The two essential fatty acids (EFA), linoleic acid (LA, C18:2 (n-6)) and α-linolenic acid (ALA, C18:3 (n-3)), are required in the diet because humans are unable to synthesise them de novo. A series of elongation and desaturation reactions creates a range of important hormone-like eicosanoids that are used for cell signalling. The long chain marine fatty acids docosahexanoic acid (DHA, C22:6 (n-3)) and eicosapentanoic acid (EPA, C20:5 (n-3)), and the plant polyunsaturated fatty acid dihomo-γ-linolenic acid (DGLA, C20:3 (n-6)) can substitute for the essential fatty acids because they feed into the same pathways and increase cellular levels of the same eicosanoids. Because the EFA are required in the diet, the developing foetus and neonate infant are dependent on their mother for their supply, through the placental blood and breast milk respectively.
The EFA are required for the development of new tissues and so play a key role in the developing foetus. In particular, the central nervous system requires high amounts of DHA in order to fully develop and a deficiency of n-3 fatty acids in the mother can lead to neurological problems. If the diet is inadequate to supply the foetus with enough EFA, body stores may be catabolised from the mother. Adipose tissue contains stores of LA, but is a poor store of ALA and so dietary sources are of great importance. Because conversion of ALA to eicosanoids is relatively slow in humans due to genetic deficiencies of the necessary enzymes, fatty fish are the preferred choice for n-3 fatty acids. This is highlighted by measurements taken from vegetarians and vegans that show lower concentrations of DHA when compared to fish eaters.
Deficiency of EFA results in increased production of a number of fatty acids found usually in much lower amounts, and these can be used as markers of essential fatty acid deficiency during early development. This negates the problem of using plasma levels of fatty acids to assess essential fatty acids status, because these are notoriously unreliable. Mead acid (MA, C20:3 (n‑9)) can be used as a marker of essential fatty acid deficiency because under normal circumstances long chain polyunsaturated fatty acids inhibit its production. Deficiency of EFA therefore results in rising levels of MA as the inhibitory effects are removed. Another fatty acid, osbond acid (OA, C22:5 (n-6)), is synthesised in response to a shortage of DHA and therefore the ratio of DHA to OA can be used as a marker of essential fatty acid function in neonates and pregnant mothers.
Generally as the foetus develops the EFA status of the mother declines. This is particularly true for DHA which plays a highly important role in growth and development of the infants nervous system. This has implications for time periods between pregnancies, because adequate time must be allowed to DHA body stores to be replenished. Declining DHA status may also have implication for breast feeding, because the infant is reliant on the mother for its supply of EFA, but the status of the mother may have declined during pregnancy. This problem may be exacerbated by intake of trans fatty acids, which are able to cross the placenta and interfere with EFA metabolism during development. Correlations between the trans fatty acid intake of the mother and the accumulated trans fatty acid in foetal tissue have been reported.
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