his section will remain Under Construction for some time. I am a severely Autistic person, and can only get words out if I do it like a jigsaw puzzle, not as a linear written letter, story, article, or paper.
Genetic diversity in species IS genetic fitness. Species that lack genetic diversity, lack genetic fitness necessary to ongoing survival of the species.
"Evolution results from natural selection acting on diversity in populations, which ultimately stems from mutations." Eviatar Nevo, Genetic variation in nature, Nov. 22, 2010, http://www.scholarpedia.org/article/Genetic_variation_in_nature (hereafter "Nevo, 2010" ). "Natural selection edits both adaptation and speciation. Darwin (1859) suggested natural selection as the major mechanism of adaptive evolution. The synthesis of Darwinian natural selection with Mendelian inheritance in the 20th century elevated the importance of natural selection as the primary force of adaptive evolution (Templeton, 2009)." (Nevo, 2010). Adaptive evolution involves more - it involves the ability to select the niche in which the species fitness for it's environment is greatest. "Evolutionary change in organisms is affected by the interaction of several major forces including mutation (broadly conceived), recombination, inbreeding, migration, natural selection, and genetic drift presently operating on past evolutionary constraints of individuals and higher levels of organization." (Nevo, 2010).
"Genetic diversity in nature, i.e., molecular genetic hereditary differences within and between populations and species, is the basis of evolutionary change (Darwin, 1859). Extensive molecular genetic diversity has been revealed in natural populations since its early discovery in enzymes (Markert and Moller, 1959), proteins (Zuckerkandl and Pauling, 1965), isozymes/allozymes (Lewontin, 1974), and DNA (Kimura, 1983)." (Nevo, 2010).
"The idea of the neutrality theory of molecular evolution (Kimura, 1983) in which nature is sharply dichotomized into phenotypes subjected to positive Darwinian selection and genotypes that are largely invisible to natural selection and governed primarily by random genetic drift (Kimura 1983) is unrealistic. Protein and DNA variation in nature do not primarily reflect evolutionary noise entering into populations through mutational input and random fixation, as maintained by the neutrality theory of molecular evolution (Kimura, 1983)." (Nevo, 2010).
"Genetic diversity of coding and noncoding genomes, including transposons and retrotransposons, is partly correlated and predictable by a combination of a few variables primarily involving climatic ecological factors, solar radiation, temperature, and drought. These patterns strongly implicate natural selection not only at the phenotypic level but also at the genotypic level." (Nevo, 2010).
"Genetic diversity is largely higher (i) in species living in broader environmental spectra, (ii) in large species with patchy population structure and limited migration, as well as in solitary or social species, and (iii) species with small body size, annuals or long-lived perennials that are older in time with diploid chromosome numbers, primarily out-crossed, and plant species reproducing sexually and pollinated by wind. Species with the above characteristics harbor, generally, more genetic diversity than their opposite counterparts."(Nevo, 2010).
"Genetic diversity in nature is nonrandom, heavily structured, and correlated with abiotic and biotic ecological diversity and stress. Explorations at the interface of ecology and genomics, combined with critical tests and strong inferences of abiotic and biotic stresses, ... highlight the understanding of the maintenance of genetic diversity in nature." (Nevo, 2010).
"DNA polymorphisms mirror protein (isozyme) polymorphisms and can highlight genome structure and evolution caused by environmental stress as indicated by wide-genome gene expression (Miyazaki et al., 2003)." (Nevo, 2010). "In genome sequencing projects, attention is now often focusing on detection of single base-pair changes in the DNA sequence" called Single nucleotide polymorphism or "SNP." (Nevo, 2010). Single nucleotide polymorphism (SNP) is the most common sequence variation in coding and noncoding genomes in diverse taxa across life from viruses and bacteria to humans (Kwok and Chen, 2003)." (Nevo, 2010)."SNPs, as with all other protein and DNA markers examined earlier, are nonrandomly distributed, correlated with diverse ecological stresses, and appear to be, to a large extent, adaptive, subjected primarily to the major evolutionary driving force of natural selection." "SNPs are best fit to answer the question about the nature and meaning of genetic diversity in natural populations in diverse ecological contests of variable stresses and changing environments." (Nevo, 2010). They do not represent neutral variation, but instead appear to be correlated with environment and partly predicting it.
"Genome-wide analyses in 52 human populations identified 139 immune response genes. They comprised 441 variant alleles involved in anti-viral immune response identified in 660,000 SNPs, which were significantly associated with virus-driven selection pressure (Fumagalli et al., 2010). ... Adaptive disease-associated SNPs in humans (lipid levels and coronary heart diseases) were described by Hao et al. (2010).... Adaptive altitudinal evolution of the dehydrogenase mitochondrial ND6 gene was described in the domestic horse in China (Ning et al., 2010). ...The human melatonin signaling pathway, particularly the melatonin receptor, appears to be subjected to a selective pressure in response to global variation in sunshine duration (Xu et al., 2010). ... Adaptive chromosomes and SNP evolution of regulatory elements were identified in ... humans by ... high-altitude adaptation to hypoxia (Beall et al., 2010; Simonson et al., 2010; Yi et al., 2010)."(Nevo, 2010).
"Mobile DNA rearrangements and major genome restructuring events at key junctures in evolution (exon shuffling, changes in cis-regulatory sites, horizontal transfer, cell fusions and whole genome doublings) highlight interactive evolutionary process, [were] emphasized by McClintock (1984). This view elucidates the molecular basis of genetic change, major genomic events in evolution, ecological changes, cellular response and control networks, and stimuli restructuring DNA. Likewise, the rapid emergence of adaptive novel complexes, coupled with a classical cytogenetic role of hybridization (allotetraploidization) in the origin of species."(Nevo, 2010).
Horizontal Gene Transfer "[HGT] is a major source of natural genetic diversity between taxa, resulting in genome innovation and evolution, particularly in prokaryotes (Gogarten and Townsend, 2005). ... Raz and Tannenbaum (2010) found that HGT has a non-trivial affect on the mean fitness of the population. They concluded that the main advantage of HGT is by promoting faster adaptation in dynamic, stressful environments." (Nevo, 2010).
"Researchers have now proven that "it is possible for genes from one organism to hop to another. This happens most often in microbes. A bacterium may jam a needle into another bacterium and inject some genes. In other cases, viruses may pick up the genes of one host and bring them to a new host. Once a gene makes this jump, it may then get carried down through normal heredity to the receiver's descendants, spreading into new species that evolve from it." Carl Zimmer, Tangling the Tree, Jul. 8, 2005, http://www.corante.com/loom/archives/2005/07/08/tangling_the_tree.php (emphasis added). During Nov. 2010, researchers from the Salk Institute for Biological Studies reported that in people with Rett syndrome, an Autism spectrum sub-type, a mutation in the MeCP2 gene mobilizes so-called L1 retrotransposons "jumping genes" in brain cells, reshuffling their genomes when they find their way into active genes. Rett Syndrome Mobilizes Jumping Genes in the Brain, ScienceDaily, Nov. 22, 2010, http://www.sciencedaily.com/releases/2010/11/101117141417.htm (hereafter "Rett Jumping Genes, 2010").
"Strong selection overrules gene flow ... across life (bacteria, soil fungi, flowering plants, Drosophila, and Acomyslocally, as well as possibly regionally and globally (Nevo, 2010). The fact that selection overrules gene flow ... is the main reason for the incipient sympatric speciation across life from bacteria to mammals." (Nevo, 2010).
"The major focus in studying genetic diversity in nature should be on population functional ecological genomics across life coupled with proteomics, metabolomics, and phenomics. A major future perspective should try to analyze the effects of stresses not only through individual genes but through genomic-biochemical networks related to individual and collective environmental stresses (solar radiation, temperature, global warming, drought, mineral and photosynthetic deprivations, biotic stresses, etc). Epigenomics should be coupled with genomics, including DNA methylation, histone modification, and the regulatory effects of small RNA, and noncoding repeat elements, including transposon and retrotransposon dynamics in both adaptation and speciation to evaluate genome-wide adaptive divergence (Andolfatto, 2005; Biemont and Vieria, 2006; Eyre-Walker, 2006; Parsons, 2005)." (Nevo, 2010).
"The basic pending problems are how much of molecular diversity in nature, at both the coding and noncoding genomic regions, is adaptive and how much of the mutations occurring in natural populations are nonrandom (adaptive, directed) rather than random, neutral, nearly neutral, non-adaptive or deleterious (see Galhardo et al., 2007)." (Nevo, 2010).
