Different quantities and quality of fat in milk products given to young children: effects on long chain polyunsaturated fatty acids and <i>trans</i> fatty acids in plasma

Abstract

In this study we compared plasma contents of long‐chain polyunsaturated fatty acids (LC‐PUFAs) and trans fatty acids in triglycerides (TG), phospholipids (PL) and cholesterolesters (CE) in young children fed milk diets containing different amounts of linoleic (LA) and α‐linolenic acid (ALA). Because the diets differed in vitamin A and E content, plasma concentrations of vitamin A and E were also studied. Thirty‐seven 1‐y‐old children were randomly assigned to one of four feeding groups: (1) low‐fat milk (LF) (1.0 g cow's milk fat/dL); (2) standard‐fat milk (SF) (3.5 g cow's milk fat/dL); (3) partially vegetable fat milk (PVF) (3.5 g fat/dL; 50% vegetable fat from rapeseed oil, 50% milk fat); and (4) full vegetable fat milk (FVF) (3.5 g fat/dL; 100% vegetable fat from palm‐, coconut‐ and soybean oil). We found higher amounts of plasma LA in the FVF group than in the LF and SF groups ( p &lt; 0.001) and higher amounts of ALA in the PVF group than in the SF ( p &lt; 0.001 in TGs, p &lt; 0.05 in CEs) and LF ( p &lt; 0.01 in PLs and CEs, p &lt; 0.05 in TGs) groups. However, amounts of plasma arachidonic acid (AA) were similar between groups as well as the amounts of docosahexaenoic acid (DHA) in CEs and PLs. Total trans FAs were lower in CEs in the PVF and FVF groups than in the SF group ( p &lt; 0.05 SF vs PVF; p &lt; 0.01 SF vs FVF). Plasma concentrations of α‐tocopherol were higher in the FVF group than in the other groups ( p &lt; 0.05 FVF vs SF, p &lt; 0.01 FVF vs SF and PVF). Conclusion : Children consuming milk diets containing high amounts of vegetable fat present with higher plasma LA and ALA without any effects on amounts of plasma LC‐PUFA. The plasma LC‐PUFA status is not adversely affected by a low‐fat milk diet. AHA and DHA in plasma are not affected by the diets studied, presumably because 15‐mo‐old children may be able to compensate for dietary influences through endogenous LC‐PUFA metabolism.