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High levels of ammonia are frequently found in those on the autism spectrum. Ammonia may be high for many reasons including, bacterial imbalances, parasites, protein consumption, and so on.  One of the most common symptoms of high ammonia, is the strong smell of ammonia in sweat, urine, stool and/or breath.  Many often experience behavioral reactions from high ammonia, and in my opinion, this may be because of  its ability to increase glutamate levels. An organic acids test (OAT) or a comprehensive stool analysis (CDSA) can give you an indication if you or your child may be struggling with high levels of ammonia.

“Like many other factors, ammonia frequently affects the brain of those with ASD. The way it does this is because excess ammonia (NH3+) is able to cross the blood brain barrier and combine with a-ketoglutarate. This brings us a three-fold problem.

A-ketoglutarate + NH3 = Glutamate (excitatory)

The first problem is obvious as more excitotoxins and excessive glutamate are never good for ASD.
The second problem is that because of the excess ammonia, a-ketoglutarate chooses to combine with ammonia and it leads to the depletion of a-ketoglutarate. A-ketoglutarate is a big word, pronouncing it isn’t important, but knowing that it is a critical biochemical step in the citric acid cycle is. The citric acid cycle is the process by which we produce a lot of ATP or energy for our cells. Trying to get the citric acid cycle functioning properly is one of the reasons why so many people are using B complex vitamins. But even with B vitamins, without adequate a-ketoglutarate, the citric acid cycle can’t function optimally. Without adequate ATP, cells die, nerves die, etc. This may be a primary problem or there still may be a third problem.
The third problem could be the decreased formation of GABA due to the increased formation of glutamine. Ammonia pushes the conversion of glutamic acid to glutamine instead of to GABA. This may be a little confusing as both glutamate and glutamine can both be beneficial or detrimental all dependent upon the proper balance. Glutamate and glutamine act as the major buffering molecules for ammonia.”


“In 1996 Dr. Kane had proposed that autism may be the aftermath of a toxic insult, a viral infection which evoked hepatic encepahlopathy, resulting in hyperammonenemia and suppression of several key enzymes, such as carbamylphosphate synthesase, glutamine synthesase and ornithine transcarbamylase.  The high levels of ammonia would cause an “increase in brain edema (water) and a deterioration in neuropsychological function.” The ammonia would also cause abnormalities in neurotransmitters and induce injury to astrocytes which are already under oxidative stress.  For this and a number of other reasons, Kane believes the oxidative stress should be viewed as the result of a toxic event, rather than the cause of autism.  Kane asserts that because of this, treating a patient with anti-oxidants is a little like pouring water on a house after it’s already burned to the ground.  She suggests “treatment should be centered on re-building membrane structure and thereby stabilizing membrane function.”  This involves clearing the body of ammonia, very long chain fatty acids, and giving the cells those building blocks which they’ve long been denied.”

” In mice also, increases in blood and brain ammonia levels after ammonia loading were prevented by the administration of biotin. The decrease in brain glutamate and aspartate after ammonia loading was lower and the brain glutamine level was higher in biotin-treated mice than in the controls. These findings indicate the protective effect of biotin against ammonia intoxication.”