Hominid Species, Ancestry, and Migration
"Recently, with more powerful geological dating methods based on fluctuations in the earth's magnetic field or electron spin resonance, the earliest Homo erectus fossils from China have been dated to 1.9 million years ago. This requires an even earlier date for the emergence of Homo ergaster in Africa, implying humans first evolved about 2.5 million years ago." Hominid Fossil Sites and Patterns of Hominid Dispersal, http://www.handprint.com/LS/ANC/disp.html (hereafter "Hominid dispersal").
First Wave of Migration Out of Africa: Homo Ergaster Evolved Into Homo Erectus / 2 mya -1 mya
"From about 2 million up to 1 million years ago, early Homo ergaster migrated outside this valley system into a larger area of Africa, and from there into central and eastern Asia -- evolving along the way into Homo erectus. The sheer geographic distances involved reduce substantially the gene flow in the total hominid population, making regional subspecies (such as eastern Homo erectus) more likely to appear." (Hominid dispersal).
Second Wave of Migration Out of Africa: Homo Heidelbergensis / 800,000 mya
"Around 800,000 years ago a large brained, robust hominid, Homo heidelbergensis, appeared in Africa and migrated throughout that continent and into Asia -- but significantly also became the first hominid to colonize Europe. Although it utilized the same Acheulean tool industry as western Homo erectus, Homo heidelbergensis probably was a more systematic hunter and relied more extensively on the economic processing of animal resources." (Hominid dispersal).
"Comparisons of the Neanderthal genome to the genomes of extant humans identified a number of genomic regions that may have been affected by positive selection in ancestral modern humans, including genes involved in metabolism and in cognitive and skeletal development (Green et al., 2010)." (Nevo, 2010).
"An extensive mtDNA analysis provides evidence that the first European farmers were not the descendants of local hunter-gatherers but immigrated into central Europe at the onset of the Neolithic Age (Bramanti et al., 2009)." (Nevo, 2010).
Inherited Red-Hair Gene From European / Middle East Ancestry
"Variation in human skin and hair color is largely explained by the levels and ratio of the two major forms of melanin—eumelanin, which is brown-black, and pheomelanin, which is red-yellow (Quevedo and Holstein 1998). The [ melanocortin 1 receptor] MC1R gene (chromosome 16q24.3) is the only gene identified, thus far, that explains substantial phenotypic variance in human pigmentation (Rees and Flanagan 1999). ...MC1R is highly polymorphic in European populations and that, in Irish, Dutch, and Swedish populations, homozygotes or compound heterozygotes for three particular variants are associated with red hair and increased sensitivity to burning from UV radiation (Valverde et al. 1995; Box et al. 1997; Smith et al. 1998). These three variants (Arg151Cys, Arg160Trp, and Asp294His) all bind α-melanocyte–stimulating hormone but show diminished intracellular ability to activate adenylate cyclase (Frändberg et al. 1998; Schiöth et al. 1999).... Arg142His—but not Val60Leu—has been found in association with red hair (authors' unpublished data). Val60Leu, however, may be associated with fair or blonde and light-brown hair colors (Box et al. 1997)." Harding, Healey, Ray, Ellis, Flanagan, Todd, Dixon, Sajantila, Jackson, Birch-Machin, & Rees, Evidence for Variable Selective Pressures at MC1R, Am J Hum Genet., 2000 April; 66(4): 1351–1361, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1288200/?tool=pubmed (hereafter "Harding et al., 2000").
"Both African and non-African data suggest that the time to the most recent common ancestor is ~1 million years and that the age of the global 314 variant is 650,000 years. On this time scale, ages for the Eurasian-distributed Val60Leu, Val92Met, and Arg163Gln variants are 250,000–100,000 years....For the European red hair–associated Arg151Cys and Arg160Trp variants, we estimate an age of ~80,000 years; for Asp294His, and Ser316Ser, we estimate an age of 30,000 years. ...MC1R alleles (Arg151Cys, Arg160Trp, Asp294His, and Arg142His) that act as recessives in the red-hair phenotype (~11% of the British and Irish population) also contribute to UV radiation sensitivity in heterozygous genotypes (~28% of the population; J. L. Rees, unpublished data)." (Harding et al., 2000).
Photo: Mary Katherine Day-Petrano, 4th Grade, circa 1965, age 9 showing her natural red-hair derived from her Caucasian European ancestry
Occipital Bun or "chignon"
"Occipital bun is a morphological term used to describe a prominent bulge, or projection, of the occipital bone at the back of the skull. The term is most often used in connection with scientific descriptions of classic Neanderthal crania. While common among many of mankind's ancestors, primarily robust relatives rather than gracile, the protrusion is relatively rare in modern Homo sapiens." http://en.wikipedia.org/wiki/Occipital_bun.
Photo: Mary Katherine Day-Petrano (hair cut especially short and color changed to get the photo), showing her occipital bun derived from her Caucasian European ancestry
Homo Neanderthalensis Had Its Own Language and Autistics, Tracking This, Have Been Found to Utter Different Pre-Verbal Vocalizations Than Cro-Magnon Neurotypicals
"A Kansas University professor has ... show[n that preverbal vocalizations of very young children with autism differ from those of typically developing children. The idea that children with autism display different vocalizations than normally developing children isn’t new.... Some parents of children with autism have pointed out that their children were displaying different vocal characteristics ..." Andy Hyland, Autism research may be used as screen, July 20, 2010, http://www2.ljworld.com/news/2010/jul/20/autism-research-may-be-used-screen/.
Epigenetics: Environmental Factors Having Long-Term and Life-Lasting Consequences For Human Genome Function And Evolutionary Adaptation
"Epigenetics, heritable changes causing differential gene expression in cells, tissues, and organisms, unfolds internal and external cues regulating the genetic code beyond DNA nucleotide changes, conferring phenotypic plasticity and complexity. Epigenetic signals affect both soma and germlines in normal and diseased conditions. Epigenomics unifies epigenetics and genomics, i.e., modification at the whole genome level, channeled by a set of chemical modifications not encoded by DNA that determine how and when genes are expressed, hence, are key elements of development and disease. Epigenetic mechanisms, switching genes on or off, or silencing repetitive elements in tissues include the following: chromatin modification, transcription factors, DNA and protein methylation, histone protein modification, nucleosome regulation, polycomb group proteins, noncoding RNA (ncRNA, e.g., small interfering RNAs, siRNA, and microRNAs, miRNA), transcription modulation, translation repression, RNA splicing, RNA stability and translation, all of which contribute to regulation and heritability of epimutations (Tost, 2008; Petronis, 2010). Nonpromoter DNA methylation by Dnmt3a facilitates transcription of neurogenic genes critical for development (Wu et al., 2010)." (Nevo, 2010).
"Genomes are plastic and responsive to environmental changes. Environmental stresses induce genomic instability in bacteria, yeast, and human cancer cells generating occasionally fitter mutants and potentially accelerating adaptive evolution. Matic (2010) emphasized that new mutations can range from deleterious through neutral to beneficial. However, when adaptation is limited by the mutation supply rates under stressful conditions, natural selection favors increased mutation rates by acting on allelic variation of the genetic systems that control fidelity of DNA replication and repair. Mutator alleles are carried to high frequency through hitchhiking with the adaptive mutations they generate." (Nevo, 2010).
"Environmental factors can have long-term and life-lasting consequences for genome function and adaptation through dynamics epigenome. Transgenerational epigenetic inheritance is transferred through meiosis, and the epigenetic component can collaborate with DNA in phenotypic inheritance. ...[T]he phenotype is the interaction of genetic, environmental, and epigenetic variables all contributing to phenotypic variation ...." (Nevo, 2010).
"[T]here are an unlimited variety of ways in which people experience the world. Even in a world that puts a high value and price on the 'normal' - there really is no such thing." Lynne Soraya, The Power of Presupposition: Presuppositions. What part do they play in our interactions? Asperger's Diary blog, April 27, 2008, http://www.psychologytoday.com/blog/aspergers-diary/200804/the-power-presupposition (hereafter "Soraya, 2008).
"Evolution, the inheritance of changed characteristics across generations, is the fundamental unifying concept underlying biology, as a National Research Council science education standards released in 1996 noted. ...[M]any U.S. adults dispute the notion of humans evolving from an ape-like ancestor within the last 6 million years, despite the genetic evidence showing a common ancestry with chimps, gorillas and orangutans, and a fossil record filled with precursor human species, including Neanderthals, now shown to be even more closely related to us by genes." Dan Vergano, Evolution teaching poor in U.S. high schools, USA Today, Jan. 28, 2011, http://content.usatoday.com/communities/sciencefair/post/2011/01/evolution-teaching-poor-/1.
