Autistic spectrum disorders (ASD) are common, comprising a range of complex and heterogeneous developmental disabilities that affect the way a person communicates and relates to people around them. Dietitians from all disciplines need an awareness of the challenges faced and posed by children with ASD. The typical characteristics of rigid thinking and resistance to change, combined with common sensory processing issues, make feeding problems, undereating and overeating common and traditional approaches to changing dietary behaviours are often inadequate.

Diagnosis of ASD involves trained professionals marking a child (or adult) in three main areas of functioning, known as the ‘triad of impairments’:

• social interaction (difficulty with social relationships, e.g. appearing aloof and indifferent to other people and difficulty with understanding others’ viewpoints and intentions)
  
• social communication (difficulty with verbal and non verbal communication)
  
• imagination (difficulty with interpersonal play and imagination, e.g. having a limited range of imaginative activities, possibly copied and pursued rigidly and repetitively)

For a diagnosis of ASD, there must be impairments in each of these three areas, i.e. functioning falls below a threshold at which it interferes with day to day living [1]. Diagnostic criteria are taken from either the international or US diagnostic manuals ICD-10 [1] or DSM-4 [2]. In addition to this triad, repetitive behaviour patterns and resistance to change in routine are often present.

ASD is an umbrella term for three diagnoses:

• autism, also known as classic autism and Kanner’s autism
  
• pervasive development disorder not otherwise specified (PDDNOS), sometimes known as atypical autism
  
• Asperger’s syndrome

Two rarer diagnoses are sometimes included under the ASD umbrella, but are not covered specifically in this chapter:

ASD was once thought of as an uncommon disorder, but prevalence is increasing and it now occurs in at least 1% of children in the UK [5–7]. Boys are affected four times more than girls [8]. The increase is partly but not wholly due to increased recognition. For the majority of cases of ASD, the cause is unknown and is likely to be varied and multifactorial; 10% have underlying medical causes including at least 60 different metabolic disorders, neurological disorders and complex chromosomal abnormalities [9]. Genetic studies have failed to find any single ‘autism gene’, but genes that are linked to higher risks of autism are being identified. For families with a child diagnosed with ASD, the likelihood of having another affected child is increased by five to ten times [10]. It is thought that for idiopathic cases of ASD there could be an inherited predisposition which is triggered by some as yet unidentified environmental factor such as an infection, immunological reaction or toxin during pregnancy or early life [11] or, indeed, maternal nutrition. A large US population based case control study found that women who reported not taking prenatal vitamins (containing folic acid) before and during the first month of pregnancy were twice as likely to have a child with ASD as women who did take supplements. The same study identified particular maternal gene variants which made the likelihood of having a child with ASD seven times as likely when not taking vitamins [12].

There is much research into the biochemistry of children with ASD in the hope it will give a clue as to cause, enabling better sub-typing and treatment. Published research reports low serum iron [13], zinc to copper ratios [14, 15], magnesium [16], calcium and vitamin D [17]; increased plasma vitamin B₆ [18]; abnormal plasma essential fatty acids [19] and amino acids [20], markers of reduced sulphation capacity [21–23], urine peptides; increased urine homocysteine; various other abnormal vitamin, oxidative stress, energy transport, sulphation and detoxification markers [24–28]. The quality and size of these studies vary, the dietary intake of the subjects tested is rarely taken into account and the clinical relevance and robustness of some of the methodology and results are yet to be clarified.

ASD is seen as a lifelong condition; however, 4%–40% of children lose their diagnosis as they get older [29–33]. Loss of diagnosis is more common for those more ‘mildly’ affected, or without other coexisting conditions. Whether these changes are due to some sort of ‘recovery’ or just a shifting of how much underlying ASD traits impede ‘normal’ life is not known.

Management, with specialised education and structured support, aims to help children maximise their skills and achieve their full potential as adults. Many individuals who were ‘disabled’ as children can get to the point where they will ‘function normally’ socially and find work, have a family and live independently.

Medical treatment is usually focused on managing common comorbidities such as ADHD, anxiety, sleep problems or epilepsy. Other treatments focus on the early implementation of education and behaviour interventions where these services are available, teaching the individual (or helping parents to teach the individual) appropriate responses to social situations they struggle with, and on developing communication.

Key strategies commonly advocated for individuals with ASD are