Let me start by saying this is neither an anti-vaccine post nor a pro-vaccine post, my intent is that the information you find here will allow you to make an INFORMED-Vaccine decision for you and your family. As parents we have a responsibility to our children to keep them safe and healthy, whether that be teaching them to look both ways before they cross the street or to wash their hands to prevent the spread of germs, or maybe it is nursing them back to health after an infection/flu or feeding them nutritious snacks and meals so they will grow up big and strong… vaccinating our children has long been touted as one of those measures to keep our children safe and healthy until recent debates have made some parents ask, “Are vaccines safe?” and leaves others gasping and wondering “How can they NOT be safe?” because they believe alternative to not vaccinating (mumps, polio, smallpox etc.) cannot be Safe either!
As a mom with my first child, I did not bat an eyelash, we went to the doctor on schedule and got every vaccine on time and on cue. Ding! Ding! Round 2, when my daughter was born we continued to vaccinate and only after MUCH research and MUCH contemplation have I come to a point where I believe as a parent I must QUESTION what is right for MY CHILD- not the “norm”, not the “average”, not the “herd” , but my little girl who cannot tolerate a few drops of food coloring in a vitamin, who cannot tolerate a fresh spray of hairspray on my head, who cannot tolerate a microgram of an alcohol containing additive in her medicine, if she cannot tolerate ALL these things, I have to wonder HOW can her body tolerate these SIMILAR ingredients being injected into her bloodstream? Why and How I have come to ask these questions has been a long road… I will try to outline my thought process here (try to follow me, I know I can jump around a bit, but I promise in my own mind it makes perfect sense!) I outline this here NOT to discourage you to vaccinate your kiddo, THAT is NOT my intention…Vaccines can save lives for some, what instead I HOPE you will do, is look at your child and vaccination with as much TIME and SCRUTINY as you would touring the 5 preschools you want to send them to and camping out at 4am to get into “the One”, or carefully journalling their milestones in their baby book, collecting each lock of hair, and recording those precious first steps and words on tape, or going to pick out the PERFECT holiday outfit for the beautiful Christmas card you will send out to friends and family… Ask Questions until you understand fully… and be confident in the VERY PERSONAL decision that each family should make for each child of their family. I will never judge ANYONE for their decision they make as a parent (for vaccines or otherwise) because whatever decision you make IS the BEST one for that little one that you know more intimately than anyone else on this earth, and I hope that you in turn will not judge any other parent for the decision they make in doing the very best they can for their child.
If you want the OVERVIEW of V is for Vaccine, Watch this VIDEO (free until Nov.5th), if you want the details and the supporting documentation, scroll down…
THE GREATER GOOD video HERE:
The great pediatric debate of the century it seems is “Do vaccines cause Autism?”
If you read about the Andrew Wakefield controversey, you would probably be quick to say: NO vaccines do not cause autism, because it appears from the media’s perspecitive it has been disproven.
BUT, I would caution you to NOT be too quick to make up your mind…based on only media reports and a very public medically/politcally charged debate and look deeper into science…
FACT: In the United states there is a special VACCINE COURT set up to try Vaccine related injuries for damages to those who have been vaccine injured. The pharmaceutical company who manufactured the vaccine is NOT financial liable in any way for ANY injury or death that results from a vaccine that it manufactures under the 1986 National Childhood Vaccine Injury Act (NCVIA)
FACT: Vaccine Injury is real and does happen. As with ANY medical treatment, there are inherent RISKS involved with Vaccines.
Press Relase on IOM adverse events
Vaccine Injury Compensation Table:
FACT: In 2008 a child who has Autism was awarded over $1.5M in damages by Vaccine Court stating:
2006 Case Study about child who Regressed into Autism after Vaccination with an underlying Mitochondrial Disorder:
Coverage of the awarding of $1.5+ Million Dollars to that same family whose child regressed into Autism
Scientific Journal article (2010): Fever plus mitochondrial disease could be risk factors for autistic regression.
J Child Neurol. 2010 Apr;25(4):429-34. Epub 2009 Sep 22.
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. http://www.ncbi.nlm.nih.gov/pubmed/19773461
2008 Interview with Dr. Bruce Cohen about link between Autism and Mitochondrial Disease. (video) http://abcnews.go.com/video/playerIndex?id=5287814
UMDF response to Vaccines and Autism: http://www.umdf.org/site/apps/nlnet/content2.aspx?c=jtJWJaMMIsE&b=4090771&ct=5315239
FACT: The number of Vaccines given to children has more than tripled in the last 27 years.
From the CDC website:
49 Doses Chart: http://www.nvic.org/Downloads/49-Doses-PosterB.aspx
FACT: Childhood vaccines once contained Mercury compounds (thimerisol ie. ethyl mercury thiosalicylate) and when it was removed it was replaced in many vaccines with Aluminum Containing Compounds. Some Vaccines (flu) still contain Mercury containing compounds.