"Reading the works of such neurologists as Oliver Sacks and V. Ramachandran - it becomes clear that the variation in the human experience is very affected by our brains interpret the world around us, and this varies widely. Being the concrete beings we are, I believe many people miss this. In a "what you see is what you get" world - where is the room to realize that what your brain "sees" when looking at an object, person, or situation, may be completely different than what my brain "sees"? And what presuppositions will that assumption cause you to make? I think this a common root of some of the social issues experienced by people on the autism spectrum, or others who have similar, invisible disabilities. People seem to make the default presupposition that your experience is similar to theirs ...." (Soraya, 2008) (emphasis added).
According to Dawson, Mottron, & Gernsbacher (2008), "[f]ew aspects of neurology have not been proposed as being atypical in autism" from the Cro-Magnon Neurotypical perspective.
"For example, regions of reported neurofunctional atypicalities range from the brainstem to the inferior frontal gyrus, while reported neuroanatomical atypicalities range from increased white and gray matter volume (e.g., Hazlett et al., 2005) to more densely packed cells and increased numbers of cortical minicolumns (Casanova et al., 2002). Neurofunctional connectivity has been suggested to be atypical (e.g., Just et al., 2004), and neural resources may be atypically allocated or rededicated (e.g., Koshino et al., 2005; Turkeltaub et al., 2004). Virtually every fundamental human cognitive and affective process, singly or as part of an overarching model, has been proposed to be dysfunctional or absent in autism, while persistent findings of superior performances by autistics are often interpreted as evidence of neurological and cognitive pathology (e.g., Beversdorf et al., 2000; Chawarska et al., 2003; Heaton et al., 1998; Just et al., 2004; Langdell, 1978; Ropar and Mitchell, 2002; Shah and Frith, 1983, 1993; Toichi et al., 2002; for analysis and perspective, see Baron-Cohen, 2005; Gernsbacher et al., 2006; Mottron et al., 2006; Mottron et al., in press). Dawson, Mottron, & Gernsbacher, 2008 (emphasis added).
"Thus, autism has been prolifically studied but remains poorly understood."Dawson, Mottron, & Gernsbacher, 2008.
"In May 2008, President George W. Bush signed into law the Genetic Information Nondiscrimination Act (GINA), which protects Americans against discrimination based on their genetic information when it comes to health insurance and employment. Genetic discrimination occurs if people are treated unfairly because of differences in their DNA that increase their chances of obtaining a certain disease." Ladan Nikravan, Discrimination Is Alive and Well, Jan. 25, 2011, Diversity Executive Magazine, http://diversity-executive.com/article.php?article=1072.'Genetic research continues to provide new insights into the causes and underlying biology of autism. Investigators from the Autism Speaks-funded Autism Genome Project (AGP) published a major paper in Nature in 2010. AGP researchers discovered that some of the Autism risk gene sets are directly involved in the development of neurons whereas other gene sets are involved in the function of neurons, particularly the ability of neurons to communicate with each other as they form and maintain synapses.' (AutismSpeaks, 2011) (citing Pinto D, et al., 2010) (Functional impact of global rare copy number variation in autism spectrum disorders. Nature. 466:368-72).
RE-INSET DAWSON genetic info here (got deleted somehow)
'Another study replicated earlier findings that parental autoimmune disease increases risk for [Autism]. ...Alexander Keil and colleagues found that there was nearly a 50% higher chance of being diagnosed with autism if the parent had an autoimmune disease, such as type-1 diabetes and rheumatic fever. The mechanisms by which parental autoimmune disease increases risk for [Autism] are now a focus of further research. What is clear from these and other studies is that the causes of autism are likely to be complex rather than simple and many rather than a few.2010: The Year in Review from Autism Speaks' Chief Science Officer, Jan. 4, 2011, http://www.autismspeaks.org/science/science_news/dawson_year_in_science_2010.php (hereafter "AutismSpeaks, 2011") (citing Keil et al., (2010) Parental autoimmune diseases associated with autism spectrum disorder in offspring. Epidemiology, 21: 805-8).
Martha Bahr Thrun Jan. __, __ -Apr. 14, 2001: My Grandmother, Mother's Side -- Auto-Immune Disease: Rheumatoid Arthritis
My "grandma," as I called her, on my Mom's side was diagnosed and suffered many years as she aged with autoimmune disease - rheumatoid arthritis.
Photo: My grandparents, from L to R: Cortez F. Day, Queen Angelica Ballard Day; Martha Bahr Thrun, Elmer Thrun circa Dec. 1955
Photo: My grandparents, from L to R: Elmer Thrun, Martha Bahr Thrun circa during the 1980s / 60th Wedding Anniversary
Photo: My grandma, Martha Bahr Thrun, as she approached her 98th Birthday
INSERT PHOTO here
'Several noteworthy papers on environmental risk factors were published in 2010. Five studies found that premature birth is associated with increased risk for autism. (Johnson, S et al., 2010) (Autism spectrum disorders in extremely preterm children. Journal of Pediatrics, 156: 525-31). Exposure to hazardous air pollutants shortly after birth also was found to be a risk factor. (Kalkbrenner, AE et al., 2010) (Perinatal exposure to hazardous air pollutants and autism spectrum disorder at age 8. Epidemiology, June 17 (Epub ahead of print)).' (AutismSpeaks, 2011).
Mother Smoking Cigarettes and Drinking Alcohol During Pregnancy With Me As A Fetus, With My Father Joining Her
"The effects of cigarettes on the pregnant woman and developing fetus are numerous with a wide range of sequelae that will remain with the fetus for the rest of her life." Krisa Van Meurs, MD, Cigarette Smoking, Pregnancy and the Developing Fetus, Sept. 5, 1999, med.stanford.edu/medicalreview/smrp14-16.pdf (hereafter "Meurs, 1999") (emphasis added).
"[N]icotine, the active ingredient in cigarettes, works in the brain to suppress smokers' appetites. The nicotine receptor in the brain has 15 subunits; they can combine in a multitude of ways to form different receptors with different jobs. Nicotine can bind to each combination and spur a cascade of distinct events; some lead to the addictive properties of cigarettes, others to an increase in blood pressure or a feeling of relaxation." http://news.sciencemag.org/sciencenow/2011/06/why-smokers-are-skinny.html?ref=hp (hereafter " Picciotto (Yale Univ.), 2011")
"It's long been known that nicotine causes a slump in appetite, and scientists suspected that this worked through receptors associated with reward and behavior reinforcement. ... But the new finding suggests that appetite has its own pathway . ... nicotine does, in fact, bind to α3β4 receptors, which then send a signal throughout the rest of the brain, signaling satiety. It's indistinguishable from the signal the brain propagates after eating a large meal. ... Females ... experience larger weight loss when they start smoking and a larger weight gain if they quit. Whether this means nicotine is working through an additional, hormone-regulated pathway in the female brain is yet to be determined." Id. The study suggests that smoking causes a 15-20 % body fat loss over 30 days.
Nicotine has been shown to be a potent vasoconstrictor reducing uterine and placental blood flow." (Meurs, 1999). "[N]icotine causes the developing fetal brain to grow millions of extra acetylcholine receptors in the cortex, striatum, and cerebellum regions ( 1995, 1999 ). ... [I]t [also] unnaturally regulates the pre-birth flow of more than 200 neurochemicals within the unborn's mind and body, including dopamine, serotonin and adrenaline.... [N]icotine is not only a teratogen but very likely a neuroteratogen inflicting lasting damage upon their nervous system ( 1991)." John R. Polito, Smoking While Pregnant or Breastfeeding: The Impact of Nicotine, Smoking and Tobacco, http://whyquit.com/whyquit/linksbirth.html (emphasis added).
"Data from the Kaiser Permanente Birth Defects Study (33,434 births) ... [was] used to assess the relationship between maternal smoking and congenital malformations," with "nine malformations ... found to be associated with maternal smoking." (Meurs, 1999) (emphasis added).
"Components of cigarette smoke are known to be transported over placental membranes and are able to act as mutagens in fetal tissues. Components of cigarette smoke have been shown in animal studies to be transplacental carcinogens." (Meurs, 1999).
"Several epidemiological studies have reported a relationship between maternal cigarette smoking and SIDS. ... Recent studies in neonatal lambs have shown that nicotine attenuated the ventilatory response to hypoxia and have led to the speculation that SIDS is related to the effects of nicotine on the central control of breathing." (Meurs, 1999).
