity and ROS production in autism LCLs may cause these cells to be more susceptible to oxidative stress and damage from any exogenous sources of ROS as compared to control LCLs.
Recent evidence indicates that the incidence of mitochondrial dysfunction in ASD may be very high, affecting up to 30% or more of children with ASD [17]. While the etiology of mitochondrial dysfunction in ASD is not known, evidence suggests that oxidative stress may be a key factor driving mitochondrial dysfunction in individuals with ASD [16, 18]. Recently, we demonstrated that LCLs derived from children with AD exhibit abnormal mitochondrial respiration at baseline as well as a more rapid decline in mitochondrial function upon exposure to increasing ROS as compared to LCLs from control children [16]. Importantly, we found that these abnormal mitochondrial parameters were driven by a subgroup consisting of 32% of the AD LCLs (termed AD-A for abnormal), whereas the other autism LCLs (termed AD-N for normal) had mitochondrial parameters similar to controls. Furthermore, we also demonstrated that pretreatment of the AD LCLs with N-acetyl cysteine (NAC) increased intracellular GSH and the GSH/GSSG redox ratio and, in the AD-A subgroup, conferred protection from mitochondrial dysfunction when ROS was increased [18].
Mitochondria are both the primary producers and targets of intracellular ROS due to the continuous low-level production of superoxide that accompanies electron transfer across the inner mitochondrial membrane during oxidative phosphorylation [19]. ROS are also generated from other sources such as activated immune cells [3,17] and prooxidant environmental toxicants such as pesticides, diesel exhaust, and mercury [20–29].
Mercury is one of several environmental toxicants that have been found to have an association with the development of ASD [28, 30–34]. Ethylmercury is an established a sulfhydryl reagent that rapidly binds to and depletes intracellular glutathione and increases intracellular ROS in a dose-dependent manner [12, 35]. We have previously demonstrated that AD LCLs have increased susceptibility to oxidative stress from exposure to ethylmercury such that exposure to ethylmercury resulted in lower intracellular GSH and GSH/GSSG and increased ROS production in AD LCLs as compared to control LCLs [12].
In the present study we tested the hypothesis that the subset of AD LCLs previously found to exhibit mitochondrial dysfunction when challenged with ROS would also exhibit mitochondrial dysfunction when exposed to ethylmercury (i.e., ethylmercury-induced mitochondrial dysfunction). Furthermore, we hypothesized that pretreatment with NAC to increase the intracellular glutathione concentration would confer protection from ethylmercury-induced mitochondrial dysfunction. To this end, we used extracellular flux analysis to measure mitochondrial oxygen consumption in AD and control LCLs transiently exposed to ethylmercury. The AD LCLs were also tested after pretreatment with NAC to determine whether changes in mitochondrial bioenergetics after exposure to ethylmercury could be prevented by NAC-induced increase in intracellular glutathione-mediated redox capacity.
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In conclusion, we have determined that a subgroup of AD LCLs exhibits abnormal mitochondrial respiratory function at baseline and increased vulnerability to mitochondrial dysfunction when exposed to the environmental toxin, ethylmercury. This subgroup of AD LCLs has previously been shown to exhibit increased mitochondrial susceptibility to ROS, suggesting that these cells may be inherently vulnerable to a wide variety of oxidative insults. Pretreatment of this subgroup with NAC improved mitochondrial function at baseline and decreased the loss of mitochondrial reserve capacity in response to ethylmercury. Our data suggest that the abnormal mitochondrial function and increased susceptibility to ethylmercury in the AD-A LCLs may be related to impaired glutathione-mediated antioxidant capacity and chronic oxidative stress, since NAC pretreatment, which could improve glutathione status, appears to partially correct the atypical mitochondrial function in the AD-A LCLs and protect the cells against the toxic effects of ethylmercury. Other prooxidant environmental toxicants associated with ASD such as pesticides and polychlorinated biphenyls (PCBs) should be tested to determine whether these autism LCLs exhibit hypersensitivity to a wide range of prooxidant environmental toxicants as our findings support the notion that a subset of individuals with autism may be vulnerable to environmental influences with detrimental effects on development through mitochondrial dysfunction.
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Full article and references available at: http://www.hindawi.com/
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