In the current study, risk factors for CVD retained from childhood to adulthood predicted CVD in young adulthood. Risk for CVD was attenuated when childhood risk factors were not maintained into adulthood, congruent with the report by Juonala et al. . Children who had high TG and retained high TG as adults had increased CVD events. Children who had normal BMI and retained normal BMI as adults had reduced CVD events. Children who had high childhood BP and TG and retained these into adulthood were more likely to have adult T2DM, children with childhood risk factors not retained were not associated with increased adult T2DM, congruent with the report by Juonala et al. .
In contrast to CVD and T2DM, adult IFG was associated with adult high BP, TG, and cigarette smoking, and was not associated with retention of risk factors from childhood to adulthood.
Our finding of a significant association of high TG retained from childhood to adulthood with young adult CVD is consistent with pediatric  and adult studies where non-fasting [23–25] and fasting TG [26–29] are independent risk factors for CVD and for ischemic stroke . The association of TG high from childhood through young adulthood with adult CVD may, speculatively, reflect the presence of pediatric metabolic syndrome, a known predictor of adult CVD . Moreover, TG levels in adolescent males have been related to coronary artery calcification 15 to 20 years later in young adults . Coronary artery streaks in 6 to 30 year olds are significantly correlated with antecedent TG and very low density lipoprotein cholesterol [32, 33]. In a post-mortem study of 15 to 34 year old men, the percentage of the right coronary arterial intima involved with atherosclerosis correlated with a combination of LDL and VLDL cholesterol levels, and was inversely associated with HDL cholesterol .
Normal childhood BMI retained to adulthood was a significant negative risk factor for adult CVD. The association of normal BMI retained from childhood to adulthood with low young adult CVD events is consistent with the report by Chen et al.  where clustering of bottom quartile BMI, HOMA IR, SBP, and the ratio of total/HDL cholesterol was associated with decreasing mean values of carotid intima-media thickness in adulthood.
High childhood BP and TG, two components of the metabolic syndrome complex, retained into adulthood were associated with adult T2DM, findings broadly in agreement with those of Everhart et al.  and Lee et al. , which suggested that the duration of the risk factor presence from childhood to young adulthood and the cumulative exposure to risk factors predict adult outcomes.
Our finding of an association of glucose levels in childhood with the development of T2DM in adulthood is consistent with a recent report from the Bogalusa Heart Study that fasting plasma glucose in childhood is a predictor of T2DM in young adulthood even when the pediatric glucose is within the normal range . Moreover, childhood insulin response during an oral glucose challenge predicts adult acute insulin response .
Given the significant tracking of risk factors for CVD and T2DM as observed in the current and previous studies [11, 38–40], failure to act on such childhood risk factors high TG, high BP, and obesity [12, 16] means the underlying pathology may continue into young adulthood, increasing the likelihood of an adverse outcome [10, 41]. These findings emphasize the importance of risk factor screening in childhood . Lifestyle  and pharmacologic intervention [1, 42, 43] in childhood-adolescence might prevent development of CVD or T2DM in young adulthood.
A weakness in the current study is the absence of knowledge concerning when (at what age) participants with normal factors in childhood developed abnormal risk factors and when participants with abnormal factors in childhood developed normal risk factors. Thus, it was not possible to evaluate more precisely the length of time the at-risk state existed.
In the current study, neither pediatric nor young adult LDLC was associated with young adult CVD, perhaps attributable to treatment of high LDLC in 26 of 770 (3. 4%) young adults at PFS, or to the fact that with only 19 CVD endpoints by mean age 38, the study may not have had adequate power to declare an LDLC effect significant. Treatment to lower LDLC might, speculatively, also have reduced the power of LDLC to predict CVD.
Conventionally, parental history of CVD serves as an indication for screening for lipid abnormalities in children [44, 45]. After detailed review of basing childhood screening on parental history, the recent Expert Panel statement  called for universal risk factor screening in children . Identification of CVD risk factors in a child can directly facilitate primary prevention  in the child through young adulthood, and also focus diagnostic attention on the potentially high-risk parent.