Polyunsaturated Fatty Acids and Infant Nutrition

Abstract

Infants consume n−6 and n−3 fatty acids both as linoleic (18:2n−6) and linolenic (18:3n−3) acids and as their 20 and 22 carbon products of elongation and desaturation. Abnormal elevation of eicosatrienoic acid (20:3n−9) occurs with diets deficient in n−6 and n−3 fatty acids since of these families only the n−9 family can be synthesized de novo by mammals. Human symptoms of deficiency include scaly dermatitis, hair loss, and impaired wound healing. If deficiency occurs during development, growth is limited. When n−3 but not n−6 fatty acids are deficient, animals grow normally but demonstrate subtle differences in retinal physiology, visual acuity, and learning.^1–6 Such an n−3 deficiency can be produced by feeding diets with very high ratios of n−6 to n−3 fatty acids to developing animals as shown by Galli and coworkers.⁷ Normally, docosahexaenoic acid (22:6n−3) is a major component of central nervous system synaptosomes and photoreceptor disk membranes. ^8–10 In n−3 deficiency, docosahexaenoic acid (22:6n−3) is partially replaced by the equivalent elongation-desaturation product of linoleic acid, docosapentaenoic acid (22:5n−6).