Healthy and unhealthy lifestyle changes during young adulthood are associated with decreased and increased risks, respectively, for subclinical atherosclerosis in middle age [
30]. Dyslipidemia is an important factor for atherosclerosis that has been shown to be associated with CIMT [
18]. Regression analysis demonstrated that the mean and maximum CIMT (CIMT[max]) are independently influenced by age, blood creatinine levels and non-high density lipoprotein (HDL) cholesterol levels [
22]. In particular, patients with familial hypercholesterolemia (FH) are at increased risk of premature CV disease. Hypercholesterolemic children [
31] and patients with FH [
32] exhibited significantly higher CIMT. Results of CIMT meta-analysis strengthen the evidence of early atherosclerotic development in children with FH. Circulating low-density lipoprotein (LDL-C) concentrations were associated with CIMT [
33,
34], and high levels of oxidized LDL (OxLDL) were significantly associated with progression and increased levels of CIMT [
35-
37]. Low levels of HDL cholesterol or relative levels of the HDL 3b subclasses and changes in the proportion of small HDL particles were significantly associated with an increased in CIMT [
20,
38] and with the presence of carotid plaques [
39]. Furthermore, among women, IMT(max) was significantly negative correlated to HDL cholesterol [
40]. In the statin group, HDL cholesterol levels were associated with CIMT; in the combined therapy group, HDL cholesterol levels were the only significant correlate of CIMT [
41]. Apoliproproteins are also important risk factors for atherosclerosis. Among them, apolipoprotein B(apoB) [
33] and ApoB/ApoA1 [
42] were significantly positively associated with CIMT, and the absence or very low levels of erythrocyte-bound apoB was associated with clinical and subclinical atherosclerosis [
43]. In contrast, other studies revealed that ApoE genotypes and CIMT were not associated [
44] and that ApoA1 has an inverse association with CIMT [
42]. Therefore, whether changes in dietary patterns affect the risk of early atherosclerosis remains under debate. One study did not find an association between dietary patterns and IMT or plaques [
45], and high versus low protein intake in infancy did not influence CIMT at 5Â years [
44]. However, several studies have demonstrated that a Mediterranean diet has a protective effect on the CV system because lower adherence to a Mediterranean diet was shown to increase the risk of subclinical atherosclerosis [
46]. Additionally, 12Â months of Mediterranean diet intervention caused a significant reduction in CIMT [
31]. Interventions to lower LDL cholesterol from the suboptimal to the optimal range were shown to have potentially significant benefits to firefighters [
34]. Atorvastatin [
47], rosuvastatin [
48] and fuvastatin [
49] treatments slowed or reduced the progression of CIMT; intensive lipid lowering and antihypertensive therapy along with a reduction in central fat [
50] may be considered a mandatory treatment strategy in young patients with FH to prevent atherosclerosis and to increase arterial stiffness. In men with CHD and high levels of Lp(a), atorvastatin use [
51] results in an average 0.06Â mm decrease in CIMT over 6Â months. Adequate statin treatment [
52] might delay carotid atherosclerosis in FH independent of Lp(a) levels. Hence, CIMT was associated with dyslipidemia and dysapoliproprotein but was not associated with protein intake. Therefore, intensive lipid-lowering therapy might be used to reduce the progression of CIMT in high-risk patients.