The scientific community now knows that children with regressive autism have hundreds of de novo and diverse gene mutations. That means that regressive autism is not genetic. It must be triggered by an external event that can create hundreds of different DNA breaks and mutations. That has been clear to us at SCPI since we were founded.
Since 2008, SCPI has been ahead of the field, doing the cutting edge biology, molecular modeling, computational informatics, and ecology to figure out what is causing so many DNA breaks and mutations in our children, long before the 2011 and 2012 publications put the hundreds of de novo mutations together. That’s because we knew that a condition associated with hundreds of different genes could not possibly be genetic. We knew that DNA and retroviral contaminants are present in some childhood vaccines and that these types of contaminants are known to cause DNA breaks and mutations.
Have we created the perfect storm for DNA breaks, mutations, and regressive autism in our children? In 1979 we started injecting our children with vaccines that are contaminated with human fetal DNA fragments and a retrovirus, and autism began to rise. Then we added more jabs with aborted fetal vaccines and thimerosal, which can also cause DNA breaks, to vaccines in 1988, and autism rose more. Then in 1995, we added much more aborted fetal DNA contaminants to the chickenpox vaccine, and autism really rose. And now we have children born to older dads who have sperm with very breakable DNA. Aborted fetal contaminated vaccines plus thimerosal plus older dads result in more DNA breaks, thus more de novo mutations, in our children.
Drugs and vaccines are too large to produce in a test tube, and therefore, they must be manufactured using cell lines. The final products contain contaminants from the cell line used to manufacture the drug or vaccine. When animal cell lines are utilized, these contaminants are recognized by our immune systems as ‘foreign’ and are eliminated from our bodies. However, when primitive human cell lines (such as an aborted fetal cell line) are used, these contaminants have the potential to trigger autoimmune diseases or genomic instability. When we use human fetal produced vaccines or cosmetics, we are also injecting or transferring DNA and viruses from the human fetus used to create the cell line into our own bodies.
SCPI is applying extensive bodies of literature from the study of meiotic recombination, DNA repair mechanisms, and gene therapy to determine the impact of aborted fetal DNA contaminants on autoimmune responses and genomic instability. During meiotic recombination, genetic material from the chromosomes of the father and mother is ‘exchanged’ so that the offspring have genetic material that is an intermixing of maternal and paternal material, creating a completely unique genetic individual. Exchange of genetic material during meiotic recombination is a beneficial process, designed to generate diversity in our offspring. However, inappropriate activation of the proteins involved in meiotic recombination can lead to genomic instability, cancer, and other diseases.
DNA repair is a process that our cells use to correct mistakes introduced into our genes on a daily basis, simply by the fact that we use our genes to make proteins and new cells during cell division. When DNA repair goes awry, genomic instability and disease can be the result. Gene therapy studies have shown us what can happen when inappropriate insertion of external genetic material occurs in our genes: 4 of 9 boys developed cancer in one of the first gene therapy trials.
The contaminants found in vaccines and drugs that are manufactured using human fetal cell lines present the perfect storm of contaminants to cause genomic instability. Some childhood vaccines contain very high levels of short human fetal DNA fragments, which gene therapy studies have taught us are the perfect size to insert into our genes. Some childhood vaccines also contain a retroviral contaminant called HERVK, which is in the same family of retroviruses as the one that caused cancer in 4 of 9 boys.
SCPI does laboratory and computer based experimentation to determine the contribution of a protein called PRDM9, the impact of 13 nucleotide long DNA sequences that bind PRDM9 (called 13 mers), the position of meiotic recombination ‘hotspots’ (areas where mom’s and dad’s genetic material exchanges the most), the amount of uptake of short human DNA fragments by varied human cells and cell lines, and the impact of this human DNA uptake on cell survival and function.
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