Follow-up with Autistic Child

Summary

Following an autistic child though testing over two-and-a-half years.

This content was created by the Metametrix Institute

History

 A 13-year-old autistic male with follow-up testing.

Age

13

Gender

Male

Description of Results

 

The initial profile revealed multiple abnormalities in almost all nutrient categories. Subsequent test results showed that many areas had significantly improved, demonstrating the effectiveness of interventions. Specifically, signs of trace element insufficiency, low vitamin A and β-carotene, PUFA imbalance, mitochondrial inefficiency, and ammonia spilling, have largely or completely cleared.

A year later, results indicated that the patient went through a period of worsening carnitine levels and concurrent worsening oxidative challenge and glutathione demand status, but these situations have been corrected.

The patient had sustained very good status for vitamin B12, folic acid, and vitamins B1, B2, and B3, but he showed persistent indication of poor status for vitamin B6 and biotin. These two members of the water-soluble family  need aggressive support. If these nutrients are already being supplemented it might be suspected that specific genetic weaknesses exist in these areas, and such a finding would give a metabolic explanation of his difficulties. Such a weakness may be overcome when tissue levels of the nutrient-derived cofactors are raised even higher. The P5P cofactor form of B6 might be used for this purpose to assure that conversion is not an issue. There are several points of biotin metabolism where weaknesses may occur.

We found a spiking of hepatic glutathione synthesis activity as indicated by the a-hydroxybutyrate (AHB) marker. This is not surprising given the oxidative challenge state at that time. However, in the last follow-up, we saw AHB perfectly normal while sulfate is quite elevated. This could be explained by increased intake of dietary sulfate. If N-acetylcysteine (NAC) is being used aggressively, it might be best to shift to agents that stimulate other Phase II conjugations.

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