Environmental Factors
Possible Environmental Factors in Autism
Many writers have commented on the beauty of a child with autism. Bernard Rimland in Infantile Autism (1964) wrote: "The child is usually exceptionally healthy and attractive, quite often precocious and alert in appearance." (p. 7). Uta Frith in Autism: Explaining the Enigma (1989) wrote: "the young autistic child strikes the observer with a haunting and somehow other-worldy beauty." (p. 1). Whether this is universally true or not, I will leave to the perception of others. However, the point is: what could be going on in the body of such a normal looking child to cause such a pervasive and devastating reaction to the world around them? That is the "enigma of autism" (to borrow Uta Frith's term). Could it be that autism is caused by environmental factors? Are the toxins, chemicals, metals, synthetics, and other things we have put into God's world somehow affecting our children? Unfortunately, we have no answers but I would like to share some of the possibilities. The following web sites will present information on the possible environmental influences in autism and related disorders. Remember, this information is presented only for your information and does not imply a causal link. These are theories, which will have to be tested and researched. Take no action without first consulting your child's physician.
Links
Life Extension Magazine - Mercury Amalgam Toxicity - An article by Jim O'Brien. Discusses the problem of dental amalgams containing mercury.
The Environmental Protection Agency - Healthy School Environments - Mercury - The EPA has "disappeared" their old page about the neurotoxic effects of Mercury, which appeared to suggest the symptoms seen in autism. This site alerts schools to the dangers of Mercury with less specificity.
Autism: Do Environmental Factors Play a Role in Causation? Dr. Ted Schettler, M.D., MPH covers the possible environmental factors in autism in great detail.
Daily University Science News - Mercury and Brain Neurons - The April 2001 edition of the British journal NeuroReport has a cover story that examines the degenerative effects of mercury on brain neurons from snails. The authors of the article support their findings with time-lapse video, which shows how the neurons degenerate when exposed to mercury.
Article Abstracts
Title: Early environmental factors in autism.
Author(s): Rodier, PM and Hyman, SL.
Source: (1998) Mental Retardation and Developmental Disabilities Research Reviews 4:121-128.
Abstract: Genetic and environmental influences are not mutually exclusive as causes of birth defects. Rather, both contribute to the etiology of many congenital anomalies. Recent results from studies of autism in twins argue that this is the case for autism spectrum disorders. thus, even after the genetic causes of autism are known, it will be necessary to identify environmental factors that contribute to the expression of the symptoms. The first half of this review describes what has been learned from research on exogenous influences in autism, discussing studies of infections, inoculations, general pre- and perinatal factors, family histories, and drug and chemical exposures. The second discusses gene-environment interactions in other birth defects and the methods by which teratogens have been discovered. The role of known genetic syndromes in the etiology of autism is discussed with attention to whether their associations with the disorder are genetic or teratologic in nature.
Title: Prenatal exposure of rats to valproic acid reproduces the cerebellar anomalies associated with autism.
Author(s): Ingram, J.L., Peckham, S.M., Tisdale, B., and Rodier, P.M.
Source: (2000) Neurotoxicology and Teratology In Press.
Abstract: Abnormalities in anatomy and function of the cranial nerve motor nuclei have been demonstrated in some people with autism and can be modeled in rats by exposure to valproic acid during neural tube closure. Reductions in Purkinje cell number and cerebellar volume, particularly of the posterior labe, have also been reproted in people with autism. Thus, a stereological examination of cerebellar morphology was undertaken in valproate-exposed rats. Compared to controls, rats exposed to a single dose of 600 mg/kg sodium valproate on embryonic day 12.5 had significantly fewer Purkinje cells in the cerebellar vermis and a reduction short of significant in the hemispheres. The diminished cell numbers reflect reductions in tissue volume throughout the cerebellum, rather than cell density, which was unaffected in all regions. Within the vermis, the reduction in volume was significantly greater in the posterior lobe than in the anterior lobe. The results parallel those reported for human cases of autism.
Title: Embryological origin for autism: developmental anomalies of the cranial nerve motor nuclei.
Author(s): Rodier PM, Ingram JL, Tisdale B, Nelson S, Romano J
Source: J Comp Neurol 1996 Jun 24;370(2):247-61.
Abstract: The underlying brain injury that leads to autism has been difficult to identify. The diagnostic criteria of the disease are not readily associated with any brain region or system, nor are they mimicked by vascular accidents, tumors, or degenerative neurological diseases occurring in adults. Fortuitously, a recent report of autism induced by thalidomide exposure provides evidence that the disease originates by an injury at the time of closure of the neural tube. The human data suggest that the initiating lesion includes the motor cranial nerve nuclei. To test this hypothesis, we first examined motor nuclei in the brainstem of a human autistic case. The autopsy brain exhibited near-complete absence of the facial nucleus and superior olive along with shortening of the brainstem between the trapezoid body and the inferior olive. A similar deficit has been reported in Hoxa-1 gene knockout mice in which pattern formation of the hindbrain is disrupted during neurulation. Alternatively, exposure to antimitotic agents just after neural tube closure could produce the observed pattern of deficits. Thus, the lesions observed in the autopsy case appear to match those predicted by the thalidomide cases in both time of origin and central nervous system (CNS) location. To produce similar brain lesions experimentally, we exposed rat embryos to valproic acid, a second teratogen newly linked to autism. Dams received 350 mg/kg of valproic acid (VPA) on day 11.5 (the day of neural tube closure), day 12, or day 12.5 gestation. Each treatment significantly reduced the number of motor neurons counted in matched sections of the earliest-forming motor nuclei (V, XII), and progressively later exposures affected the VIth and IIIrd cranial nerve nuclei. All treatments spared the facial nucleus, which forms still later. Counts from the mesencephalic nucleus of trigeminal, the dorsal motor nucleus of the vagus, and the locus ceruleus were not affected by exposure to VPA, even though these nuclei form during the period when exposure occurred. Despite its effects on the motor nuclei, valproic acid exposure did not alter the further development of the brain in any obvious way. Treated animals were robust and had no external malformations. The autopsy data and experimental data from rats confirm that CNS injuries occurring during or just after neural tube closure can lead to a selective loss of neurons derived from the basal plate of the rhombencephalon. The results add two new lines of evidence that place the initiating injury for autism around the time of neural tube closure.
DISCLAIMER: This site is intended to provide basic information resources on Autistic Disorder. It is not intended to, nor does it, constitute medical or other advice. The author of the web site is not a medical doctor. Readers are warned not to take any action with regard to medical treatment or otherwise based on the information on this web site or links without first consulting a physician. This web site does not necessarily endorse any of the information obtained from any of the links on this page or links that other pages may lead you to. Neither does this web site promote or recommend any treatment, therapy, institution or health care plan. The information contained in this site is intended to be for your general education and information only and not for use in pursuing any treatment or course of action. Ultimately, the course of action in treating a given patient must be individualized after a thorough discussion with the patient's physician(s) and family.