## 4 Discussion
A total of 30% of them had mothers who gained >20 kg during their pregnancy, 25% had mothers with autoimmune thyroiditis, 10% had mothers with gestational diabetes mellitus, and 5% had mothers with gestational hypertension (Figure 2). These patients presented significantly increased values in CIMT compared to obese children born to healthy mothers (\(p\) = 0.047, Table 3). In overweight children, the proportion of cases that came from abnormal pregnancies dropped to 53%, and we also detected increased CIMT mean values compared to the overweight children with healthy mothers (\(p\) = 0.049, Table 4). For normal-weight children, the proportion of unhealthy pregnancies was even smaller, at 32% (Table 5). Overall, the most predominant risk factor was by far maternal obesity (>20 kg weight gain). The mechanism behind its effects on the fetus is based on placental insufficiency, which promotes intrauterine growth restriction [54]. This can lead to structural and functional alterations on the fetus' cardiovascular system that may persist throughout childhood [55]and can remain permanent risks or predispositions for high blood pressure, increased CIMT, and arterial stiffness [56]. Family medical history should play an important role in shaping an individual's cardiometabolic risk profile. Family history alone is not enough to place blame, but it surely helps to evaluate the genetic risk of the individual in order to estimate prognostics on the onset and severity of the disease's evolution [57]. In our study, 75% of obese children had a family history positive for risk, 40% had obese first-grade relatives, followed by a long distance by autoimmune thyroiditis, type 2 diabetes mellitus, and cardiovascular diseases (Figure 3). Although CIMT values were higher for children with a family history of risk in all three groups of study, significance was found only in the overweight group (\(p=0.049\)). Smoking is a well-known risk factor for vascular dysfunction, affecting the integrity of endothelial cells and promoting lipid and monocyte invasion of endothelial walls [58], and thus accelerating the stiffness of the arterial wall. We addressed the problem of adolescent smoking, but cannot rely on our findings due to the small amount of smoking teenagers in our group. Obese smokers had the most increased CIMT mean: \(\overline{X}=0.61\) mm, \(p=0.015\) (Table 3). We note the only case of a 16-year-old male normal-weight smoker, who presented neither of the evaluated risk factors and who had a CIMT value of 0.56, higher than anyone in his group (group CIMT \(\overline{X}=0.39\) mm); see Table 5. Because both age and the presence of metabolic syndrome are closely linked to inflammation and oxidative stress, and ultimately the damage of the vasculature structure, which is easily detectable starting in young adulthood [59], in young adults with such conditions, smoking will strengthen the adverse effects of age and all the other risk factors by directly damaging endothelial integrity. High blood pressure in obese children and young adults is a consequence of the mixture of insulin resistance, sympathetic nervous system overactivity, and damage to the endothelial wall [60]. With regard to CIMT values, once installed, hypertension is an aggravating factor [61]. Moreover, hypertensive children present increased CIMT values, regardless of their BMI [62]. Our study confirmed the higher CIMT values among hypertensive children compared to normotensive ones (\(p=0.012\)) with similar BMIs. Hypertensive subjects in the obese group reached 20%. Our approach to lifestyle as a risk was focused on the level of sedentary behavior of each subject. We considered a subject sedentary when they practiced no sport and/or had less than 1 h of physical activity/day. Lack of physical activity is the factor that completes the big picture of obesity [63]. Although we did not find statistically meaningful differences, our study showed a tendency toward higher CIMT based on sedentary habits in all weight categories.