Excipient Table: Ingredients in Vaccines: http://www.vaccinesafety.edu/components-Excipients.htm
Johns Hopkins School of Public Health Thimerosal Content Table and links to Package inserts for US Licensed Vaccines/Flu Shots: http://www.vaccinesafety.edu/thi-table.htm
FACT: Mercury (Thimerisol) and Aluminum have toxicity to the body, including the mitochondria and neurotoxicity.
Thimerosal induces neuronal cell apoptosis by causing cytochrome c and apoptosis-inducing factor release from mitochondria.
“Our data suggest that thimerosal (at nanamolar concentrations) causes apoptosis in neuroblastoma cells by changing the mitochondrial microenvironment.”
Biochemical and molecular basis of thimerosal-induced apoptosis in T cells: a major role of mitochondrial pathway.
The major source of thimerosal (ethyl mercury thiosalicylate) exposure is childhood vaccines. It is believed that the children are exposed to significant accumulative dosage of thimerosal during the first 2 years of life via immunization. Because of health-related concerns for exposure to mercury, we examined the effects of thimerosal on the biochemical and molecular steps of mitochondrial pathway of apoptosis in Jurkat T cells. Thimerosal and not thiosalcylic acid (non-mercury component of thimerosal), in a concentration-dependent manner, induced apoptosis in T cells as determined by TUNEL and propidium iodide assays, suggesting a role of mercury in T cell apoptosis. Apoptosis was associated with depolarization of mitochondrial membrane, release of cytochrome c and apoptosis inducing factor (AIF) from the mitochondria, and activation of caspase-9 and caspase-3, but not of caspase-8. In addition, thimerosal in a concentration-dependent manner inhibited the expression of XIAP, cIAP-1 but did not influence cIAP-2 expression. Furthermore, thimerosal enhanced intracellular reactive oxygen species and reduced intracellular glutathione (GSH). Finally, exogenous glutathione protected T cells from thimerosal-induced apoptosis by upregulation of XIAP and cIAP1 and by inhibiting activation of both caspase-9 and caspase-3. These data suggest that thimerosal induces apoptosis in T cells via mitochondrial pathway by inducing oxidative stress and depletion of GSH. http://www.ncbi.nlm.nih.gov/pubmed/12140745
Aluminum hydroxide injections lead to motor deficits and motor neuron degeneration.
Gulf War Syndrome is a multi-system disorder afflicting many veterans of Western armies in the 1990-1991 Gulf War. A number of those afflicted may show neurological deficits including various cognitive dysfunctions and motor neuron disease, the latter expression virtually indistinguishable from classical amyotrophic lateral sclerosis (ALS) except for the age of onset. This ALS “cluster” represents the second such ALS cluster described in the literature to date. Possible causes of GWS include several of the adjuvants in the anthrax vaccine and others. The most likely culprit appears to be aluminum hydroxide. In an initial series of experiments, we examined the potential toxicity of aluminum hydroxide in male, outbred CD-1 mice injected subcutaneously in two equivalent-to-human doses. After sacrifice, spinal cord and motor cortex samples were examined by immunohistochemistry. Aluminum-treated mice showed significantly increased apoptosis of motor neurons and increases in reactive astrocytes and microglial proliferation within the spinal cord and cortex. Morin stain detected the presence of aluminum in the cytoplasm of motor neurons with some neurons also testing positive for the presence of hyper-phosphorylated tau protein, a pathological hallmark of various neurological diseases, including Alzheimer’s disease and frontotemporal dementia. A second series of experiments was conducted on mice injected with six doses of aluminum hydroxide. Behavioural analyses in these mice revealed significant impairments in a number of motor functions as well as diminished spatial memory capacity. The demonstrated neurotoxicity of aluminum hydroxide and its relative ubiquity as an adjuvant suggest that greater scrutiny by the scientific community is warranted. http://www.ncbi.nlm.nih.gov/pubmed/19740540
Hepatic response to aluminum toxicity: dyslipidemia and liver diseases.
Aluminum (Al) is a metal toxin that has been implicated in the etiology of a number of diseases including Alzheimer’s, Parkinson’s, dialysis encephalopathy, and osteomalacia. Al has been shown to exert its effects by disrupting lipid membrane fluidity, perturbing iron (Fe), magnesium, and calcium homeostasis, and causing oxidative stress. However, the exact molecular targets of aluminum’s toxicity have remained elusive. In the present review, we describe how the use of a systems biology approach in cultured hepatoblastoma cells (HepG2) allowed the identification of the molecular targets of Al toxicity. Mitochondrial metabolism is the main site of the toxicological action of Al. Fe-dependent and redox sensitive enzymes in the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) are dramatically decreased by Al exposure. In an effort to compensate for diminished mitochondrial function, Al-treated cells stabilize hypoxia inducible factor-1α (HIF-1α) to increase ATP production by glycolysis. Additionally, Al toxicity leads to an increase in intracellular lipid accumulation due to enhanced lipogenesis and a decrease in the β-oxidation of fatty acids. Central to these effects is the alteration of α-ketoglutarate (KG) homeostasis. In Al-exposed cells, KG is preferentially used to quench ROS leading to succinate accumulation and HIF-1α stabilization. Moreover, the channeling of KG to combat oxidative stress leads to a reduction of l-carnitine biosynthesis and a concomitant decrease in fatty acid oxidation. The fluidity and interaction of these metabolic modules and the implications of these findings in liver-related disorders are discussed herein. http://www.ncbi.nlm.nih.gov/pubmed/21787768
FACT: Many pediatiricians recommend giving acetominophen to children who develop fever after vaccines. Some propose pre-medicating children before shots are given.
