During the last trimester of gestation and for the first 18 months after birth, AA, and Docosahexaenoic acid (DHA) are deposited within the cerebral cortex at a rapid rate (Martinez et al., 1974; Clandinin et al., 1980). As noted above, this stage of human development is known as the brain growth spurt (Martinez and Mougan, 1998), when neuronal development is particularly vulnerable to nutritional insufficiencies (Nyaradi et al., 2013).
Numerous expert and government authorities worldwide agree that dietary Docosahexaenoic acid (DHA) requirements are increased during pregnancy and lactation when a minimum of 200 mg of Docosahexaenoic acid (DHA) per day is recommended (Van Elswyk and Kuratko, 2009).
The decline in breast milk Docosahexaenoic acid (DHA) may plausibly be explained by dietary shifts overtime. Formula-fed infants may also be at risk of sub-optimal Docosahexaenoic acid (DHA) supply during this period. Evidence that infant Docosahexaenoic acid (DHA) supplementation conveys significant benefit on visual acuity is derived from a systematic review of 12 clinical studies from the Harvard School of Public Health (SanGiovannietal.,2000). San Giovanni et al.(2000) incorporated the results from both randomized and non-randomized studies of DHA supplemented formula and concluded that increased dietary Docosahexaenoic acid (DHA) improved visual acuity in term infants at two and four months of age.
Preterm infants are especially vulnerable to Docosahexaenoic acid (DHA) deficiency as they have not had access to maternal lipid stores for the normal period of gestation (Haggarty, 2002).
It has been identified that children born preterm have higher rates of learning disabilities, language impairment, attention deficits, hyperactivity, and reduced cognitive test scores compared to (gender- and age-matched) children born at term (Bhutta et al., 2002; Perricone and Morales, 2011).
It is possible that Docosahexaenoic acid (DHA) deficiency during critical periods of brain growth and structural organization may render the brain vulnerable to neurological or neurodegenerative diseases later in life (Farquharson et al., 1995). The development of the brain’s architecture prenatally and during infancy lays down the foundation on which the structure of the adult brain is based. It is therefore possible that early modification of LC-PUFA levels will have long-term structural and functional consequences which may be too long-term and/or subtle to detect in healthy infants and children (McNamara and, 2006).