Risk factors for cardiovascular disease and type 2 diabetes retained from childhood to adulthood predict adult outcomes: the Princeton LRC Follow-up Study
© Morrison et al.; licensee BioMed Central Ltd. 2012
Received: 2 December 2011
Accepted: 19 March 2012
Published: 16 April 2012
Pediatric risk factors predict adult cardiovascular disease (CVD) and type 2 diabetes (T2DM), but whether they predict events independently of adult risk factors is not fully known.
Assess whether risk factors for CVD and T2DM retained from childhood to adulthood predict CVD and T2DM in young adulthood.
770 schoolchildren, ages 5–20 (mean age 12), 26-yr prospective follow-up. We categorized childhood and adult risk factors and 26-year changes (triglycerides [TG], LDL cholesterol, BMI, blood pressure [BP] and glucose ≥, and HDL cholesterol < pediatric and young adult cutoffs). These risk factors and race, cigarette smoking, and family history of CVD and T2DM were assessed as predictors of CVD and T2DM at mean age 38.
Children who had high TG and retained high TG as adults had increased CVD events as adults (p = .0005). Children who had normal BMI and retained normal BMI as adults had reduced CVD events as adults (p = .02). Children who had high BP or high TG and retained these as adults had increased T2DM as adults (p = .0006, p = .003).
Risk factors for CVD and T2DM retained from childhood to adulthood predict CVD and T2DM in young adulthood and support universal childhood screening.
KeywordsRisk factors Cardiovascular disease Type 2 diabetes mellitus Obesity High blood pressure Tracking
Recently, an expert panel recommended screening all American children for risk factors for cardiovascular disease (CVD) , not just children of parents with known CVD or high risk factors. Pediatric risk factors for atherosclerosis have been shown to associate with young adult atherosclerotic lesions , carotid intima-media thickening (CIMT) [3–7], and cardiovascular disease (CVD) events . Moreover, adolescent CVD risk factor status predicts increased adult CIMT, independent of adult risk factors [9, 10], and children with metabolic syndrome (MetS) have 2–3 times greater risk of high CIMT and type 2 diabetes mellitus (T2DM) as adults versus children free of MetS . Obese children who remained obese as adults have increased type 2 diabetes (T2DM), hypertension, dyslipidemia, and increased CIMT, but risks for these outcomes are attenuated in obese children who became non-obese adults, with outcomes similar to those non-obese in both childhood and adulthood .
It is not well understood whether childhood risk factors cause adult CVD directly, independent of adult risk factors, or only in those individuals whose risk factors tracked into adulthood, thereby increasing the length of exposure to high risk factors [10, 13]. The best predictor of high blood pressure (HBP) in adulthood has been reported to be adult obesity or change in obesity; pediatric obesity does not predict adult HBP when adult obesity is in the model . However, HBP is itself a risk factor, not a CVD event. Positive associations between childhood BMI and adult CIMT are generally attenuated once adjusted for adult BMI . Child-adult relationships may be dependent on tracking of BMI from childhood to adulthood , since risk of events increases with the length of exposure [15, 16]. There is a stepwise increase in the incidence of T2DM with the duration of obesity .
In the current study, our specific aim was to assess whether risk factors for CVD and T2DM retained from childhood to adulthood predict CVD and T2DM in young adulthood or whether childhood risk factors are attenuated  by changes in risk factors from childhood to young adulthood.
We used data from the NHLBI Princeton Follow-up Study (PFS, 1999–2003), a 22–30 year follow-up of black and white former schoolchildren first studied in the NHLBI Lipid Research Clinics (LRC, 1973–1976) [8, 17]. PFS collected data following a protocol approved by the Children’s Hospital Institutional Review Board, with signed informed consent .
Princeton LRC and PFS studies
The Princeton LRC  study was a multistage survey of lipids and other CVD risk factors in students in grades 1–12 and a 50% random sample of their parents by household. The student population in LRC was 72% white and 28% black, with a mean age of 12.3 ± 3.4 years. Participation rates did not differ significantly between races.
The PFS  was conducted in adults, 22 to 30 years after their initial pediatric LRC sampling to assess relationships of pediatric risk factors to subsequent adult health events. The subjects’ CVD, T2DM and high blood pressure (HBP) status and use of prescribed medications for lipids, diabetes mellitus, and blood pressure were obtained by questionnaire with an interviewer .
After an overnight fast, blood was drawn for measurements of plasma triglyceride (TG), high density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC), systolic blood pressure (SBP), diastolic blood pressure (DBP), BMI, and glucose in children and their parents at the LRC assessment and at the subsequent PFS study 26 years later. There was no contact with the former schoolchildren or their parents during the 26-year interval between the LRC and PFS studies.