Despite my father's denial of these facts to numerous friends, relatives, courts, and investigators, my Father, Kenneth G. Day, knew all about my Mom's smoking and drinking during her pregnancy with me causing my life-long Autism, because HE JOINED HER - that is also why my father consented in his marital dissolution with my mother during April 1970 when I was age 14, to pay Autism adult child support for my developmental disabilities.
Photo: My Father, Kenneth G. Day, joining with my Mom (see above-photo) drinking himself, with full knowledge she was smoking cigarettes and drinking during her pregnancy with me as a fetus, Dec. 1955 (I was born Apr. 16, 1956)
People with Autism "are much more likely to have defects in a cellular structure called the mitochondria, which is responsible for producing the energy used by brain cells." Jenifer Goodwin, Cell Dysfunction May Play Part in Autism: Mitochondria, energy center of cell, found impaired in some, researchers report, HealthDay News, Nov. 30, 2010 (hereafter "Goodwin, 2010") (emphasis added).
"Mitochondria, sometimes called cellular 'powerhouses,' produce energy that's used to fuel a cell's activity -- an especially important function in the brain.... When mitochondria don't function properly, the results can be devastating." (Goodwin, 2010).
A recent issue of the Journal of the American Medical Association, Cecilia Giulivi, and colleagues reported a much higher prevalence of mitochondrial dysfunction in children with [Autism] than had previously been found. Mitochondria, found within cells, contain enzymes that are responsible for producing energy. Unlike previous studies, researchers studied lymphocytes (white blood cells) which have a higher number of mitochondria. The children with [Autism] had lower mitochondrial enzyme activity and other indications that the mitochondria were not functioning optimally. Five of the 10 children with [Autism] had more copies of their mitochondrial DNA than expected, suggesting that the body may be trying to compensate for poor mitochondria functioning.'' (AutismSpeaks, 2011) (citing Giulivi, C., Zhang, Y., Omanska-Klusek, A., Ross-Inta, C., Wong, S., Hertz-Picciotto, I,, F., Pessah, I.N. (2010) Mitochondrial dysfunction in autism. JAMA, 304: 2389-2396).
People with Autism as compared to others, are "far more likely to have mitochondrial dysfunction, including defects in mitochondrial DNA and abnormalities in the levels of various enzymes produced by the mitochondria."Among the various mitochondrial defects," the mitochondria of people with Autism have been found to "consume less oxygen" than mitochondria from Neurotypical people, "suggesting less mitochondrial activity." (Goodwin, 2010) (emphasis added).
"Mitochondrial disease can lead to symptoms including muscle weakness, exercise intolerance (pain and muscle cramps during exercise), gastrointestinal disorders, seizures, liver disease, vision and hearing problems, developmental delays and increased susceptibility to infection." (Goodwin, 2010) (emphasis added).
'It is not known whether the mitochondrial dysfunction is a cause or effect of autism. However, mitochondrial dysfunction can amplify brain dysfunction because the brain requires a high level of energy and depends on the mitochondria to supply that energy' (AutismSpeaks, 2011).
'The role of the immune system in autism was also highlighted in several other 2010 studies. Paul Ashwood and colleagues from UC Davis found that children with [Autism] had increased levels of cytokines, small molecules that are secreted by the immune system. Increased cytokine levels were pronounced in children with regressive autism and those with more severe [Autism Spectrum] symptoms.' (AutismSpeaks, 2011) (citing Ashwood, P. et al., (2010) Elevated plasma cytokines in autism spectrum disorders provide evidence of immune dysfunction and are associated with impaired behavioral outcome. Brain Behavior Immunology, August 10. (Epub ahead of print)).
"Individuals with autism more often had microscopic deletions in their chromosomes that affected the function of specific genes. The specific deletions (called “copy number variations”) are extremely rare in the general population, and many were “de novo,” meaning that they occurred for the first time in the individual with [Autism], and were not inherited from parents. De novo mutations can arise spontaneously through errors in DNA replication or be caused by environmental factors, such as viruses or chemicals." (AutismSpeaks, 2011).
"The need for better assessments and treatments of medical conditions in people with [Autism], including GI, sleep, and seizures, among others, was the topic of a 2010 presentation to the IACC." (AutismSpeaks, 2011). "'[A] central difficulty in recognizing and characterizing gastrointestinal dysfunction with [Autism] is the communication difficulties experienced by many affected individuals.'” AutismSpeaks, 2011) (citation omitted, emphasis added).
Preference for Geometric Patterns, Pictures, Objects & Things -- Early Autism Identifier
Photo: Oct. 20, 1956 - Mary at 6 months, gazing at pictures & patterns:
"Only autistic babies looked at the geometric patterns more than 69 percent of the time. 'It's pretty clear that showing heightened interest in geometric patterns and repetitive moving objects is a risk factor for autism.'" http://www.nlm.nih.gov/medlineplus/news/fullstory_103003.html.
A recent study identified preference for geometric patterns over social images as an early risk factor for the development of Autism. Marlena Smith, Preference for Geometric Patterns Identified as a Possible Early Sign of Autism, Feb. 25, 2011 (citing Pierce, K., Conant, D., Hazin, R., Stoner, R., & Desmond, J. (2011), Preference for geometric patterns early in life as a risk factor for autism. Archives of General Psychiatry, 68, 101-109), http://blog.centerforautism.com/2011/02/25/preference-for-geometric-patterns-identified-as-a-possible-early-sign-of-autism/.
Lower Than Expected 2:4D Digit Ratio Demonstrating High Fetal Testosterone Marker for Autism
"[A]utism may arise as the result of exposure to high concentrations of prenatal testosterone. There is evidence that the ratio of the lengths of the 2nd and 4th digit (2D:4D) may be negatively correlated with prenatal testosterone." People with Autism "had lower than expected 2D:4D ratios and children with AS higher ratios than expected in relation to their fathers' 2D:4D ratio. It was concluded that 2D:4D ratio may be a possible marker for autism which could implicate prenatal testosterone in its aetiology." J T Manning, S Baron-Cohen, S Wheelwright, and G Sanders, The 2nd to 4th digit ratio and autism, Developmental Medicine & Child Neurology (Apr. 9, 2001), 43: pp. 160-164, http://journals.cambridge.org/action/displayAbstract;jsessionid=E90C8762C880668EBE80B4E16016CDC6.tomcat1?fromPage=online&aid=68749
Left (ring finger longer than index finger):
Right (ring finger longer than index finger):
"Vaccines kill children in more than rare occurrences. In 1986, Congress officially acknowledged the reality of vaccine-caused injuries and death by creating and passing The National Childhood Vaccine Injury Act (Public Law 99-660) which requires doctors to provide ... information about the benefits and risks of childhood vaccines prior to vaccination. Doctors are required by law to report suspected cases of vaccine damage. The Vaccine Adverse Event Reporting System (VAERS) -- operated by the CDC and FDA." http://www.naturalnews.com/031172_vaccines_children.html (hereafter "NaturalNews, 2011").
"The National Vaccine Information Center (NVIC) reported that, "In New York, only one out of 40 doctor's offices [2.5%] confirmed that they report a death or injury following vaccination," -- 97.5% of vaccine related deaths and disabilities go unreported there. Implications about the integrity of medical professionals aside (doctors are legally required to report serious adverse events), these findings suggest that vaccine deaths actually occurring each year may be well over 1,000." (NaturalNews, 2011").
A research team from Wake Forest University School of Medicine in North Carolina examined children with regressive autism and bowel disease occurring after vaccination with the MMR vaccine - "and of the 82 tested so far, 70 prove positive for the measles virus. ... [S]o far, all are vaccine strain and none are wild measles. 'This research proves that in the gastrointestinal tract of a number of children who have been diagnosed with regressive autism, there is evidence of measles virus.'" The new research supports the previous discovery of British doctor Andrew Wakefield of "a new bowel disease, autism enterocolitis. ... This is the second independent study to back up Dr Wakefield. In 2001 John O'Leary, Professor of Pathology at St James's Hospital and Trinity College, Dublin, replicated his findings." Sally Beck, Scientists fear MMR link to autism, http://www.dailymail.co.uk/news/article-388051/Scientists-fear-MMR-link-autism.html.
My Paralytic Poliomyelitis Autism Vaccine Injury
The U.S. Center for Disease Control (CDC) “admitted that the vaccine has become the dominant cause of polio in the US today, with 87% of cases between 1973 and 1983 caused by the vaccine. More recently, 1980-1989, every case of polio in the US was caused by the vaccine.” Polio Information & Polio Vaccine Dangers, http://www.nccn.net/~wwithin/polio2.htm.
