## 4 Discussion
Inflammation and an early onset of subclinical atherosclerosis makes the arterial walls of pre-pubertal obese children have similar characteristics to the arterial walls of normal-weight or slightly overweight post-pubertal children and even young adults. In adults, CIMT reaches higher values in men [8]; however, in children, differences on behalf of sex are insignificant. In our analysis, in the obese group, the mean valuesfor CIMT in boys and girls were identical, whereas in the overweight group, boys scored higher values for CIMT (\(p\) = 0.043); see Table 2.  
An essential part of our study was the analysis of potential factors that increase risk for higher CIMT from an early age. Most of these factors overlap their influence on CIMT with that of weight excess predisposition. We analyzed each risk factor within the respective group. Although discussions on postnatal nutrition's role in cardiometabolic risk is still being researched, most studies are in agreement that breastfeeding has a protective cardiovascular role only when it is not prolonged, being inversely associated with mortality by coronary disease [10]. A 65-year longitudinal study showed that breastfeeding reduces the progression of atherosclerosis, which translates into a lower CIMT [13]. On the other hand, artificial feeding is known to be associated not only with obesity [12], but also with high blood pressure [14] and insulin resistance [15]. Our analysis showed that although in all three groups, children who were bottle-fed presented higher CIMT values, the results were not statistically significant, except for the overweight group (\(p\) = 0.023). Although the results concerning CIMT were inconclusive, the proportions of formula-fed/breast-fed children in each group clearly suggest that artificial nutrition represents a risk factor for weight excess in childhood: 65% of the obese group, 47% of the overweight group, and only 37% of the normal-weight group were bottle-fed. Data on birth weight and its influence on cardiometabolic risk over time are more conclusive. Children born large for gestational age have a predisposition for obesity and an increased CIMT in young adulthood, although they seem to have an otherwise healthy cardiovascular risk [17]. Children with low birth weight have increased CIMT values in young adulthood only if they have experienced severe intrauterine growth retardation followed by exaggerated postnatal growth [50]. A recent meta-analysis showed that in children born small for gestational age, CIMT has increased values in infants rather than in older children, which may prove that fetal growth restriction is an important factor that may increase the child's risk trajectory [51]. Our findings are in accord with previous studies, although our sample cases were smaller. In all three study groups, approximately half of the children had normal birth weights (2500-3500 g) and the other half had either low birth weight (<2500 g) or high birth weight (>3500 g) (Tables 3-5). Although we did not detect significant differences, CIMT had higher values for children with high birth weight in both overweight children and controls. However, in the obese group, the mean values for low birth weight were higher than for high birth weight (Table 3). Low birth weight might have more of impact on endothelial suffering, as it is associated with in utero cardiac remodeling and reduced arterial compliance [52]. Previous studies have shown that the more severe fetal growth impairment is, the more significant the data [51]. Because a mother's health and health-related habits during pregnancy are directly connected to the intrauterine development of the child [53], we analyzed how some maternal risk factors for child obesity and cardiovascular risk influence our subjects. A total of 70% of our obese patients were born to unhealthy mothers.