Epidemiology

Globally, in 2016, approximately 52.9 million children reportedly had identifiable

developmental problems delay. Since 95% of the population resides in low and middle-
income countries (LMICs), there is an increased risk for developmental delays and disorders.
[13] Although the exact prevalence of developmental delay is unknown, according to the
World Health Organization (WHO), 10% of the population in each country population has a
disability of one or another kind.[14] In the United States, roughly 15% of children have been
reported to have at least one developmental problem.[15] In England, the prevalence of ID in
children under age five and adults is 2.7% and 2.17%, respectively. The GDD incidence rate
is 1% to 3% in school-age children or younger.[6] Autism prevalence is approximately 2.5%.
[16] 
The prevalence of delay in development involving respective domains among children
(which is based on data reported in children getting services in 2007 by USPSTF on their
respective website) is given below:[15]
 Cognitive (1% to 1.5%)
 Learning disability (8%)
 Speech and language (2% to 19%)
 Any delay (15%)
According to Drakenstein Child Health Study (DCHS) conducted in Western Cape, South
Africa, the risk of low developmental performance in the high-risk environment was high
among boys. Likewise, several other studies have also reported a slightly increased incidence
in males, possibly due to genetic variability on the X-chromosome.[6][12]
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Pathophysiology
Except for specific syndromes that include developmental delay, the vast majority of
developmental delay is idiopathic.  Although the exact underlying pathophysiology is
unknown, several mechanisms have been proposed by epidemiologic studies that lead to
some sort of developmental delay and/or disabilities. Since some forms of developmental
delay may run in families, genes have been assumed to play a significant role in
developmental delay. 
A multitude of genes and mechanisms for genetic transmission have been proposed.  While
some causes of developmental delay such as Fragile X or Down syndrome have known
genetic etiologies, for most others, it is unclear. Even for well-characterized disorders like
autism spectrum disorder, there are over 100 risk alleles. Perinatal complications, profound
deprivation, and poverty, among other environmental stressors, can play a role in causing
developmental delays, but special causal links remain elusive.
The hypothalamic-pituitary axis (HPA) is responsible for the normal regulation of stress
response in progenies. Psychosocial stressors during pregnancy, maternal immune activation
(MIA), and modification of HPA may significantly affect fetal brain development, but there
are no specific cause and effect relationships for most disorders. Boyce and his colleagues
offered the concept of differential susceptibility. This suggests that the risk for developmental
anomalies is increased by a variety of factors that create a biological vulnerability to
environmental stressors but are only expressed when the environmental stresses occur.
Furthermore, even vulnerable children can do well if environmental circumstances are highly
favorable and foster resilience.