“Doctors and scientists on the staff of the National Institute of Health during the 1950’s were well aware that the Salk vaccine was ineffective and deadly. Some … stated that it was ‘worthless as a preventative and dangerous to take’. The Salk ‘inactivated’ or ‘killed-virus’ was actually regulated to permit 5,000 live viruses per million doses.” Id. “A large vaccine trial in 1955 showed a total failure of the Salk vaccine to protect against poliomyelitis. During a 1959 epidemic in Massachusetts, 77.5% of the paralytic cases had received three or more doses of the inactivated vaccine.” Id. “In 1956 with the … Francis Field Trials they discovered large numbers of children contracted polio after receiving the vaccine.” Id.“In 1958 mass vaccination triggered a disastrous increase in polio, the highest being 700% in Ottawa, Canada. The highest incidence in the USA occurred in those states which had been induced to adopt compulsory polio shots. … Where polio vaccination programs have been instituted worldwide, reported polio infections show a 700% increase as a result of compulsory vaccination.” Id.
“In most people with a normal immune system, a poliovirus infection is asymptomatic.” See Poliomyelitis, http://en.wikipedia.org/wiki/Poliomyelitis. Factors that increase the risk of polio infection or affect the severity of the disease include immune deficiency. Id. “In the 4% to 8% of cases in which there are symptoms (called symptomatic polio), the illness appears in three forms, including: a more serious form associated with aseptic meningitis called nonparalytic polio (1%-5% show neurological symptoms such as sensitivity to light and neck stiffness), and a severe, debilitating form called paralytic polio (this occurs in 0.1%-2% of cases).” Joel Kline, M.D., Polio, Sept. 10, 2010, http://kidshealth.org/parent/infections/bacterial_viral/polio.html. “Although the acute illness usually lasts less than 2 weeks, damage to the nerves [can] last a lifetime.” Id., at http://kidshealth.org/parent/infections/bacterial_viral/polio.html#.
“[A]ffected individuals can exhibit a range of symptoms if the virus enters the blood stream.In about 1% of cases the virus enters the central nervous system, preferentially infecting and destroying motor neurons, leading to muscle weakness and acute flaccid paralysis. ... [In] cases progress[ing] to paralytic disease, ... the muscles become weak, floppy and poorly controlled, and finally completely paralyzed; this condition is known as acute flaccid paralysis.” See Poliomyelitis, http://en.wikipedia.org/wiki/Poliomyelitis.
“Different types of paralysis may occur, depending on the nerves involved. Spinal polio is the most common form, characterized by asymmetric paralysis that most often involves the legs. Bulbar polio leads to weakness of muscles innervated by cranial nerves. Bulbospinal polio is a combination of bulbar and spinal paralysis.” “Depending on the site of paralysis, paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal. Encephalitis, an infection of the brain tissue itself, can occur in rare cases and is usually restricted to infants. It is characterized by confusion, changes in mental status, headaches, fever, and less commonly seizures and spastic paralysis. Id.
“Poliomyelitis is caused by infection with a member of the genus Enterovirus known as poliovirus (PV). This group of RNA viruses colonize the gastrointestinal tract — specifically the oropharynx and the intestine.” Id. “Poliovirus divides within gastrointestinal cells for about a week, from where it spreads to the tonsils (specifically the follicular dendritic cells residing within the tonsilar germinal centers), the intestinal lymphoid tissue including ... the deep cervical and mesenteric lymph nodes, where it multiplies abundantly. The virus is subsequently absorbed into the bloodstream. ... Poliovirus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks. In a small percentage of cases, it can spread and replicate in other sites such as brown fat, the reticuloendothelial tissues, and muscle. ...sustained replication causes a major viremia .... Rarely, this may progress and the virus may invade the central nervous system, provoking a local inflammatory response. In most cases this causes a self-limiting inflammation of the meninges, the layers of tissue surrounding the brain, which is known as non-paralytic aseptic meningitis. ... In around 1% of infections, poliovirus spreads along certain nerve fiber pathways, preferentially replicating in and destroying motor neurons within the spinal cord, brain stem, or motor cortex. This leads to the development of paralytic poliomyelitis, the various forms of which (spinal, bulbar, and bulbospinal) vary only with the amount of neuronal damage and inflammation that occurs, and the region of the CNS that is affected.” The destruction of the neuronal cells causes brain stem and spinal damage of various types. See Poliomyelitis, http://en.wikipedia.org/wiki/Poliomyelitis.
Bulbar polio – In “about 2% of cases of paralytic polio, bulbar polio occurs when poliovirus invades and destroys nerves within the bulbar region of the brain stem. ... The destruction of these nerves weakens the muscles supplied by the cranial nerves, producing symptoms of encephalitis, and causes difficulty breathing, speaking and swallowing.” See Poliomyelitis, http://en.wikipedia.org/wiki/Poliomyelitis.
Critical brain stem (bulbar) Cranial Nerves affected include “the glossopharyngeal nerve, which partially controls swallowing and functions in the throat, tongue movement and taste; the vagus nerve, which sends signals to the heart, intestines, and lungs; and the accessory nerve, which controls upper neck movement. Due to the effect on swallowing, secretions of mucus may build up in the airway causing suffocation. Other signs and symptoms include facial weakness, caused by destruction of the trigeminal nerve and facial nerve, which innervate the cheeks, tear ducts, gums, and muscles of the face, among other structures; double vision; difficulty in chewing; and abnormal respiratory rate, depth, and rhythm, which may lead to respiratory arrest.” See Poliomyelitis, http://en.wikipedia.org/wiki/Poliomyelitis.
Bulbospinal polio – “Approximately 19% of all paralytic polio cases have both bulbar and spinal symptoms; this subtype is called respiratory polio or bulbospinal polio. ...[T]he virus affects the upper part of the cervical spinal cord (C3 through C5), and paralysis of the diaphragm occurs. The critical nerves affected are the phrenic nerve, which drives the diaphragm to inflate the lungs, and those that drive the muscles needed for swallowing. By destroying these nerves this form of polio affects breathing, making it difficult or impossible for the patient to breathe .... It can lead to paralysis of the arms and legs and may also affect swallowing and heart functions.” See Poliomyelitis, http://en.wikipedia.org/wiki/Poliomyelitis.
“Treatment of polio often requires long-term rehabilitation, including physical therapy, braces, corrective shoes and, in some cases, orthopedic surgery. Bulbar polio often causes death if respiratory support is not provided; with support, its mortality rate ranges from 25 to 75%, depending on the age of the patient. ... Other mechanisms that occur during the rehabilitation phase, and contribute to muscle strength restoration, include myofiber hypertrophy—enlargement of muscle fibers through exercise and activity.... In addition to these physiological processes, the body possesses a number of compensatory mechanisms to maintain function in the presence of residual paralysis. These include the use of weaker muscles at a higher than usual intensity relative to the muscle's maximal capacity, enhancing athletic development of previously little-used muscles, and using ligaments for stability, which enables greater mobility. See Poliomyelitis, http://en.wikipedia.org/wiki/Poliomyelitis.
In 1955 the [pre-polio vaccine era] criteria were changed to conform more closely to the definition used in the 1954 Salk polio vaccine field trials: “residual paralysis was determined 10 to 20 days after onset of illness and again 50 to 70 days after onset.... This change in definition meant that in 1955 we started reporting a new disease, namely, paralytic poliomyelitis with a longer-lasting paralysis.” See Hiding Polio, http://www.whale.to/vaccine/polio1.html.
"Polio has not been eradicated by vaccination, it is lurking behind a redefinition and new diagnostic names like viral or aseptic meningitis….” “After the Salk vaccine was introduced, the definition of polio was changed by the CDC. Now, in order to have paralytic polio, you had to have it longer than 60 days. Because the Salk vaccine was promoted as being incapable of causing polio, cases that occurred following administration of the vaccine were denied” initially by doctors – i.e., the dramatic decline in polio cases to a change in arbitrary, capricious, and fraudulent reporting practices by physicians. See Hiding Polio, http://www.whale.to/vaccine/polio1.html
'Having poliomyelitis paralysis more than 60 days' under definition existing when I was Autism Vaccine injured 
I was born on April 16, 1956. My earliest photos do not show proof that I had yet suffered my Autism Vaccine injury as evident from my perfectly symmetrical Cranial Nerves -- in particular my left eye does not partly close with a paralysis to my brain stem Cranial nerves and the right side of my mouth does not curve downward from a paralysis to my Cranial Nerves while the left side curves upward.
