Thursday, March 27, 2014
Study supports that Autism originates during pregnancy
For moms who worry that autism is somehow vaccine - related, please read. That theory is false and has been thoroughly and clearly debunked by the scientific community. Andrew Wakefield's "study" was completely false and his reputation destroyed. Jenny McCarthy is simply a irresponsible celebrity, not medical authority. Do not refuse to vaccinate your children, there is no link between vaccines and autism. Two strong evidence points suggest that 1) autism begins prenatally and 2) genetics most likely play a role.
Researchers at the University of California, San Diego School of Medicine and the Allen Institute for Brain Science have published a new study that shows new evidence that autism begins during pregnancy. The authors are: Eric Courchesne, PhD, professor of neurosciences and director of the autism Center of Excellence at UC San Diego, Ed S. Lein, PhD, of the Allen Institute for Brain Science in Seattle, and first author Rich Stoner, PhD, of the UC San Diego Autism Center of Excellence. The peer-reviewed study analyzed post-mortem brains of children with autism, finding that key genetic markers were absent in brain cells in multiple layers. "This defect," Courchesne stated, "indicates that the crucial early developmental step of creating six distinct layers with specific types of brain cells -- something that begins in prenatal life -- had been disrupted."
These results add to the already-considerable evidence that autism starts in the womb; according to Professor Stanley Nelson of UCLA's David Geffen School of Medicine, "The overwhelming set of data is that the problems are existing during [very early] brain development, probably as an embryo or fetus." The prenatal origin of autism Spectrum Disorder (ASD) also supports the prevailing view of ASD expressed by Professor Daniele Fallin of the Johns Hopkins Bloomberg School of Public Health: “If there is environmental risk or interaction with genes, it’s likely to either [occur around the time of conception] or very early in development in utero” and thus risk of ASD cannot be attributed to postnatal vaccines.
As noted in this study, autism has been previously associated with abnormal prenatal proliferation of neurons leading to an excess of neurons in prefrontal cortex. Moreover, children who regressed into autism followed an abnormal trajectory of brain growth consistent with this abnormal prenatal development, which is also consistent with the recent data that demonstrates that gene networks associated with autism tend to be expressed during mid-fetal development in pre-frontal cortex. Other children who developed ASD were shown to have abnormal accumulations of fluids in their brains in a pattern previously shown to begin to develop before birth.
Both genetic and environmental data point to early to mid gestation as the critical period for the development of ASD. Both rare and common genetic variations contribute to ASD risk; and both inherited and spontaneous mutations play a role. Environmental factors identified as drivers of ASD risk include maternal infection, preterm birth, advanced parental age, short inter-pregnancy interval, prenatal exposure to air pollution, phthalates and pesticides, and inadequate intake of appropriate prenatal vitamins around the time of conception.
The authors of a recently-published, long-term follow-up of all of the 1.5 million children born in Denmark between 1980-2004 found that "the difference in the recurrence risk between full- and half-siblings supports the role of genetics in ASDs, while the significant recurrence risk in maternal half-siblings [greater than in paternal half-siblings] may support the role of factors associated with pregnancy and the maternal intrauterine environment in ASDs." [Grønborg TK1, Schendel DE, Parner ET. Recurrence of Autism spectrum disorders in full- and half-siblings and trends over time: a population-based cohort study. JAMA Pediatr. 2013 Oct;167(10):947-53.]
Original Study in the NEJM: http://www.nejm.org/doi/full/10.1056/NEJMoa1307491
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