FACT: Children with Austim (and some with Mitochondrial Disease) have noteably LOWER levels of Glutathione (GSH, a tripeptide antioxidant which is one of the body’s most important detoxifying compounds) and Sulfate (plasma sulfate) than controls .
FACT: One dose of Acetaminophen (Tylenol/Practamol) can reduce a child’s sulfate levels in the liver by reducing the amount of glutathione available for detoxification (leaving little glutathione left over to detoxify anything else (adjuvents, food and environmental toxins) (http://emedicine.medscape.com/article/1008683-overview#a0104)
Cellular and mitochondrial glutathione redox imbalance in lymphoblastoid cells derived from children with autism.
Research into the metabolic phenotype of autism has been relatively unexplored despite the fact that metabolic abnormalities have been implicated in the pathophysiology of several other neurobehavioral disorders. Plasma biomarkers of oxidative stress have been reported in autisticchildren; however, intracellular redox status has not yet been evaluated. Lymphoblastoid cells (LCLs) derived from autistic children and unaffected controls were used to assess relative concentrations of reduced glutathione (GSH) and oxidized disulfide glutathione (GSSG) in cell extracts and isolated mitochondria as a measure of intracellular redox capacity. The results indicated that the GSH/GSSG redox ratio was decreased and percentage oxidized glutathione increased in both cytosol and mitochondria in the autism LCLs. Exposure to oxidative stress via the sulfhydryl reagent thimerosal resulted in a greater decrease in the GSH/GSSG ratio and increase in free radical generation in autism compared to control cells. Acute exposure to physiological levels of nitric oxide decreased mitochondrial membrane potential to a greater extent in the autism LCLs, although GSH/GSSG and ATP concentrations were similarly decreased in both cell lines. These results suggest that the autism LCLs exhibit a reduced glutathione reserve capacity in both cytosol and mitochondria that may compromise antioxidant defense and detoxification capacity under prooxidant conditions. http://www.ncbi.nlm.nih.gov/pubmed/19307255
Evaluation of oxidative stress in autism: defective antioxidant enzymes and increased lipid peroxidation.
Autism is a neurodevelopmental disorder of childhood with poorly understood etiology and pathology. This pilot study aims to evaluate the levels of antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and levels of malondialdehyde (MDA), a marker of lipid peroxidation, in Egyptian autistic children. Autism is a neurodevelopmental disorder of childhood with poorly understood etiology and pathology. The present study included 20 children with autism diagnosed by DSM-IV-TR criteria and Childhood Autism Rating Scale. Controls included 25 age-matched healthy children. Cases were referred to Outpatient Clinic of Children with Special Needs Department, National Research Center, Cairo, Egypt. We compared levels of SOD, GSH-Px, and MDA in children with autism and controls. In children less than 6 years of age, levels of SOD, and GSH-Px were significantly lower in autistic children compared with their controls, while MDA was significantly higher among patients than controls. In children older than 6 years, there was no significant difference in any of these values between cases and controls. We concluded that children with autism are more vulnerable to oxidative stress in the form of increased lipid peroxidation and deficient antioxidant defense mechanism especially at younger children. We highlight that autistic children might benefit from antioxidants supplementation coupled with polyunsaturated fatty acids. Moreover, early assessment of antioxidant status would have better prognosis as it may decrease the oxidative stress before inducing more irreversible brain damage. http://www.ncbi.nlm.nih.gov/pubmed/20845086
Sulphation deficit in “low-functioning” autistic children: a pilot study.
Parents of autistic children and autism support groups often report that autistic episodes are exacerbated when the children eat certain foodstuffs such as dairy products, chocolates, wheat, corn sugar, apples, and bananas. The hypothesis that autistic behavior might be related to metabolic dysfunctions has led us to investigate in a group of “low functioning” autistic children and in an age-matched control group each made up of 20 subjects, the sulphation capacity available.
Utilizing the biochemical characteristics of paracetamol we evaluated by high performance liquid chromatography, the urine paracetamol-sulfate/paracetamol-glucuronide (PS/PG) ratio in all subjects following administration of this drug.
The PS/PG ratio in the group of autistic subjects gave a significantly lower results than the control group with p < .00002.
The inability to effectively metabolize certain compounds particularly phenolic amines, toxic for the CNS, could exacerbate the wide spectrum of autistic behavior.
Overview of Acetminophen Toxicity