WHEN?

[Guest guest]

WHEN WILL ALL THIS MADNESS STOP? AUTISM a GENETIC ILLNESS or a TOXIC ILLNESS Genetic testing of patients with AUTISM has found changes to most of the chromosomes. BUT does this indicate the parents have the same genotype or is it unique to the child with autism? If the parents have normal genotypes then the only likely explanation is that the change occurred as the result of a TOXIC INSULT. I have looked at many papers, but where are the papers that look and find all these genotypes that they say proves AUTISM is genetic and compare to the mother and father? They are not there or not done. WHY? The answer is quite clear to me. The tests are not done because the parents are not AUTISTIC. The findings of the same genotype for a parent would present a dilemma. Why is this parent not AUTISTIC too? The finding of completely normal or no similarity of the chromosome with either parent would demand the answer to the question – How did the child get this change in its chromosomes? We know that very many chemicals have the ability to change the make up of chromosomes and the one which is the world’s most likely non-radioactive candidate is the element mercury, specifically organomercury and particularly ethylmercury. At the level in ONE vaccine such changes to lymphocytes do occur. The vaccine companies themselves would be the first to admit to all this knowledge and often they are the berst sources of information. The chosen toxicologist for Wyeth used a scientist fully conversant with mercury but also organophosphates. These have a short but bloody history and the changes to the chromosomes have been charted extensively due to the massive applications of these products in the home and on our food. In Vitro Data Using Human Lymphocytes. A host of studies have examined mutagenic behavior of OPs and carbamates in human lymphocytes in vitro (Bianchi-Santamaria et al., 1997; Bonatti et al., 1994; Cid et al., 1990; Cid and Matos, 1984; Dolara et al., 1994; Garry et al., 1990; Lieberman et al., 1998; and Carrascal, 1987; Kappas et al., 1990; Kevekordes et al., 1996; et al., 1979; Perocco and Fini, 1980; Veronesi and Ehrich, 1993; Rupa et al., 1991; Rupa et al., 1989; Rupa et al., 1988; Sobti et al., 1982). These studies examined a variety of OPs (including microtophos, malathion, chloracetophone, parathion, azinphos-methyl, dimethoate, pirimphos-methyl, diazinon) and carbamates (methomyl, aldicarb, propoxur, benomyl), as well as pesticide combinations, and reported interference in reparative DNA synthesis; increased damage to human lymphocyte DNA and interference with DNA repair processes after damage exerted by ultraviolet rays; and OP-associated increases in mitotic index, sister-chromatid exchanges (Perocco and Fini, 1980), chromatid breaks, gaps, deletions, fragments, exchanges, dicentrics, and endoreduplications (Rupa et al., 1988). One study examined a variety of OP and carbamate compounds using a micronucleus test, with chemical doses based on subjects’ estimated daily intake. Weak genotoxicity at these doses was seen in three of the four tested OPs and in the tested carbamate (benomyl); additive effects were not seen (Bianchi-Santamaria et al., 1997). The timing of exposure of the cell culture was also found to influence the susceptibility to chromosomal aberrations (tested with diazinon) ( and Carrascal, 1987). One study used a cell cloning assay to study genotoxicity of malathion to human T lymphocytes in vitro. Cells in phase G0 were exposed to doses of malathion ranging from 10 to 600 µg/ml (Pluth et al., 1996). In seven in vitro experiments using cells from four different individuals, and one experiment in an individual exposed in vivo, one or more independent mutants containing a partial deletion of exon 3 were isolated from each individual. In five of the seven mutants, the deleted regions overlapped extensively, indicating an area within exon 3 that is exceptionally prone to deletions upon exposure to malathion. It is uncertain what the molecular mechanism is, and how this could relate to agricultural workers’ increased risk of cancer. Neuroblastoma cell lines have also been examined (in humans and mice), and evidence suggests that interspecies selectivity in response to OP-related cytotoxicity is influenced by intercellular differences in metabolism and baseline esterase activity, as well as cytochrome-P450-associated monooxidase activity (Veronesi and Ehrich, 1993). This is a little technical but you can realise that these chemicals have an ENORMOUS effect on chromosomes and just one brief exposure to these products has resulted in MILLIONS of pounds in compensation for HARM. Sadly the vast majority of these cases end rather like the BLACKWELL case with everyone making MOUNTAINS of MONEY except the ONE person almost or totally destroyed with his ‘inherited’ chromosome damaged lymphocytes not altered by the world’s most toxic non-radioactive MUTAGEN in the shape of ETHYLMERCURY present in vaccines given yesterday and today to all and sundry. It’s a good way to make a living to chart all these changes to lymphocytes in autistic children and not follow up with the ONLY possible explanation even in a COURT of LAW. But to have the destruction of a MILLION lives of babies dying coincidently after receiving a TOXIC INSULT and TENS OF MILLIONS of babies through to young adults with the cost to the COMMUNITY? Now that is SCIENCE FOR SALE! AUTISM GENETIC ILLNESS or a TOXIC ILLNESS WHEN WILL ALL THIS MADNESS STOP?