Diagnosis of CVD, type 2 diabetes and impaired fasting glucose
At PFS, CVD was defined as myocardial infarction, coronary artery bypass graft, angioplasty, ischemic stroke, and carotid or peripheral artery bypass surgery . Diagnosis of diabetes (T2DM) was based on World Organization of Health criteria, fasting glucose ≥ 7 mmol/l (126 mg/dl) and/or self-report of diabetes with treatment by a physician . We excluded from these analyses 10 subjects who had reported type 1 diabetes mellitus as children at LRC. However, in PFS we did not have a measurement of C-peptides or diabetes autoantibody levels, the gold standard methods of distinguishing type 1 from type 2 diabetes . Diagnosis of impaired fasting glucose (IFG) was made when fasting blood glucose was ≥ 100 but <126 mg/dl.
Pediatric and young adult risk factor cutoffs
Pediatric risk factor cutoffs included high LDLC (≥110 mg/dl [2.82 mmol/l]) , high BMI (≥85th CDC 2000 age-gender specific percentile), high BP (SBP and/or DBP >90th age-height specific percentiles in current cohort), and cutoffs published for pediatric metabolic syndrome : high TG (≥110 mg/dl [1.24 mmol/l]), low HDLC (≤50 mg/dl [1.28 mmol/l] in girls, ≤40 [1.03 mmol/l] in boys), and high glucose (≥100 mg/dl [5.6 mmol/l]).
Risk factor cutoffs at the PFS were those of the NCEP/AHA Metabolic syndrome (waist ≥ 102 cm men, ≥ 88 cm women, SBP ≥ 130 mmHg and/or DBP ≥ 85, TG ≥ 150 mg/dl [1.69 mmol/l], HDLC <40 mg/dl [1.03 mmol/l] men, <50 mg/dl [1.28 mmol/l] women, glucose ≥ 100 mg/dl [5.6 mmol/l]) . BMI and LDLC cutpoints at the PFS respectively were ≥ 30 kg/m2 (CDC, US Obesity Trends, Trends by State 1985–2009), and the current cohort’s gender-race-specific 90th percentile levels.
CVD risk factor measures in the cohort in childhood (LRC) and adulthood (PFS) were summarized.
To assess for possible selection bias, comparisons were made between the 770 subjects with complete CVD risk factor measures at both the LRC visit and the PFS visit 26 years later, and 695 subjects without complete measures. Comparisons were made by Wilcoxon test or by chi-square test.
Risk factor measures at LRC and PFS were categorized as high vs. not high (for TG, LDLC, BMI, SBP-DBP, and glucose) or low vs. not low (for HDLC) using the above-mentioned cutoffs. The change in status for each risk factor from LRC to PFS was indicated by 4 dummy variables (normal to normal vs. others; abnormal to normal vs. others; normal to abnormal vs. others; abnormal to abnormal vs. others).
Stepwise logistic regression analysis was used to identify significant independent risk factors for young adult CVD, T2DM and IFG at PFS in multivariate analyses. Explanatory variables included age at follow-up and categorical variables: race, pediatric and young adult risk factor status group (high vs. not high) for TG, LDLC, BMI, glucose, blood pressure, HDLC (low vs. not low), cigarette smoking (yes vs. no), and parental history (yes vs. no) of CVD or T2DM, as well as changes in risk factor status from childhood to young adulthood. Including only significant explanatory variables from stepwise selection, logistic regression models were re-evaluated allowing more observations to be used.
From the logistic regression model, the changes in TG, BMI or BP from LRC to PFS were significant predictors for the CVD or T2DM at PFS. The associations of these risk factor changes with CVD or T2DM status were graphed. Pediatric to adult changes in risk factors were ordered to represent increasing risk, with lowest risk being normal to normal, then abnormal to normal, normal to abnormal and highest being abnormal to abnormal. The Mantel-Haenszel test was used to measure the significance of associations between the risk factor status groups in childhood and adulthood and the adult development of CVD or T2DM.