My Baby Photo Nov. 1956 - Age 6 1/2 Months Showing NO Paralytic Brain Stem Cranial Nerves
My Baby Photo Dec. 1956 - Age 7 1/2 Months Showing NO Paralytic Brain Stem Cranial Nerves
"The Vaccine Injury Table (Table)... lists and explains injuries/conditions that are presumed to be caused by vaccines. It also lists time periods in which the first symptom of these injuries/conditions must occur after receiving the vaccine. If the first symptom of these injuries/conditions occurs within the listed time periods, it is presumed that the vaccine was the cause of the injury or condition unless another cause is found." Paralytic polio in an immuno-deficient recipient in polio vaccine containing live virus "0-6 months." Vaccine Injury Table, National Vaccine Injury Compensation Program, http://www.hrsa.gov/vaccinecompensation/table.htm
"The National Foundation For Infantile Paralysis (NFIP) used the "The March Of Dimes" to fund its polio research which lead to the Salk vaccine field trials in 1954. April 12, 1955, Salk vaccine began on large scale. ... April 25, vaccination program encountered disaster via faulty vaccines manufactured by the Cutter Laboratory in California, which were discovered by EIS. The incidence rate (17 per 100,000 for one month) was higher than with that found with other manufacturer's vaccines, yet this rate was not at all an impossibility since incidence rates of over 400 per 100,000 per month were found in Detroit in 1958. The EIS found 204 Cutter polio cases, by assuming contagion, and then highly publicized these cases (Jane Smith, Patenting The Sun) though only 79 cases were documented (Fields Virology). It was decided that because Cutter did not filter its vaccine thoroughly, that tissue particles had contributed to allergic reactions and live polioviruses." Three injections – Salk vaccine, 1956, http://www.harpub.co.cc/pol_all.htm
On May 8, 1955, the Surgeon General of the United States suspended the entire US production of the Salk polio vaccine and called for emergency meetings with Salk and the manufacturers. They then agreed that these cases were caused by polioviruses surviving the formaldehyde poisoning by being inside ‘lumps in the vaccine'. Thus, for purposes of the Vaccine Table, the early Salk polio vaccines containing live virus falls under the "polio vaccine containing live virus '0-6 months'" portion of the Vaccine Injury Table, see Vaccine Injury Table, National Vaccine Injury Compensation Program, http://www.hrsa.gov/vaccinecompensation/table.htm
By 1955 US children were receiving three injections with Salk’s polio vaccine, as well as the smallpox and whooping cough vaccines.
The New York Times of May 11, 1956 reported the ‘Supplement No. 15 of the Poliomyelitis Surveillance Report' for that year revealed there was 12% more paralysis in 1956 than in 1955. By January 1957 seventeen US states had stopped distributing the polio vaccine. The New York Times reported that nearly half of all polio cases reported were in vaccinated children.
An eight-year-old Chicago boy who had received three injections of "Salk vaccine in 1956 came down with paralytic polio in May of 1957, see Chicago Sun-Times. August 25, 1957, just like I did during 1957.
In January of 1957. Tommy Mohr. a child from Albuquerque, N.M., contracted polio four months after his third inoculation with Salk vaccine; it was confirmed at Johns Hopkins Hospital that the death was due to polio. See Chicago Daily News, March 14, 1957.
My Baby Photo first of Jan. 1958 - Age 1 Year 8 1/2 Months Showing The House With The Staircase I Was Carried Up While My Entire Body Was Paralyzed and I was Dying Of Paralytic Poliomyelitis Autism Vaccine Injury With a Fever as High as 107 Degrees (105 degrees can produce convulsions in people), and Showing First Evidence Of My Left Eye and Right Mouth Residual Brain Stem Cranial Nerve Paralysis 'Having poliomyelitis paralysis more than 60 days' While My Father Still Had To Carry Me Everywhere
Photo: April 1958 Showing Me Having To Sit In A Baby Walker Because I Lost My Ability To Walk After Entire Body Paralysis And Marked Evidence Of My Left Eye and Right Mouth Residual Brain Stem Cranial Nerve Paralysis Autism Vaccine Injury 'Having poliomyelitis paralysis more than 60 days'
Photo: June 1958 Showing Me Having To Learn To Walk All Over Again After Entire Body Paralysis And Marked Evidence Of My Left Eye and Right Mouth Residual Brain Stem Cranial Nerve Paralysis Autism Vaccine Injury 'Having poliomyelitis paralysis more than 60 days'
My Second Grade Photo, 1963 - Age 7 Showing More Marked Evidence Of My Left Eye and Right Mouth Residual Brain Stem Cranial Nerve Paralysis Autism Vaccine Injury 'Having poliomyelitis paralysis more than 60 days'
My Seventh Grade Photo, 1968 - Age 13 Hiding Evidence Of My Left Eye and Right Mouth Residual Brain Stem Cranial Nerve Paralysis Autism Vaccine Injury 'Having poliomyelitis paralysis more than 60 days' with my hair so I would not be taunted, mocked, and Autism BULLIED for my Paralytic Polio Autism Vaccine Injury
Photo: President Lyndon Baines Johnson Bestowed a Presidential Physical Fitness Award On Me For Efforts To Overcome As Best I Could My Paralytic Polio Autism Vaccine Injury 'Having poliomyelitis paralysis more than 60 days'
Photo: January 1976 U.S. National Equestrian Title "Edencroft Trophy" Derived From Countless Hours Of Autism Horse Riding Therapy, Showing Evidence Of My Left Eye and Right Mouth Residual Brain Stem Cranial Nerve Paralysis Autism Vaccine Injury 'Having poliomyelitis paralysis more than 60 days'
Photo: May 1990 Graduation From University of San Francisco School of Law Showing Evidence Of My Left Eye and Right Mouth Residual Brain Stem Cranial Nerve Paralysis Autism Vaccine Injury 'Having poliomyelitis paralysis more than 60 days' But California and Florida Refuse To Let Me Become A Lawyer Because They Won't Accommodate My Paralytic Polio Autism Vaccine Injury In Their Bar Admission Process Or Their Courts
Photo: When The Sonoma County, California Superior Court Used A "Grandparent Visitation" Case To Take My Own Daughter Away From Me Because I Have A Paralytic Polio Autism Vaccine Injury And They Refused To Provide Me Title II Americans With Disabilities Act Accommodations So I Could Defend My Fundamental Constitutional Right To Be A Mother And Parent My Own Child, Other People Had To Write Out My Legal Arguments For Me Because A Paralytic Polio Autism Vaccine Injury Damaged Motor Neurons In My Brain Stem And Spinal Cord
Medical Reports Documenting My 'Having poliomyelitis paralysis more than 60 days' Evidenced In Cranial Nerve Brain Stem Autism Vaccine Injury Shown In My Baby Photos From 1957 To The Present Date, 2011
Michael W. Hoffmann, M.D.’s medical reports of Jul. 18, 2008, pg. 1 reported I had meningitis (“She had meningitis”) paralytic poliomyelitis Autism Vaccine injury.
Murthy Ravipati, M.D.'s medical report of May 23, 2008, pg. 2 reported I had at least one paralytic injury to a Cranial Nerve, thereby reporting residual paralytic poliomyelitis Autism Vaccine brain stem injury to my Cranial Nerves.
Loren Bartels, M.D.’s medical report of Apr. 10, 2008, pg. 2 reported I had only six of 12 Cranial Nerves that were “normal,” thereby reporting residual paralytic poliomyelitis Autism Vaccine brain stem injury to Cranial Nerves I, II, III, IV, VI, and VIII.
 Vaccination, The Medical Assault on the Immune System—Dr V.Scheibner, cited in Polio Information & Polio Vaccine Dangers, http://www.nccn.net/~wwithin/polio2.htm. “Four of the five Salk vaccine companies ceased producing this vaccine due to its failure, and because of the lawsuits against them. ‘Use of either Salk or Sabin vaccine will increase the possibility that your child will contact the disease. …’—Dr Mendelsohn M.D.(1984).” Id. “‘Some of the vaccines that are being currently being used are still laced with viruses,’—Leonard Horowitz., D.M.D., M.A., M.P.H.”Id.
 Davis L, Bodian D, Price D, Butler I, Vickers J (1977), "Chronic progressive poliomyelitis secondary to vaccination of an immunodeficient child". N Engl J Med 297 (5): 241–5. doi:10.1056/NEJM197708042970503. PMID 195206.
