Polyunsaturated Fatty Acids and Infant Nutrition

  • Susan E. Carlson

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).

Keywords

Preterm Infant Human Milk Docosahexaenoic Acid Plasma Phospholipid Eicosatrienoic Acid 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1989

Authors and Affiliations

  • Susan E. Carlson
    • 1
  1. 1.Newborn CenterThe University of TennesseeMemphisUSA

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