Risk factors for cardiovascular disease and type 2 diabetes mellitus, measured during childhood (LRC) and 26 years later in young adulthood (PFS) in 770 subjects
W 561 (73%), B 209 (27%)
M 351 (46%), F 419 (54%)
Spearman correlation Between LRC and PFS
Mean ± SD
Mean ± SD
Adjusted for BMI at LRC
Adjusted for BMI at PFS
Adjusted for BMI at LRC and at PFS
r = 0.33, p < .0001
r = 0.34, p < .0001
r = 0.38, p < .0001
r = 0.44, p < .0001
r = 0.44, p < .0001
r = 0.46, p < .0001
107 ±30 106 ±29*
121 ±36 121 ±36*
r = 0.48, p < .0001 r = 0.49, p < .0001*
r = 0.48, p < .0001 r = 0.50, p < .0001*
r = 0.48, p < .0001 r = 0.50, p < .0001*
2.05 ±0.76 2.03 ±0.75*
2.94 ±1.34 2.94 ±1.33*
r = 0.44, p < .0001 r = 0.44, p < .0001*
r = 0.45, p < .0001 r = 0.45, p < .0001*
r = 0.46, p < .0001 r = 0.46, p < .0001*
r = 0.18, p < .0001
r = 0.18, p < .0001
r = 0.18, p < .0001
Pediatric and adult CVD risk factor measures 26 years later were highly correlated, Table 1. Twenty-six of the 770 subjects (3.4%) were taking cholesterol-lowering medications at their PFS visit, Table 1. Excluding their LDLC values from the analyses of correlations between LRC and PFS did not appreciably affect the correlation coefficients, Table 1. After adjusting for BMI at mean ages 12 and 38, age 12 and age 38 risk factors remained closely correlated, Table 1.
Incidence rate (%) of cardiovascular disease (CVD) by triglyceride (TG) and BMI classification in childhood and adulthood and of type 2 diabetes mellitus (T2DM) by blood pressure and triglyceride classification in childhood and adulthood
Normal - Normal
High - Normal
Normal - High
High - High
Trend of incidence rate by Mantel-Haenszel χ 2 test
χ2 = 22.4, p < .0001
χ2 = 12.1, p = .0005
χ2 = 17.8, p < .0001
χ2 = 20.3, p < .0001
Childhood (LRC) and adulthood (PFS) predictors for cardiovascular disease (CVD), type 2 diabetes (T2DM) and impaired fasting glucose (IFG) at PFS
Young adult outcome
Odds Ratio, 95% Confidence Intervals
CVD (19 Yes, 751 no) a 770 observations used AUC = 0.843
TG at LRC and PFS (high to high vs others)
Age at PFS (year)
BMI at LRC and PFS (low to low vs others)
T2DM (29 Yes, 417 normal) b 446 observations used AUC = 0.842
BP at LRC and PFS (high to high vs others)
TG at LRC and PFS (high to high vs others)
BMI at PFS (high vs not high)
Glucose at LRC (high vs not high)
Age at PFS
IFG (88 Yes, 617 normal) b 705 observations used AUC = 0.699
BP at PFS (high vs not high)
TG at PFS (high vs not high)
Cigarette smoking (yes vs no)
Adult T2DM (29 yes, 417 no) was associated with BP and TG high in childhood and retained into adulthood (p = .0006, .003), with childhood glucose (p = .006), with adult age (p = .002), and with black race (p = .04), Table 3.
Adult IFG (88 yes, 617 no) was positively associated with adult BP and TG (high vs not high), p < .0001, p = .0009, respectively, and with cigarette smoking, p = .018, Table 3.
Neither pediatric nor young adult LDLC was associated with young adult CVD, p > .05.
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.
Risk factors for CVD and T2DM retained from childhood to adulthood predict CVD and T2DM in young adulthood and support universal childhood screening.
Lipid Research Clinics
Princeton School Follow-up Study
coronary heart disease
carotid intima-media thickening
impaired fasting glucose
type 2 diabetes mellitus
high blood pressure
diastolic blood pressure
systolic blood pressure
high density lipoprotein cholesterol
low density lipoprotein cholesterol
body mass index
National Cholesterol Education Program
National Heart, Lung, and Blood Institute
American Heart Association.
Supported by American Heart Association (National) 9750129 N and NIH-HL62394 (Dr Morrison), Lipoprotein Research Fund of the Jewish Hospital of Cincinnati (Dr Glueck).
- Expert panel on integrated guicelines for cardiovascular health and risk reduction in children and adolescents: Summary Report. Pediatrics. 2011, 128 (Supplement 5): S1-S45.
