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Autism

Globally, the number of people suffering from autism has been increasing at an alarming

rate over the past few years. Some of the most recent reports estimate the global pervasive rate to

be over 30 percent. This worrying prevalence statistic has sparked off debates about autism

among various quotas. Whereas some health psychologists argue that autism is a genetic

condition, others believe that it is a prenatal and environmental disorder. These divergent

perspectives affirm the magnitude of the health problem that the world continues to grapple with

in the 21

Century. Therefore, a detailed understanding of the etiology and symptoms of the

illness presents a more proactive approach to diagnosing and managing autism.

By definition, autism, commonly known as autism spectrum disorder (ASD), is a

multifaceted developmental condition that manifests during childhood and may progress to

adulthood if not properly managed. Repetitive stereotypic behavior, impaired communication,

and social interaction inability are the main defining features of autism disorder. Research has

also identified anxiety, eating and sleeping turbulences, temper irritabilities, and self-instigated

aggressions as other forms of autism.

There exists a widespread consensus among mental health and behavioral psychologists

that autism spectrum disorder has no single known cause. According to Holt and Anthony

(pp.442) autism results from the interaction among genetic and non-genetic risk factors that

individuals endure as they develop through childhood to adult life. Foremost, the primary

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genetic causes of autism are gene defectiveness and chromosomal abnormalities. These defects

and abnormalities have been reported in at least 10% of people with ASD. Besides, children born

in households with an ASD history have a 50% chance of contracting the illnesses, with a relapse

rate of up to 8%. The concordance rate ranges between 80% and 94% in monozygotic twins,

while it ranges between 1% and 10% in dizygotic twins. Chromosomes 2q, 7q, and 15q harbor

most of the genes susceptible to autism. Additionally, metabolic errors account for less than 6%

of ASD incidences. Moreover, cerebellar developmental modeling gene ENGRAILED 2

explains more than 41% of ASD cases. Therefore, autism a hereditary neurobehavioral disorder

that may become more pervasive the number of families with a rich history of ASD increases.

Nevertheless, there are myriads of environmental factors that may contribute to ASD.

These factors are categorized into three major sets namely prenatal, prenatal, and postnatal

causes. Autism in children may results from such prenatal factors as advanced parental age,

exposure to agrochemicals and household inhalants, maternal diabetes, and viral infections.

Empirical studies have established that children sired by males aged 29 or younger are less likely

to develop ASD compared to those sired by men aged above 50. Among the leading perinatal

causes include premature birth, low birth weight, and birth complications. Arguably, an

incomplete development in the womb and underweight may render a newborn vulnerable to

autism. Expectant mothers should adhere to the prescribed dietetic plans to achieve the correct

weight for the newborn and avoid birth complications. Finally, postnatal causes such poor

immune response, hypoxia, viral infections, and mercury toxicity plays an important role in

understanding the pathophysiology of ASD. The symptoms of ASD vary according to age.

Notably, preschool children experience either delayed or lack of spoken language. Other

identifiable behaviors at this stage include lack of awareness for one’s self and others, little

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imagination, impaired non-verbal communication, and abnormal expressions and reactions.

Children of school age portray muteness, inappropriate reference and use of unfamiliar

vocabulary for age, disruptive behavior, lack of cognition for rules, extreme responses and lack

of creativity, disorganization, and resistance to change.

Furthermore, adolescents show the most complex symptoms of autism typical in all ages.

Kincaid (pp.102) observed that those in adolescence stage experience long-standing

externalizing behaviors, communication, and adaptation to change. It is true that they portray

disharmonies between academic success and social intelligence. In most cases, they fail to

exercise common sense. Again, children at this age tend to be quiet, offer a lot of information on

topics they enjoy, have speech fetishes, and may fail to appreciate the metaphorical nature of

language. Murphy (pp.1669) further reported that adolescents with ASD undergo social

problems such as difficulties in making and building relationships, discriminatory behavior, lack

of awareness, and rigid thinking. There is no doubt that such indicators are evident of poor

cognitive development in children that may affect their relationships in the future. Emotional

intelligence is an integral aspect of social learning whereby children construe and reconstruct

their experiences in terms of others’ perspectives as well as feelings.

Adults are not immune to the manifestation of ASD indicators. According to the

behavioral school of thought, the ADS symptoms identified in childhood persist in adulthood

because they become repeated habits. However, adults develop a sense of seclusion, adamant

positions, and career challenges because they are interact and communicate at a higher level than

children. They always follow stringent schedules, and are less responsive to colleagues. Adults

with ASD do not show empathy for other people, and instead resist change let alone adjusting

their behaviors to the prevailing social circumstances.

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In brief, the war against autism may be far from over if the healthcare system cannot

address the comorbid conditions that promote its recurrence. It is a product of both genetic and

non-genetic risk factors. The symptoms of ASD are distributed throughout the human

development stages. ASD manifests strongly in people with eating and sleep disturbances as well

as antisocial behaviors. However, severity of the disorder largely depends on early diagnosis and

adherence to both medical and psychosocial interventions. Therefore, going forward, more active

interventions should focus on community involvement and evidence-based practice.

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Work Cited

Holt, Richard, and Anthony P. Monaco. "Links between genetics and pathophysiology in the

autism spectrum disorders." EMBO Molecular Medicine 3.8 (2011): 438-450.

Kincaid, Debbie L., et al. "What is the prevalence of autism spectrum disorder and ASD traits in

psychosis? A systematic review." Psychiatry Research 250 (2017): 99-105.

Murphy, Clodagh M., et al. "Autism spectrum disorder in adults: diagnosis, management, and

health services development." Neuropsychiatric Disease and Treatment 12 (2016): 1669.

Volkmar, Fred, et al. "Practice parameter for the assessment and treatment of children and

adolescents with autism spectrum disorder." Journal of the American Academy of Child

& Adolescent Psychiatry 53.2 (2014): 237-257.

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