Nexus Magazine - Vol 23 #3, April—May 2016 by Nexus various

Author:Nexus various
Language: eng
Format: epub
Tags: conspiracy, alternative, news, commentary
Published: 2016-04-10T00:00:00+00:00

Implications for Autism

From the above studies regarding the observations and measurements of the corpus callosum, it is clear that the fibre density (density of the axon[s] in all regions including anterior, middle and posterior subregions), cross-sectional area and average thickness in female subjects are significantly higher and/or greater than in male subjects. These findings are very important in explaining why autism is primarily a male disorder.

Cohen (1999) was the first researcher to illustrate extremely high gamma-aminobutyric acid (GABA) levels in the plasma and urine and high plasma ammonia levels as possibly the root cause of autism. GABA is a major inhibitory neurotransmitter in the mammalian brain.

It is responsible for axon(s)-to-oligodendrocyte signalling in the corpus callosum. Located in the centre of the brain, the corpus callosum is responsible for language processing, speech and intelligence. When this area is damaged, cognitive disorders and language delays are usually found.

The finding of elevated levels of GABA in the plasma and urine could explain why autistic features such as self-stimulatory behaviour and language delays are found. This is possibly due to the abnormal development of the axon(s) in the corpus callosum (Cohen, 1999, 2001, 2002, 2004, 2015).

Cohen (2002, 2004) proposed a possible link between the liver and infantile autism via the measurements of elevated plasma ammonia and lower gamma-aminobutyric acid-transaminase (GABA-T, EC 2.6.1.19) enzyme activity. GABA-T is the enzyme responsible for GABA catabolism (chemical breakdown in the liver during regulation). Cohen (2002, 2004) illustrated that the GABA-T enzyme activity in an autistic child was approximately 45.5 per cent (approximately half) lower than in the average control (normal) group.

Elevated levels of ammonia in the plasma result in a decrease in the efficiency of the enzyme GABA-T, and this results in higher GABA concentrations in the plasma after liver regulation (Cohen, 2002, 2002a, 2004).

In addition, Cohen (2002, 2004) postulated that a link (a cause and effect) between plasma ammonia and plasma GABA exists, where the concentration of plasma ammonia and plasma GABA is directly related to one another.

In fact, a ratio of approximately 0.3 of plasma ammonia to plasma GABA seems to exist for normal subjects as well as for autistic subjects and individuals with liver disorders (e.g., hepatic encephalopathy) (Cohen, 2002, 2004).

Cohen (2015) also described that epigenetic transgenerational changes due to nuclear or atomic radiation exposure in paternal grandparents could be responsible for "switches" turning on or off genes in subsequent generations. Cohen (2004, 2004a, 2015) illustrated that these genes affect chromosome 16p13.3.

This chromosome region is important for the regulation of GABA-T enzyme activity since the enzyme GABA-T implicates a mapping region of chromosome 16p13.3 (Cohen, 2004, 2004a, 2015).

The finding that the fibre density (density of the axon[s] in all regions including anterior, middle and posterior subregions), cross-sectional area and average thickness of the corpus callosum in female subjects are significantly higher and/or greater than in male subjects could explain why autism is primarily a male disorder.

Cohen (1999, 2001, 2002, 2002a, 2004) has postulated in numerous studies that high plasma GABA affects axon(s)-to-oligodendrocyte signalling in the corpus callosum.

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