- McMahan CA, Gidding SS, Malcom GT, Tracy RE, Strong JP, McGill HC: Pathobiological determinants of atherosclerosis in youth risk scores are associated with early and advanced atherosclerosis. Pediatrics. 2006, 118: 1447-1455. 10.1542/peds.2006-0970.View ArticlePubMedGoogle Scholar
- Juonala M, Magnussen CG, Venn A, Dwyer T, Burns TL, Davis PH, Chen W, Srinivasan SR, Daniels SR, Kahonen M, Laitinen T, Taittonen L, Berenson GS, Viikari JS, Raitakari OT: Influence of age on associations between childhood risk factors and carotid intima-media thickness in adulthood: the Cardiovascular Risk in Young Finns Study, the Childhood Determinants of Adult Health Study, the Bogalusa Heart Study, and the Muscatine Study for the International Childhood Cardiovascular Cohort (i3C) Consortium. Circulation. 2010, 122: 2514-2520. 10.1161/CIRCULATIONAHA.110.966465.View ArticlePubMedGoogle Scholar
- Juonala M, Viikari JS, Kahonen M, Taittonen L, Laitinen T, Hutri-Kahonen N, Lehtimaki T, Jula A, Pietikainen M, Jokinen E, Telama R, Rasanen L, Mikkila V, Helenius H, Kivimaki M, Raitakari OT: Life-time risk factors and progression of carotid atherosclerosis in young adults: the Cardiovascular Risk in Young Finns study. Eur Heart J. 2010, 31: 1745-1751. 10.1093/eurheartj/ehq141.View ArticlePubMedGoogle Scholar
- Magnussen CG, Venn A, Thomson R, Juonala M, Srinivasan SR, Viikari JS, Berenson GS, Dwyer T, Raitakari OT: The association of pediatric low- and high-density lipoprotein cholesterol dyslipidemia classifications and change in dyslipidemia status with carotid intima-media thickness in adulthood evidence from the cardiovascular risk in Young Finns study, the Bogalusa Heart study, and the CDAH (Childhood Determinants of Adult Health) study. J Am Coll Cardiol. 2009, 53: 860-869. 10.1016/j.jacc.2008.09.061.PubMed CentralView ArticlePubMedGoogle Scholar
- Freedman DS, Dietz WH, Tang R, Mensah GA, Bond MG, Urbina EM, Srinivasan S, Berenson GS: The relation of obesity throughout life to carotid intima-media thickness in adulthood: the Bogalusa Heart Study. Int J Obes Relat Metab Disord. 2004, 28: 159-166.View ArticlePubMedGoogle Scholar
- Davis PH, Dawson JD, Riley WA, Lauer RM: Carotid intimal-medial thickness is related to cardiovascular risk factors measured from childhood through middle age: the Muscatine Study. Circulation. 2001, 104: 2815-2819. 10.1161/hc4601.099486.View ArticlePubMedGoogle Scholar
- Morrison JA, Glueck CJ, Horn PS, Yeramaneni S, Wang P: Pediatric triglycerides predict cardiovascular disease events in the fourth to fifth decade of life. Metabolism. 2009, 58: 1277-1284. 10.1016/j.metabol.2009.04.009.PubMed CentralView ArticlePubMedGoogle Scholar
- Raitakari OT, Juonala M, Kahonen M, Taittonen L, Laitinen T, Maki-Torkko N, Jarvisalo MJ, Uhari M, Jokinen E, Ronnemaa T, Akerblom HK, Viikari JS: Cardiovascular risk factors in childhood and carotid artery intima-media thickness in adulthood: the Cardiovascular Risk in Young Finns Study. JAMA. 2003, 290: 2277-2283. 10.1001/jama.290.17.2277.View ArticlePubMedGoogle Scholar
- Daniels SR: Can lipid and lipoprotein concentrations in childhood predict adult atherosclerosis?. J Am Coll Cardiol. 2009, 53: 870-871. 10.1016/j.jacc.2008.11.037.View ArticlePubMedGoogle Scholar
- Magnussen CG, Koskinen J, Chen W, Thomson R, Schmidt MD, Srinivasan SR, Kivimaki M, Mattsson N, Kahonen M, Laitinen T, Taittonen L, Ronnemaa T, Viikari JS, Berenson GS, Juonala M, Raitakari OT: Pediatric metabolic syndrome predicts adulthood metabolic syndrome, subclinical atherosclerosis, and type 2 diabetes mellitus but is no better than body mass index alone: the Bogalusa Heart Study and the Cardiovascular Risk in Young Finns Study. Circulation. 2010, 122: 1604-1611. 10.1161/CIRCULATIONAHA.110.940809.PubMed CentralView ArticlePubMedGoogle Scholar