 Atkinson W, Hamborsky J, McIntyre L, Wolfe S (eds.) (2009), "Poliomyelitis" (PDF), Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book) (11th ed.), Washington DC: Public Health Foundation, pp. 231–44. http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/polio.pdf.
 Cohen JI (2004). "Chapter 175: Enteroviruses and Reoviruses," in Kasper DL, Braunwald E, Fauci AS, et al. (eds.), Harrison's Principles of Internal Medicine (16th ed.), McGraw-Hill Professional. pp. 1144. ISBN 0-07-140235-7.
 Yin-Murphy M, Almond JW (1996), "Picornaviruses: The Enteroviruses: Polioviruses," Baron's Medical Microbiology (Baron S et al., eds.) (4th ed.), Univ of Texas Medical Branch. ISBN 0-9631172-1-1. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.2862.
 “Virus invasion causes inflammation of the nerve cells, leading to damage or destruction of motor neuron ganglia. When spinal neurons die, Wallerian degeneration takes place, leading to weakness of those muscles formerly innervated by the now dead neurons.” See Poliomyelitis, http://en.wikipedia.org/wiki/Poliomyelitis (citing Cono J, Alexander LN (2002), "Chapter 10, Poliomyelitis," (PDF), Vaccine Preventable Disease Surveillance Manual (3rd ed.), Centers for Disease Control and Prevention, pp. 10–1. http://www.cdc.gov/vaccines/pubs/surv-manual/3rd-edition-chpt10_polio.pdf).
 Atkinson W, Hamborsky J, McIntyre L, Wolfe S (eds.) (2009), "Poliomyelitis" (PDF), Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book) (11th ed.), Washington DC: Public Health Foundation, pp. 231–44. http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/polio.pdf.
 Leboeuf C (1992) (PDF), The late effects of Polio: Information For Health Care Providers, Commonwealth Department of Community Services and Health. ISBN 1-875412-05-0. Archived from the original on June 25, 2008. http://web.archive.org/web/20080625212726/http://www.health.qld.gov.au/polio/gp/GP_Manual.pdf. Retrieved 2008-08-23.
 Atkinson W, Hamborsky J, McIntyre L, Wolfe S (eds.) (2009), "Poliomyelitis" (PDF), Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book) (11th ed.), Washington DC: Public Health Foundation, pp. 231–44. http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/polio.pdf.
 Atkinson W, Hamborsky J, McIntyre L, Wolfe S (eds.) (2009), "Poliomyelitis" (PDF), Epidemiology and Prevention of Vaccine-Preventable Diseases (The Pink Book) (11th ed.), Washington DC: Public Health Foundation, pp. 231–44. http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/polio.pdf; Miller AH, Buck LS (1950), "Tracheotomy in bulbar poliomyelitis," California medicine 72 (1): 34–6. PMC 1520308. PMID 15398892.
 In 1956, the health authorities instructed doctors that they were in future only to diagnose polio if a patient has paralytic symptoms for 60 days or more. This definition was not changed until 1958. I got paralytic poliomyelitis Autism Vaccine injury during 1957 -- before Jan. 1, 1958.
 See Tinnerholm v. Parke, Davis & Co., 411 F.2d 48 & fn. 4(2d Cir. 1969)
Sudden Infant Death SYNDROME (SIDS)
"CDC itself admits, 'The age at which infants begin their primary course of vaccinations (2 to 4 months old) is also the peak age for the incidence of sudden infant death syndrome (SIDS).'" (NaturalNews 2011)."
Sleep Disorders and Seizures Occur In Significant Numbers in the Autism Population
Autism Speaks' Autism Treatment Network's patient registry, .. reported that 65% of children with [Autism] experience sleep disturbances, and 14% of those with sleep problems also have seizures." (AutismSpeaks, 2011).
"GI problems were also reported in 50% of children [with Autism], and children with GI problems were more likely to have sleep disturbances, behavioral problems, and a lower health-related quality of life. Other health issues identified include seizures, food sensitivities, anxiety and depression." (AutismSpeaks, 2011).
"[T]he Internet and its assorted devices are not merely tools for human use, but rather the future of human evolution." http://www.washingtonpost.com/wp-dyn/content/article/2011/01/28/AR2011012806446.html (hereafter "Internet a basic human right, 2011" ).
Further, "[i]t's right there in Article 19 of the U.N. Universal Declaration of Human Rights: 'Everyone has the right to freedom of opinion and expression; this right includes freedom . . . to seek, receive and impart information and ideas through any media and regardless of frontiers.'" "Internet access is a basic human right...." (Internet a basic human right, 2011).
"Formation of a functional synapse is a complex process requiring stabilization of initial synaptic contacts by adhesive protein interactions, organization of presynaptic and postsynaptic specializations by scaffolding proteins, regulation of growth by intercellular signaling pathways, reorganization of the actin cytoskeleton, and proper endosomal trafficking of synaptic growth signaling complexes. Many neuropsychiatric disorders, including autism ..., have been linked to inherited mutations which perturb these processes." Jan E. Melom & J Troy Littleton, Synapse development in health and disease, Jan. 27, 2011, http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VS0-52226V0-3&_user=10&_coverDate=01%2F27%2F2011&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=47682e0e1890a6a4608ff6dac78d71cf&searchtype=a.
Neurological Map of Brain Connectivity Changes During Development
The "Connectome" -- Connectivity of Neural Highways In The Human Brain
"Connected highways of nerve cells carry information to and from different areas of the brain and the rest of the nervous system. Scientists are trying to draw a complete atlas of these connections ... referred to as the 'connectome' -- to gain a better understanding of how the brain functions in health and disease." Study Shows Map Of Brain Connectivity Changes During Development, MedicalNewsToday, Jan. 28, 2011, http://www.medicalnewstoday.com/articles/214929.php (hereafter "Scripps, 2011") (emphasis added).
"In the nervous system, information is handed from one nerve cell to another through two arms, called dendrites and axons, stretching out from opposite sides of each cell. The axon carries information away from a nerve cell, or neuron, and passes it to the dendrite of another; dendrites receive the information, which travels through the cell to the axon. The region where the information is transferred from one neuron to another (and where the axons and dendrites connect) is called the synapse." (Scripps, 2011) (emphasis added).
Synapse Formation - The Courtship Dance Before Selection Of A Life Partner
In synapse formation, it has been thought that "as dendrites extend new branches, each branch forms an immature synapse with a target axon that is later either maintained or eliminated." (Scripps,, 2011). However, the Scripps research "shows instead the process is not as selective. Each growing dendrite samples not one but many possible partners before selecting one with which to maintain contact. As new branches grow from dendrites, they form many immature synapses on axons. Then as each new dendrite matures, most immature synapses are eliminated; the ones not eliminated mature into stable synapses." (Scripps, 2011) (emphasis added).
Moreover, brain activity is the impetus that helps new connections to form; brain activity is needed for selecting which synapses should be eliminated and without such brain activity many more immature synapses occurred. (Scripps, 2011) (emphasis added).
Recent research by The Scripps Institute shows this road grid map of connected highways in the brain "undergoes constant revisions" as the brain of the young develop "with new routes forming and others dropping away in a matter of hours. 'We have shown that the connectome is dynamic during development, but ... will also change according to an individual's experience and in response to disease...." (Scripps, 2011) (emphasis added).
"[E]xperience" includes "the different sights and sounds and other environmental cues picked up by neurons-change connections and activities in the brain through a process known as plasticity." (Scripps, 2011).
See discussion, supra: Autism-Specific Implicit Learning Disabilities, Autistic People's Implicit Learning May Not Map Directly Onto Non-Autistics' Implicit Learning Or Be Governed By The Same Constraints, "autistics’ implicit learning may not map directly onto non-autistics’ implicit learning or be governed by the same constraints." Dawson, Mottron, & Gernsbacher, 2008.
"The effectiveness of comprehensive early intervention programs is judged against autism’s presumed poor prognosis, and according to the extent to which typical skills have successfully been acquired and atypical autistic behaviors have successfully been extinguished (Handleman and Harris, 2001; Smith, 1999)." Dawson, Mottron, & Gernsbacher, 2008 (emphasis added).
"The possibility that a typical developmental trajectory and repertoire of behaviors may not be adaptive for autistics or beneficial for autistic learning has not yet been considered. Researchers have “studied the effectiveness of programs, not the appropriateness of various goals” (NRC, 2001) ...." Dawson, Mottron, & Gernsbacher, 2008 (emphasis added).
