Altered composition of polyunsaturated fatty acids (PUFA) has been observed in allergic individuals and it has been proposed that this is due to an impairment of delta-6-desaturase activity. We have studied the composition of PUFA in serum phospholipids in twenty-two 12-15 year old children with asthma and/or allergic dermatitis and 23 non-atopic controls of similar age. The relative levels of docosahexaenoic acid (DHA, C22:6n-3) and total n-3 long-chain polyunsaturated fatty acids (LCP) were lower (1.46% +/- 0.54 vs. 1.90% +/- 0.58, P = 0.01 for DHA and 2.34% +/- 0.67 vs. 2.80% +/- 0.77, P < 0.05 for total n-3 LCP) and the ratio of total n-6 to n-3 LCP was higher (P < 0.01) in the allergic children than in the controls. In addition to these differences, the relative levels of docosapentaenoic acid (DPA, C22:5n-3) and the ratio of arachidonic acid (AA, C20:4n-6) to dihomo-gamma-linolenic acid (DHGLA, C20:3n-6) were also lower in the 12 allergic children with positive skin prick test, as compared with the SPT negative children (both P < 0.05). In non-allergic children, the levels of total n-3 correlated with n-6 LCP (r = 0.76, p < 0.001). Furthermore, the n-3 LCP, i.e. EPA, DPA and DHA, correlated significantly with each other (r = 0.52-0.78, all p < 0.01) and correlated with n-6 LCP, i.e. C20:2, DHGLA and AA respectively (r = 0.56-0.83, all P < 0.01). Most of these correlations were absent in allergic children. Higher levels of C20:2n-6 and lower levels of eicosapentaenoic acid (EPA, C20:5n-3) were recorded in 11 allergic children with serum IgE above the median level (56 kU/l), as compared to 11 with lower IgE levels (both P < 0.05). Furthermore, the levels of C20:2n-6 correlated with the IgE levels in the children (r = 0.65, P = 0.001). The findings could not confirm an impaired delta-6-desaturase activity in allergic school children and suggest that a disturbance of LCP metabolism is associated with allergic diseases.

The fatty acid composition of umbilical cord serum phospholipids was investigated by gas chromatography in 33 infants with allergic and 35 babies of non-allergic mothers. The relative levels of the linoleic acid metabolites C20:3, arachidonic acid (AA, C20:4) and C22:4n-6, and two alpha-linolenic acid metabolites, i.e. eicosapentaenoic acid (EPA, 20:5) and docosahexaenoic acid (DHA, C22:6) were significantly higher in infants of allergic mothers than in non-allergic mothers (all p < 0.05). Furthermore, an altered proportional relationship between the various fatty acids in n-6 series fatty acids and between n-3 and n-6 series fatty acids was present already at birth in infants who developed allergic disease during their first 6 years of life. These observations cannot be employed for the prediction of allergy, however, as the individual variations were considerable.

The fatty acid composition of total lipids was analysed in colostrum and mature human milk samples obtained at 1, 3, 4 and 6 months from 17 non‐atopic and at 1 and 3 months from 17 atopic mothers. The relative levels of linoleic acid and α‐linolenic acid increased up to 3 months after delivery and then declined. In contrast, the levels of their metabolites were higher in colostrum than in mature milk. The levels of dihomo‐γ‐linolenic acid, eicosapentaenoic acid, docosapentaenoic acid and docosahexaenoic acid were all lower in atopic than non‐atopic mothers in milk samples obtained after 1 month of lactation (all p < 0:05). The ratio of total n‐6 to n‐3 long‐chain polyunsaturated fatty acids (LCP) in milk at 1 and 3 months was higher in atopic than non‐atopic mothers (all p < 0:05). Lower levels of the monounsaturated fatty acids (MUFA) were also observed in atopic mothers, as compared to non‐atopic mothers. In the non‐atopic mothers, the levels of individual n‐6 LCP correlated and also correlated with n‐3 LCP in colostrum and early mature milk (r= 0:60‐0.92, all p < 0:01). These correlations within n‐6 and between n‐6 and n‐3 LCP were mostly absent in atopic mothers. The findings suggest that the LCP metabolism in human milk is disturbed in atopic mothers, as indicated by the lower relative levels of some LCP at 1 month, higher ratios of n‐6 to n‐3 LCP and poor correlations between the levels of the various compounds during the first 3 months of lactation.

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The fatty acid composition of total lipids was analysed in colostrum and mature human milk samples obtained at 1, 3, 4 and 6 months from 17 non-atopic and at 1 and 3 months from 17 atopic mothers. The relative levels of linoleic acid and alpha-linolenic acid increased up to 3 months after delivery and then declined. In contrast, the levels of their metabolites were higher in colostrum than in mature milk. The levels of dihomo-gamma-linolenic acid, eicosapentaenoic acid, docosapentaenoic acid and docosahexaenoic acid were all lower in atopic than non-atopic mothers in milk samples obtained after 1 month of lactation (all p < 0.05). The ratio of total n-6 to n-3 long-chain polyunsaturated fatty acids (LCP) in milk at 1 and 3 months was higher in atopic than non-atopic mothers (all p < 0.05). Lower levels of the monounsaturated fatty acids (MUFA) were also observed in atopic mothers, as compared to non-atopic mothers. In the non-atopic mothers, the levels of individual n-6 LCP correlated and also correlated with n-3 LCP in colostrum and early mature milk (r = 0.60-0.92, all p < 0.01). These correlations within n-6 and between n-6 and n-3 LCP were mostly absent in atopic mothers. The findings suggest that the LCP metabolism in human milk is disturbed in atopic mothers, as indicated by the lower relative levels of some LCP at 1 month, higher ratios of n-6 to n-3 LCP and poor correlations between the levels of the various compounds during the first 3 months of lactation.