Arachidonic acid [AA, 20:4(n-6)], an important precursor of the prostaglandin compounds, cannot be synthesized de novo from FFA in mammals and must be derived from another EFA in the diet, namely linoleic acid [LA, 18:2(n-6)]. In the case of life long low oral fat intake, as in our patient, clinical EFA deficiency might occur with depletion of n-3 and n-6 FA stored in adipose tissue. Therefore, her source of EFA would be entirely from recent dietary intake and deficiency might occur sooner than in individuals with normal LPL and abundant EFA storage [
23]. Eicosatrienoic acid [ETA, 20:3(n-9)], on the other hand, is not an EFA because it can be synthesized in mammals from palmitic acid [16:1(n-9)]. In the event of diminishing pool of both n-3 and n-6 fatty acids due to absence or deficiency in the diet, more ETA are produced and the amount parallels the degree of deficiency [
24‐
26]. EFA deficiency syndrome commonly results from a combined deficiency in both n-3 and n-6 fatty acids. A ratio of ETA to AA > 0.2, is suggestive of EFA deficiency [
24‐
26]. Clinical manifestations in EFA deficiency are unusual on a diet containing > 2% of the calories as linoleic acid [
27]. While the clinical symptoms of dryness and desquamation of the skin are annoying at best, a more serious consequence could be impaired fetal brain and visual development. The proband did not develop signs of clinical EFA deficiency, nor did the ratio of 20:3(n-9) to 20:4(n-6) exceed 0.2 at any stage of her pregnancy, although an upward trend did occur. Additionally, the report that infants fed a formula low in EFA grew poorly and developed multiple medical complications was a concern [
28]. Several reports have documented a reversal of biochemical and clinical manifestations of EFA deficiency in infants and adults by cutaneous administration of EFA-rich oil, such as sunflower oil [
29‐
35]. Therefore, application of sunflower oil to the proband's skin was initiated at week 25 and may have had prevented progression of EFA deficiency in mother, as suggested by the stabilization of the 20:3(n-9) to 20:4(n-6) ratio. Surprisingly, we found low levels of n-3, n-6, and PUFA precursor levels in the cord blood taken during the delivery, and yet there was abundant long chain PUFA in the infant circulation. This would suggest that other adaptive mechanisms were involved in maintaining the critical levels of long chain EFA in fetal circulation in the face of inadequate maternal supply.