*Geek Box: Nutritional Abnormalities in ASD

*Geek Box: Nutritional Abnormalities in ASD

The caveat before we outline some of the nutritional characteristics of ASD is that, as stated above, most of the evidence is derived from children. Nevertheless, these analyses have provided some fascinating insights into the nutritional abnormalities associated with ASD.

First off, what do we mean by ‘abnormalities’? We are referring to a normal distribution, i.e., the statistical concept represented by a bell-curve with the mean [i.e., the average] in the middle, and the percentages of a population covered by standard deviations[ SD] from the mean: one SD [68.72%], two SD [95.45%], and three SD [99.73%].

Children with ASD are defined by abnormally distributed nutrient intakes; while for most micronutrients children with ASD will exhibit levels within the 10th to 90th percentile, up to 25% lie below or above these reference ranges, depending on the nutrient. For example, abnormally uneven distribution of vitamin B6, from subsets ranging high in red blood cell B6 levels to subsets with pronounced B6 deficiency.

Such abnormal distributions are observed across several nutrients, indicative of the multifaceted presentations and different phenotypes in ASD. Some interesting nutrient characteristics have been observed. For example, low lithium levels in children with ASD have been characterised, and lithium is required as a co-factor in the function of two enzymes linked to ASD symptoms. Another observed abnormal nutritional characteristic is elevated copper-to-zinc ratio, which has been associated with behavioural disorders. Biotin has also been shown to be lower in children with ASD compared to non-ASD controls, and biotin is required as a co-factor in fatty acid synthesis, while deficiencies in biotin in experimental models result in neurological deficits.

Certain underlying metabolic dysfunctions have been identified, which may also relate to ASD symptoms and behavioural disorders, including elevated oxidative stress levels and damage to cell membrane phospholipid layers. The latter appears to be associated with fatty acid metabolism abnormalities, which may be relevant for omega-3 status and related central nervous system disorders. A very important point to bear in mind is that whether these nutritional correlates of ASD are a consequence or cause of the condition is unknown.