1. Allow ultrasound technicians to “date” your pregnancy, see if you have twins, check the growth of your baby. Even one ultrasound affects your baby’s brain. Multiple ultrasounds will move cells in the brain around and also affect future generations of your family.
2. Eat whatever you like in pregnancy. Don’t take the time and trouble to study the effects of over-processed, high fat diets. Don’t worry about buying organic produce and meat.
3. Let your physician induce you. Induction drugs over-ride Nature’s pace of the birth process. They cause prolonged periods of oxygen deprivation similar to holding a pillow over your child’s face. Any form of hurrying you into the birth process or, once into it, hurrying the process faster than it goes naturally will damage cells in the baby’s brain.
4. Take pain-killing drugs during your child’s birth. Every anesthetic goes immediately to the baby so choose whatever one you like. The longer the baby is medicated, the more brain damage is done.
5. Continue on with the interventions in birth by having a cesarean, forceps or vacuum pull out of your baby. None of these procedures are gentle. All involve incredible traction on the baby’s neck and head. Sometimes all three are used on the same baby. Risks of all 3 are increased when inductions and epidurals were brought into the birth.
6. Once your baby is born, feed him/her solutions made by pharma giants like Mead Johnson.
7. Be sure to inject your baby with every toxic pharmaceutical vaccine that your doctor recommends. Don’t do any research. 36 vaccines is the modern North American child’s recommended allotment of mercury preserved toxic waste.
For more information on childhood autism go to Non Toxic Childhood.
Raine Study on the importance of Breastfeeding for mental development.
Update, June 7, 2011
J Atten Disord. 2011 Jul;15(5):423-31. Epub 2011 Apr 28.
Perinatal pitocin as an early ADHD biomarker: neurodevelopmental risk?
Kurth L, Haussmann R.
Colorado State University, Fort Collins, CO, USA. Lisa.Kurth@ColoState.edu.
Objective: To investigate a potential relationship between coincidental increases in perinatal Pitocin usage and subsequent childhood ADHD onset in an attempt to isolate a specific risk factor as an early biomarker of this neurodevelopmental disorder. Method: Maternal labor/delivery and corresponding childbirth records of 172 regionally diverse, heterogeneous children, ages 3 to 25, were examined with respect to 21 potential predictors of later ADHD onset, including 17 selected obstetric complications, familial ADHD incidence, and gender. ADHD diagnosis and history of perinatal Pitocin exposure distinguished groups for comparison. Results: Results revealed a strong predictive relationship between perinatal Pitocin exposure and subsequent childhood ADHD onset (occurring in 67.1% of perinatal Pitocin cases vs. 35.6% in nonexposure cases, χ(2) = 16.99, p < .001). Fetal exposure time, gestation length, and labor length also demonstrated predictive power, albeit significantly lower. Conclusion: The findings warrant further investigation into the potential link between perinatal Pitocin exposure and subsequent ADHD diagnosis.
[PubMed - in process]
Med Hypotheses. 2010 Jul;75(1):53-8. Epub 2010 Feb 9.
Potential teratogenic effects of ultrasound on corticogenesis: implications for autism.
Williams EL, Casanova MF.
Department of Psychiatry and Behavioral Sciences, University of Louisville, Louisville, KY, USA.
The phenotypic expression of autism, according to the Triple Hit Hypothesis, is determined by three factors: a developmental time window of vulnerability, genetic susceptibility, and environmental stressors. In utero exposure to thalidomide, valproic acid, and maternal infections are examples of some of the teratogenic agents which increase the risk of developing autism and define a time window of vulnerability. An additional stressor to genetically susceptible individuals during this time window of vulnerability may be prenatal ultrasound. Ultrasound enhances the genesis and differentiation of progenitor cells by activating the nitric oxide (NO) pathway and related neurotrophins. The effects of this pathway activation, however, are determined by the stage of development of the target cells, local concentrations of NO, and the position of nuclei (basal versus apical), causing consequent proliferation at some stages while driving differentiation and migration at others. Ill-timed activation or overactivation of this pathway by ultrasound may extend proliferation, increasing total cell number, and/or may trigger precipitous migration, causing maldistribution of neurons amongst cortical lamina, ganglia, white matter, and germinal zones. The rising rates of autism coincident with the increased use of ultrasound in obstetrics and its teratogenic/toxic effects on the CNS demand further research regarding a putative correlation.
Copyright 2010 Elsevier Ltd. All rights reserved.
[PubMed - indexed for MEDLINE]
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LinkOut – more resources Source http://www.ncbi.nlm.nih.gov/pubmed/20149552