Abstract:
Autism Spectrum Disorder (ASD), also known as Autism, is a common, highly heritable and heterogeneous neurodevelopmental disorder that has underlying cognitive features and commonly co-occurs with other conditions. Traits may be detected in early childhood, but ASD is often diagnosed later. ASD, more common in males than in females (ratio from 2:1 to 5:1), occurs in all racial, ethnic, and socioeconomic groups and data report it globally affects 52 million people (approximative prevalence of 1 in 132 individuals). ASD has unclear multifactorial etiology, although genetic/environmental interaction appears to be decisive. More than 100 genes and genomic regions have been confidently associated to ASD; main environmental factors related to ASD development are: neonatal hypoxia, gestational diabetes, preterm birth, valproate use during pregnancy, prenatal exposure to pesticides, inadequate intake of protective folic acid, maternal obesity, maternal age > 40 and paternal age > 50 years.
The ASD phenotype is defined, according to DSM-5 criteria, as a heterogeneous "spectrum" of persistent deficit in communication/social interaction and repetitive/stereotypic behaviors with sectoral interests/activities, variously combined and with variable expressivity. ASD can affect nutritional status and increase the likelihood of developing eating problems; food selectivity is the most frequent feeding disorder, followed by picky eating up to food refusal. ARDIF, Anorexia/Bulimia, BED and PICA are “typical” DSM-5 eating disorders that can coexist with ASD. In these patients were found alterations in both Serotonin and Dopamine Systems; moreover, demodulations in both Gabaergic and Endocannabinoid systems and appetite hormones imbalances (Leptin, Adiponectin, Ghrelin) were also found. Finally, morpho-structural alterations in some brain regions involved in food intake regulation (Insula, Amygdala, Caudate nucleus) have been demonstrated in ASD patients.
Therefore, ASD may be associated with inadequate dietary intake; prevalence of obesity, overweight and underweight in children, adolescents and adults with ASD is higher, as well as incidence of Type 2 diabetes, developing diabetes risk and risks of dyslipidemia and heart disease. Some side effects, particularly hyporexia and/or increased hunger, of drugs predominantly used in ASD (Risperidone, Aripiprazole, Methylphenidate, Atomoxetine), as well as tendency to sedentary lifestyle and poor aptitude for physical activity, can affect the nutritional status in these patients.
On the other hand, type of diet can influence ASD; moreover, ASD children are more likely to have food allergy and Coeliac disease, worsening ASD symptoms; Gut dysbiosis, more frequent in ASD, can also worsen digestive and neurological symptoms. This is the why children with ASD sometimes undergo to non-intentional and dangerous dietary restrictions protocols, based on non-evidence-based attempt, to improve behavioral disturbances or digestive symptoms. There is a lack of clear evidence on the benefits of gluten/casein-free, sugar-free or ketogenic or GAPS diet and, although many studies have demonstrated clinical improvement in these patients, the evidence is not strong enough to recommend them as a treatment for ASD; better well-designed, and high-quality clinical trials are needed to validate their potential. However, any dietary therapy requiring strict adherence may be extremely difficult to manage for patients and families/caregivers, thus increasing stress and discomfort. Personalized diet, based on behavioral disorders severity, patients compliance and dietary adherence should be preferred.
Audience Take Away:
- Useful in daily clinical practice.
- Helpful in nutritional management of ASD patients.
- Provide a practical solution to a problem that could simplify or make a designer’s job more efficient.
- Improve the accuracy of a design, or provide new information to assist in a design problem.