Incredibly (!), U.S. "behavior analysts" beginning in the 1960's, "characterized autistics as being governed by the same laws of learning as all other organisms, while being distinguished by failing to learn from the typical, every-day environment (e.g., Lovaas, 1987; Green, 1996; Smith and Lovaas, 1998; Lovaas and Smith, 2003; Koegel et al., 2001)." Dawson, Mottron, & Gernsbacher, 2008 (emphasis added). Huh ??? !!!
Yet, None of the Cro-Magnon Neurotypical human types could see the total disconnect in the scientific reasoned logic of pursuing their line of thinking ?
The Autistic Perspective Of Cro-Magnon Neurotypical Traits
Malleability in character
"Perhaps one of the most frustrating things about neuro-typical people is their malleability in character. Neuro-typical people often play a different part for each person they meet and while they are not in anyway being inauthentic, as a person on the autistic spectrum, I feel completely fake when I try to emulate this." Comment posted to aspietribe on Topic: People with Autism Rarely Judge Others, by Mark Wharton,
"The identification of early signs of [Autism] is crucial to the advancement of early detection. As research studies have shown time and again, early intervention significantly improves treatment outcomes for children with [Autism]; however, early intervention heavily depends upon the time at which a child is diagnosed. Thus, it is important that researchers identify and explore early signs of [Autism] that may be useful in detecting [Autism] sooner." __
"However, the only empirical investigation to date found that autistics acquired the specific trained behaviors (labeling pictures expressing facial affect), but did so without producing the desired neurofunctional changes (increased task-related activity in the fusiform gyrus, Bölte et al., 2006)." Dawson, Mottron, & Gernsbacher, 2008 (emphasis added).
You Can't Forcibly Change A Cat Into A Dog - Or, How Cro-Magnon Neurotypicals Lightbulbs Went Off In The Brain After Numerous Failed Efforts To Extinguish & Wipe Out The Neurological Differences Of The Autistic Indigenous People Whom Cro-Magnon Labeled "Not Recognizably Human"
"[B]ehavior analytic literature in autism presents autistics as having an extremely restricted behavioral repertoire that is not recognizably human, as lacking in human
experience to the point of being tabula rasa, as requiring the explicit teaching of virtually every human behavior ...." Dawson, Mottron, & Gernsbacher, 2008 (emphasis added).
"[M]y brain is not particularly efficient in decoding sounds and speech. The net result is that sometimes there's a noticeable delay between my hearing a sound, and my brain decoding it. I'll hear some muffled, unrecognizeable sound, say "What?", then a second later my brain will decode it as speech. What does this lead to when the other person makes the assumption that my hearing/neurology is "normal"? The presupposition that I really heard them in the first place then lied about it, which is not true at all. Many articles about autism written from the outside perspective fall prey to this type of thinking ...." (Soraya, 2008) (emphasis added).
A Cro-Magnon Neurotypical] person "who looks at typical autistic behavior - avoiding eye contact, not talking, and avoiding personal contact - tends to make the assumption that this behavior means the same thing that it would mean in a person who does not have autism. This leads to blanket statements such as 'People with autism have no desire for human contact.' The question is - do you know this, or is it a presupposition? Especially if the person in non-verbal - can you make that presupposition? Or could it be that the person wants interaction, but finds it painful or difficult to do so?" (Soraya, 2008) (emphasis added).
The Ability Of People With Autism To Learn Has Historically Been Characterized From The Cro-Magnon Neurotypical Perspective As "Non-Existent" And Singled Out As "Subhuman""[T]he ability of autistics to learn is considered nonexistent in the typical everyday environment (Lovaas and Smith, 2003) and fundamentally impaired (Klinger et al., 2006), but so astounding that the ognitive literature as a whole is insufficient to explain it (Atkin and Lorch, 2006). Autistic learning is recognized as distinctive (Volkmar et al., 2004) and singled out as subhuman (Tomasello et al., 2005)..." Dawson, Mottron, & Gernsbacher, 2008.
Autistic People's Implicit Learning May Not Map Directly Onto Non-Autistics' Implicit Learning Or Be Governed By The Same Constraints
"[L]earning in autism is characterized both by spontaneous—sometimes exceptional—mastering of complex material and an apparent resistance to learning in conventional ways. Learning that appears to be implicit seems to be important in autism, but autistics’ implicit learning may not map directly onto non-autistics’ implicit learning or be governed by the same constraints." Dawson, Mottron, & Gernsbacher, 2008.
Cro-Magnon Neurotypical Teaching Methods Do Not Work For People With Autism -
"In both cases (perception and procedural memory), procedures (e.g., repeated performance of tasks) that reliably resulted in learning in non-autistics appeared
not to do so in autistics, while autistics appeared to learn in ways (e.g., apparently passive exposure to materials) that did not necessarily benefit non-autistics." Dawson, Mottron, & Gernsbacher, 2008 (emphasis added).
Autistic People Who Are "Taught" Cro-Magnon Neurotypical Skills Are Neurologically Unable To GENERALIZE Those Skills Across Contexts Or To Related-Neurotypical Skills
"A common finding ... is that autistics, when explicitly taught typical skills, fail to generalize those skills across contexts or to related typical skills (e.g., Hwang and Hughes, 2000; Lovaas et al., 1973; Lovaas and Smith, 1989; Ozonoff and Miller, 1995).This failure to generalize is widely regarded as an autistic learning deficit ...." Dawson, Mottron, & Gernsbacher, 2008 (emphasis added).
Analogy to Feminine Male Humans - "Young “feminine boys” who underwent early intensive behavioral interventions to impose stereotypically male behaviors also demonstrated a failure to generalize (Rekers and Lovaas, 1974; Rekers et al., 1974)." Dawson, Mottron, & Gernsbacher, 2008.
Recent research has found that "identical twins, who share their genetic make-up, did more similarly in [English, maths and science] tests than ... fraternal twins, who share half their genetic make-up. ...'The results were striking, indicating that even when previous achievement and a child's general cognitive ability are both removed, the residual achievement measure is still significantly influenced by genetic factors.'" Katherine Sellgren, Genes 'play key role in classroom performance,' BBC News, Feb. 2, 2011, http://www.bbc.co.uk/news/education-12339798 (hereafter "Sellgren, 2011").
"[T]he findings point to a need to re-examine what schools, colleges and universities offer young people, particularly in the light of modern technology. This genetic perspective on learning suggests a return to the original meaning of education [and testing].... "'[I]nstead of a model of instruction in which [people] are the passive recipients of knowledge, a genetically sensitive approach to education suggests an active view of learning in which children select, modify and create their own education in part on the basis of their genetic propensities'" (Sellgren, 2011).
"[A]utistics are often divided into high- and low-functioning subgroups, based on a
snapshot measurement of intelligence or developmental level. While this division is an efficient shorthand to denote whether participants fall into the range of diagnosable mental retardation, instruments normed for the non-autistic population are potentially misleading when applied to autistics (e.g., Mottron, 2004) ...." Dawson, Mottron, & Gernsbacher, 2008 (emphassis added).
Weschler IQ - A Measure of Cro-Magnon g-Intelligence
"Autistics’ average scores on intelligence test batteries (e.g., Wechsler scales) mask widely scattered subtest scores, raising the question of whether level of functioning can definitively be assigned even at any single point in time." Dawson, Mottron, & Gernsbacher, 2008 (emphasis added).
"[A]utistics’ performance on Raven’s Progressive Matrices, the pre-eminent measure of fluid intelligence, may significantly exceed their performance on Wechsler scales, suggesting that the high- versus low-functioning division is of questionable validity ...."Dawson, Mottron, & Gernsbacher, 2008 (emphasis added, citation omitted).
Due to the nature of autism, and individual's difficulties with social interaction and communication, anyone assessing or judging person with Autism must have an understanding of the condition in order to ascertain Autistic people's needs. Personal Budgets Must Be Supported Warns The National Autistic Society, UK. Nov. 18, 2010, http://www.medicalnewstoday.com/articles/208235.php.
"It is not always apparent that someone with autism has a disability because autism can be a hidden disability and the needs of the person with the condition can fluctuate on a daily basis depending on their environment and levels of anxiety. It can be very difficult for someone who has not been specifically and specially trained in Autistic Spectrum Condition's to effectively determine the impact that the disability has on the person with the condition in a relatively short assessment process. ...[A] radical overhaul of the assessment process is urgently required. At the moment the assessment is not wrapped around a realistic works model. There is an overriding emphasis on what the person ‘can do’ as opposed to what they ‘can not do’ but it is almost impossible to decide what an autistic person can do without first understanding what they can not do." ACT NOW (Autism Campaigners Together), http://networkedblogs.com/dM4rh.