Abstract
Humans consume large amounts of TFA due to the extensive use of hydrogenated fats in food production. TFA consumption is considered safe for man, but side effects including impaired synthesis of LCP (20 & 22 carbons) have been observed in animal studies. We have previously documented materno-fetal transfer of TFA in humans. Therefore, we looked for possible effects of TFA on LCP status during early life, when LCP modulate tissue growth and development. Methods: Blood plasma samples were obtained in 29 clinically well-premature infants (gest. age 34.0±1.8 wks., birthwt. 1694±173 g, M±SD) prior to feeding in the morning of day 3 post partum, when milk intake was still very low. No infant had received fat infusions. Fatty acids in lipid classes were determined by high-resolution gas-liquid-chromatography. Results: Both total TFA and elaidic acid (18:1t), the main dietary TFA, were inversely correlated to LCP in plasma lipids. In triglycerides, linear correlation coefficients (r) for 18:1t were significant (P<0.05* & 0.01**) for LCP (n-6-LCP: -0.41*, n-3-LCP: -0.50**, total LCP: -0.55**) and for product substrate ratios of LCP biosynthesis (20:4/18:2n-6: -0.47**, 22:6/18:3n-3: -0.50**). Similar results were found in other lipid classes for 18:1t and total TFA. Conclusions: 1. TFA exposure may impair biosynthesis of n-6- and n-3-LCP in man. 2. Since the capacity for LCP biosynthesis is limited during early life and LCP accretion is essential for normal functional development of membrane rich tissues (e.g. brain), a high intrauterine TFA exposure may have serious risks for fetus and neonate. 3. This observation is the first indication of possible untoward effects of TFA in man.
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