Objective: Development of atherosclerotic changes starts in the early postnatal life and is influenced by nutrition. We aimed to map the development of selected risk factors of atherosclerosis in infants with regard to breast feeding. Design: Prospective, observational study. Material and Method: We enrolled 47 mother + infant pairs that were followed until the infant’s 6th postnatal month (samples before and after the delivery, from umbilical cord, 3 and 6 months after the labor). We determined the levels of total cholesterol (TC), HDL cholesterol (HDL), triglycerides (TG), apolipoprotein AI (apoA), apolipoprotein B (apoB), oxidized LDL (oxLDL), antibodies against oxidized LDL, thiobarbituric acid reacting substances (TBARS) and activity of paraoxonase (PON1). LDL cholesterol (LDL) was calculated according to Planell. Results: In the 3rd month fully breast fed infants (vs. formula fed infants) showed higher levels of TC (P < 0.001), apoB (P < 0.001), LDL (P < 0.01), oxLDL (P < 0.005), TBARS (P < 0.001) and lower titers of oxLDLAb (P < 0.001). Differences between breast and formula fed infants in the 3rd month were not statistically significant after a correction for LDL (oxLDL/ LDL and TBARS/LDL). In the 6th month the fully breast fed infants had higher TC (P < 0.05), apoB (P < 0.05), LDL (P < 0.01) and TBARS (P < 0.05), however the difference in concentrations of oxLDL (P = 0.21) and oxLDLAb (P = 0.055) was not statistically significant any more. TBARS levels of the breast fed infants after the correction for LDL was not statistically different from formula fed infants in the 6th postnatal month. Neither in the 3rd nor in the 6th postnatal month we found any statistically significant difference in PON1 activities between both groups. There was a statistically significant difference between the breast and formula fed infants in changes in the 3rd month (value in the 3rd month – value at birth) in u TC (P = 0.001; higher increase in breast fed), apoB (P < 0.005; higher increase in breast fed), oxLDL (P < 0.005; higher increase in breast fed) and oxLDLAb (P < 0.001; increase in formula fed, decrease in breast fed). Conclusions: Our data suggest that the breast fed (vs. formula fed) infants have a burden of classical lipid risk factors of atherosclerosis (TC, LDL). Higher concentrations of oxLDL and TBARS in the breast fed infants are probably caused by better supply of substrate (LDL) than by enhanced oxidative stress in the breast fed infants. The breast fed infants are characterized by a low immune response to oxidatively modified LDL.

        Key words: atherosclerosis, LDL, oxidative stress, breast feeding.