Can Prenatal N-3 Fatty Acid Deficiency Be Completely Reversed after Birth? Effects on Retinal and Brain Biochemistry and Visual Function in Rhesus Monkeys

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Abstract
Our previous studies of rhesus monkeys showed that combined prenatal and postnatal n-3 fatty acid deficiency resulted in reduced visual acuity, abnormal retinal function, and low retina and brain docosahexaenoic acid content. We now report effects of n-3 fatty acid deficiency during intrauterine development only. Rhesus infants, born to mothers fed an n-3 fatty acid deficient diet throughout pregnancy, were repleted with a diet high in alpha-linolenic acid from birth to 3 y. Fatty acid composition was determined for plasma and erythrocytes at several time points, for prefrontal cerebral cortex biopsies at 15, 30, 45, and 60 wk, and for cerebral cortex and retina at 3 y. Visual acuity was determined behaviorally at 4, 8, and 12 postnatal weeks, and the electroretinogram was recorded at 3–4 mo. Total n-3 fatty acids were reduced by 70–90% in plasma, erythrocytes, and tissues at birth but recovered to control values within 4 wk in plasma, 8 wk in erythrocytes, and 15 wk in cerebral cortex. At 3 y, fatty acid composition was normal in brain phospholipids, but in the retina DHA recovery was incomplete (84% of controls). Visual acuity thresholds did not differ from those of control infants from mothers fed a high linolenic acid diet. However, the repleted group had lower amplitudes of cone and rod ERG a-waves. These data suggest that restriction of n-3 fatty acid intake during the prenatal period may have long-term effects on retinal fatty acid composition and function.

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