Breast milk levels of zinc and omega-6 polyunsaturated fatty acids and growth of healthy Chinese infants

AIM: To examine the concentrations of zinc and omega-6 polyunsaturated fatty acids (omega-6 PUFAs) in breast milk, the impact of zinc on omega-6 PUFA metabolism, and the growth rate of infants. METHODS: Forty-one mother-term infant pairs from a rural area of northern Beijing, China, who were 1 month (n = 18, group I) and 3 months (n = 23, group II) old and exclusively breastfed, were studied. The dietary records and the concentrations of zinc and omega-6 PUFAs in the milk of lactating women and the increase in weight and length of their infants during 1 and 3 postnatal months were analysed. RESULTS: The dietary intakes of mothers in the two groups were the same, i.e. high in carbohydrate and low in fat, protein and energy. The maternal zinc intake was 7.5mg/d and thus reached only 34.6% of the current Recommended Nutrient Intake (RNI). The levels of zinc and arachidonic acid (AA, C20:4 omega-6) in the milk of group I were significantly higher than those in group II. Furthermore, significant positive correlations were found between the concentrations of zinc and AA in the breast milk and between the level of milk AA and weight gain. CONCLUSION: Zinc may be a co-factor and essential for essential fatty acids (EFA) metabolism. Thus suboptimal zinc intake may cause EFA imbalance. Further studies of Chinese rural mother-infant pairs are necessary to determine whether zinc supplementation should be recommended when lactation exceeds 3 months.

Polyunsaturated fatty acids in the pathogenesis and treatment of multiple sclerosis

Epidemiological, biochemical, animal model and clinical trial data described in this overview strongly suggest that polyunsaturated fatty acids, particularly n-6 fatty acids, have a role in the pathogenesis and treatment of multiple sclerosis (MS). Data presented provides further evidence for a disturbance in n-6 fatty acid metabolism in MS. Disturbance of n-6 fatty acid metabolism and dysregulation of cytokines are shown to be linked and a "proof of concept clinical trial" further supports such a hypothesis. In a randomised double-blind, placebo controlled trial of a high dose and low dose selected GLA (18:3n-6)-rich oil and placebo control, the high dose had a marked clinical effect in relapsing-remitting MS, significantly decreasing the relapse rate and the progression of disease. Laboratory findings paralleled clinical changes in the placebo group in that production of mononuclear cell pro-inflammatory cytokines (TNF-alpha, IL-1 beta) was increased and anti-inflammatory TGF-beta markedly decreased with loss of membrane n-6 fatty acids linoleic (18:2n-6) and arachidonic acids (20:4n-6). In contrast there were no such changes in the high dose group. The improvement in disability (Expanded Disability Status Scale) in the high dose suggests there maybe a beneficial effect on neuronal lipids and neural function in MS. Thus disturbed n-6 fatty acid metabolism in MS gives rise to loss of membrane long chain n-6 fatty acids and loss of the anti-inflammatory regulatory cytokine TGF-beta, particularly during the relapse phase, as well as loss of these important neural fatty acids for CNS structure and function and consequent long term neurological deficit in MS.