Autism is characterized by a spectrum of behaviors and developmental delays that are  attributed to a complex set of neurological disturbances that result from a combination of genetic and environmental factors. Many of the alternative treatment approaches or adjunct therapies for patients with autism are designed to improve methylation and detoxification pathways.

These treatments generally view the environment or other external sources, like mercury in vaccines, as the origin of neurotoxic substances. Neurotoxins are defined as chemical substances that are lethal to neurons. While the environment certainly can be a source of neurotoxins, these therapeutic protocols overlook the fact that neurotoxic substances may originate within the body and can actually be formed within the neurons themselves.

Neurotoxin Synthesis
Neurotransmitters are metabolized in a two-step process that utilizes the enzymes monoamine oxidase (MAO) and aldehyde dehydrogenase. The first step involves MAO, which is present within the cytoplasm of neurons, and breaks down neurotransmitters to form highly reactive aldehyde intermediates. The dopamine metabolite DOPAL (3-, 4-dihydroxyphenylethanol) is one of the reactive aldehyde intermediates formed by MAO and is a potent neurotoxin.

Studies have found that Parkinson's-like brain lesions can be induced with DOPAL and that the cognitive impairment seen has similarities to autism1. MAO is a mitochondrial enzyme and is present inside the neurons, but not inside the neurotransmitter vesicles within the neuron. As such, DOPAL and related reactive neurotransmitter aldehydes are formed from neurotransmitter pools that are present inside a neuron, but outside of the intracellular vesicles. Excessive catecholamine (dopamine, norepinephrine, and epinephrine) neurotransmitter turnover, the sum of neurotransmitter fi ring and reuptake, increases the production of these neurotoxins. In order to limit the formation of these aldehydes, it is necessary to limit the supply of neurotransmitters present in the cytoplasm.

A common misconception regarding neurotransmitter turnover and degradation is that neurotransmitter molecules are only released from the vesicles via synaptic release and that the neurotransmitters degraded by MAO are only those that have been returned to the neuron through an active reuptake mechanism. While it is true that this is one source of neurotransmitter degradation products, neurotransmitters can also leak out of vesicles directly. This leaking process is a signifi cant source of neurotransmitters degraded by MAO and therefore neurotoxin formation.

In summary, neurotoxic aldehyde formation comes from two sources:

  • reuptake degradation
  • vesicle leakage degradation

In a normal heathy situation, the active release of neurotransmitters and subsequent reuptake contributes only a very small fraction <2% of the neurotransmitters metabolized by MAO to form the neurotoxic reactive aldehydes. The primary source >98% is the constant non-specific leaking of neurotransmitters directly from the vesicles. This situation changes dramatically when neurons are highly stimulated. In this situation >60% of the neurotransmitters susceptible to MAO degradation and aldehyde formation originate from the active release and reuptake of  neurotransmitters and <40% are from the non-specific leaking of vesicles. This high rate of firing can be pathogenic because it significantly increases the formation of toxic metabolites within the neuron and increases the risk of neurological damage.

Neurotoxins & Autism
Many patients with autism have high urinary levels 
of neurotransmitters indicating an increased rate of neurotransmitter turnover. Insufficient regulation of excitatory neurotransmitters increases the high rate of neurotransmitter release and reuptake and increases neurotransmitter exposure to MAO.

Unchecked, excitatory neurotransmitters will cause rapid and repeated neuron firing and increase neurotoxin formation. Interventions that reduce high rates of neurotransmitter turnover will also reduce the formation of toxic aldehydes and as a consequence can reduce neurological damage.

Raising the level of inhibitory neurotransmitters will decrease the rate of firing and decrease aldehyde formation. Because over-stimulation results in the formation of toxic compounds and neurological damage, it may also contribute to the development of symptoms seen in autistic patients. Urinary testing of neurotransmitter levels confirms that supporting the inhibitory neurotransmitters with Targeted Amino Acid Therapy (TAAT) will reduce the excretion of excitatory neurotransmitters.

Supporting inhibitory neurotransmitters with a TAAT program has been shown to decrease urinary levels of catecholamines and therefore is a  method to decrease the rate of catecholamine turnover. TAAT can be used to decrease the rate of neurotoxic aldehyde formation by MAO, and reduce the risk of further neurological damage in patients with autism.

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  1. Burke WJ, Li SW, Williams EA, Nonneman R, Zahm DS. 3,4-Dihydroxyphenylacetaldehyde is the toxic dopamine metabolite in vivo: implications for Parkinson's disease pathogenesis. Brain Res. 2003 Nov 7;989(2):205-13.
  2. Eisenhofer G, Kopin IJ, Goldstein DS. Leaky catecholamine stores: undue waste or a stress response coping mechanism? Ann N Y Acad Sci. 2004 Jun;1018:224-30.