Cause of Autism Part II

Cause of Autism Part II

Etiology theories for physical disorder models

While the etiology of autism is largely unknown, there is no shortage of theories in the area. In part, the mystery what can be the cause of autism has been slow to resolve due to its relatively recent identification as a disorder, and because government funding of autism research lags far behind that of less common diagnoses , such as juvenile diabetes. What funding is available has largely been directed toward epidemiological research, rather than clinical studies investigating possible environmental triggers. In addition, since the 1970s the recorded incidence of autism has risen dramatically in the west.

Genetics theory

Autism is known to be highly inheritable. Research done by some institutions seek to find a way for early and more accurate detection of autism similar to Rett syndrome. Instead of searching for one particular gene as the cause for autism, many of the studies tend to search for complex interactions between a number of genes.

A 2005 study done by the Duke Center for Human Genetics at Duke University finds some evidence that complex interactions between GABA (gamma aminobutyric acid) receptor genes might be part of the cause of autism. One of the functions of the GABA genes is to inhibit the nerve system from firing. The theory is that somehow GABA genes suffer damage of some kind, leading to an overwhelmed sensory system which causes the characteristics or symptoms of autism.

Brain testosterone theory

Simon Baron-Cohen has proposed a model for autism based in his empathising-systemising (E-S) theory[8]. His team at the Autism Research Centre in Cambridge, UK, measured testosterone levels in the amniotic fluid of mothers while pregnant. This was presumed to reflect levels in the babies themselves. The team found that the babies with higher fetal testosterone levels had a smaller vocabulary and made eye contact less often when they were a year old.

His group has looked at the original 58 children again, at age four. The researchers found that the children with higher testosterone in the womb are less developed socially, and the interests of boys are more restricted than girls. The results are published in the Journal of Child Psychology and Psychiatry in a 2004 issue.

Baron-Cohen theorizes that high fetal testosterone levels push brain development towards an improved ability to see patterns and analyze complex systems. Males supposedly tend to be better at such spacial tasks than females. But the high levels are thought to inhibit the development of communication and empathy. (New Scientist, May 24, 2003).

In 2004 Dr. Geier and his son, David Geier published a paper in the journal Medical Hypotheses on the potential importance of lowering testosterone as part of the treatment of autistic spectum disorders, which they claim involve mercury toxicity. In 2006 the Geiers published in the peer-reviewed Hormone Research journal, a paper titled "A Clinical and Laboratory Evaluation of Methionine Cycle-Transsulfuration and Androgen Pathway Markers in Children with Autistic Disorders." This paper presented data from Geier's clinic, suggesting a cyclical interaction between the methionine cycle-transsulfuration and androgen pathways in children with autistic disorders.

Nutritional deficiencies

Children exhibiting behavioral and learning disorders may do so in part because of diets deficient in vital nutrients needed for their brains to function and develop normally.

In 1998, a small study published in the medical journal Lancet found a consistent set of bowel disorders among a dozen autistic children. Although an emphasis was placed by the authors on a possible link to the MMR vaccine, the study also suggested nutritional deficits caused by bowel disorders may have contributed to the onset of neurological disorders. It should be noted that the sample was very small, and the results have not been replicated by other researchers.

Leaky Gut Syndrome and related

Some children with autism are said to have responded well to dietary intervention such as eliminating gluten (a protein found in most grains) and casein (the protein found in milk) as well as phenyls and food coloring (see Feingold diet). Most data regarding the validity of these interventions have been the subjective observations of parents and caretakers and no scientific study with proper subject elimination has taken place.

Possible determining factors regarding the effectiveness of this as a treatment involve coincidence of a combination of asthma, eczema, diarrhea and constipation, strange "yeasty" diaper rash, and uncharacteristic eating habits (eating an entire loaf of bread).

Several unproven theories behind the effectiveness of this as a treatment involve damage to the lining of the stomach and/or intestines allowing the proteins to be improperly metabolized as glutomorphine and casomorphine which are both opiates. The damage to the gut lining is theorized to be caused by immunio-abnormalities and possibly the incidence of early oral-antibiotic use combined with a genetic predisposition. However, this is speculation and there is as yet no proof.

Folic acid

Increased intake of folic acid by pregnant women roughly coincides with the reported increase in the prevalence of autism. The explanation offered is that folic acid allows more brain cells to survive than should. This hypothesis is untested at this point.

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