Objective: To evaluate whether levels of n-6 long chain polyunsaturated fatty acids (LCPs) in human breast milk are related to the mother's atopic constitution, and whether a decreased level can be restored by gamma-linolenic acid supplementation. Design: Cross-sectional study and dietary supplementation trial. Subjects: 20 atopic mothers and 20 non-atopic mothers (controls), all lactating. Setting: General population. Interventions: The atopic mothers were randomly assigned to low (n 10) or high (n 10) dosage oral supplementation with oral borage oil for one week (230 or 460 mg gamma-linolenic acid (18:3n-6) per day). Main outcome measures: Essential fatty acid composition of the breast milk total fat fraction, determined by gas liquid chromatography. Results: Arachidonic acid (20:4n-6) was lower in breast milk of atopic mothers compared with non-atopic mothers (0.39 wt% vs 0.46 wt%, difference 7 0.07% wt% (95% con®dence limits 7 0.13, 7 0.01 wt%; P`0.05). The ratio between linoleic acid and the sum of n-6 derivatives did not differ between these groups, indicating no difference in delta-6-desaturase (D6D) activity. Supplementation of the atopic mothers signi®-cantly increased the levels of gamma-linolenic acid and dihomo-gamma-linolenic acid in breast milk in a doserelated way, but the level of arachidonic acid was not increased. Conclusion: We found a decreased level of arachidonic acid in breast milk in atopic compared to non-atopic mothers, but no indication that the rate-limiting enzymatic step (D6D) is involved. Supplementation increased the precursor pool but did not restore the level of arachidonic acid. We conclude that atopy is related to a metabolic disturbance beyond the D6D enzymatic step. A low level of arachidonic acid in breast milk may be a risk factor for the development of atopy in the infant, especially when the possible underlying metabolic disturbance of EFA metabolism is inherited by the child.
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