Several in vitro studies have shown that ALA (omega-3 fatty acid) aids in the differentiation and functioning of brain cells. It has been shown that ALA deficiency alters the course of brain development, disrupts the composition and physicochemical properties of brain cell membranes, neurons, oligodendrocytes, and astrocytes, bringing about minor cerebral dysfunctions. These deficiency symptoms have been observed in animals as well as human infants. The effects of these types of deficiencies are manifested in neurosensory and behavioral disorder.
Recent studies have shown that dietary ALA deficiency causes distinct abnormalities in certain brain regions. The frontal cortex and pituitary gland are severely affected, which could lead to behavioral disorders affecting certain tests (habituation, adaptation to new situations). The deficiency of ALA reduces the perception of pleasure, slackening the efficacy of sensory organs and affecting certain cerebral structures. Age-related impairment of hearing, vision and smell is linked to decreased efficacy of the brain parts of the brain and disorders of sensory receptors, particularly of the inner ear or retina. For example, a given level of perception of a sweet taste requires a larger quantity of sugar in subjects with ALA deficiency.
The organization of the neurons is almost complete several weeks before birth. Any disturbance to the neurons or any disruption of their connections or depleted reservoir of their constituents at any stage of life is known to accelerate aging. Brain lacks the ability to synthesize LA and ALA. AA and cervonic acid, which are derived from diet unless human liver synthesizes LA and ALA, are essential for the brain, The age-related reduction of hepatic desaturase activities (which participate in the synthesis of long chains, together with elongases) can impair turnover of cerebral membranes. In many structures, especially in the frontal cortex, a reduction of cervonic and AA is observed during aging.
Many studies have shown that (n-3) fatty acid deprivation during development results in decreased DHA in brain membrane phospholipids, reduced performance in learning tasks, altered activity of membrane receptors and proteins, and altered metabolism of several neurotransmitters, including dopamine. Low DHA status is also associated with poorer development of visual acuity and lower indices of neural development in human infants. It is also suggested that (n-3) fatty acid deficiency decreases the mean cell body size of neurons in the hippocampus, hypothalamus, and parietal cortex. Furthermore, higher DHA intakes during pregnancy and lactation increase measures of cognitive performance in infants.
Recent studies have suggested that pregnant women following Westernized diets consume less than the recommended intakes of (n-3) fatty acids.
Studies with rats have shown that fatty acid deficiency has long term effects on a developing brain. In a study with rats, the cerebral hemispheres of the (n-3) fatty acid deficient embryos were noticeably reduced compared with those of the control group (not fatty acid deficient). A decrease in size of the cortical plate, primordial hippocampus, and dentate gyrus was associated with n-3 fatty acid deficiency. In the primordial cerebral cortex, the mean thickness of the cortical plate was 25 percent lower in the fatty acid deficient embryos than in controls.