- Juonala M, Magnussen CG, Berenson GS, Venn A, Burns TL, Sabin MA, Srinivasan SR, Daniels SR, Davis PH, Chen W, Sun C, Cheung M, Viikari JS, Dwyer T, Raitakari OT: Childhood adiposity, adult adiposity, and cardiovascular risk factors. N Engl J Med. 2011, 365: 1876-1885. 10.1056/NEJMoa1010112.View ArticlePubMedGoogle Scholar
- Lauer RM, Clarke WR: Childhood risk factors for high adult blood pressure: the Muscatine Study. Pediatrics. 1989, 84: 633-641.PubMedGoogle Scholar
- Lloyd LJ, Langley-Evans SC, McMullen S: Childhood obesity and adult cardiovascular disease risk: a systematic review. Int J Obes (Lond). 2010, 34: 18-28. 10.1038/ijo.2009.61.View ArticleGoogle Scholar
- Everhart JE, Pettitt DJ, Bennett PH, Knowler WC: Duration of obesity increases the incidence of NIDDM. Diabetes. 1992, 41: 235-240. 10.2337/diabetes.41.2.235.View ArticlePubMedGoogle Scholar
- Lee J, Gebremariam A, Vijan S, Gurney JG: Excess body mass index-years, a measure of degree and duration of excess weight and risk for incident diabetes. Archives of Pediatrics and Adolescent Medicine. 2011, 166 (1): 42-48.Google Scholar
- Morrison JA, Friedman LA, Wang P, Glueck CJ: Metabolic syndrome in childhood predicts adult metabolic syndrome and type 2 diabetes mellitus 25 to 30 years later. J Pediatr. 2008, 152: 201-206. 10.1016/j.jpeds.2007.09.010.View ArticlePubMedGoogle Scholar
- Morrison JA, Friedman LA, Gray-McGuire C: Metabolic syndrome in childhood predicts adult cardiovascular disease 25 years later: the Princeton Lipid Research Clinics Follow-up Study. Pediatrics. 2007, 120: 340-345. 10.1542/peds.2006-1699.View ArticlePubMedGoogle Scholar
- Dabelea D, Bell RA, D'Agostino RB, Imperatore G, Johansen JM, Linder B, Liu LL, Loots B, Marcovina S, Mayer-Davis EJ, Pettitt DJ, Waitzfelder B: Incidence of diabetes in youth in the United States. JAMA. 2007, 297: 2716-2724.View ArticlePubMedGoogle Scholar
- Magnussen CG, Raitakari OT, Thomson R, Juonala M, Patel DA, Viikari JS, Marniemi J, Srinivasan SR, Berenson GS, Dwyer T, Venn A: Utility of currently recommended pediatric dyslipidemia classifications in predicting dyslipidemia in adulthood: evidence from the Childhood Determinants of Adult Health (CDAH) study, Cardiovascular Risk in Young Finns Study, and Bogalusa Heart Study. Circulation. 2008, 117: 32-42. 10.1161/CIRCULATIONAHA.107.718981.View ArticlePubMedGoogle Scholar
- Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH: Prevalence of a metabolic syndrome phenotype in adolescents: findings from the third National Health and Nutrition Examination Survey, 1988–1994. Arch Pediatr Adolesc Med. 2003, 157: 821-827. 10.1001/archpedi.157.8.821.View ArticlePubMedGoogle Scholar
- Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC, Spertus JA, Costa F: Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute scientific statement. Curr Opin Cardiol. 2006, 21: 1-6. 10.1097/01.hco.0000200416.65370.a0.View ArticlePubMedGoogle Scholar
- Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM: Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA. 2007, 298: 309-316. 10.1001/jama.298.3.309.View ArticlePubMedGoogle Scholar
- McBride PE: Triglycerides and risk for coronary heart disease. JAMA. 2007, 298: 336-338. 10.1001/jama.298.3.336.View ArticlePubMedGoogle Scholar
- Nordestgaard BG, Benn M, Schnohr P, Tybjaerg-Hansen A: Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA. 2007, 298: 299-308. 10.1001/jama.298.3.299.View ArticlePubMedGoogle Scholar
- Sarwar N, Danesh J, Eiriksdottir G, Sigurdsson G, Wareham N, Bingham S, Boekholdt SM, Khaw KT, Gudnason V: Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation. 2007, 115: 450-458. 10.1161/CIRCULATIONAHA.106.637793.View ArticlePubMedGoogle Scholar
- Austin MA, McKnight B, Edwards KL, Bradley CM, McNeely MJ, Psaty BM, Brunzell JD, Motulsky AG: Cardiovascular disease mortality in familial forms of hypertriglyceridemia: a 20-year prospective study. Circulation. 2000, 101: 2777-2782. 10.1161/01.CIR.101.24.2777.View ArticlePubMedGoogle Scholar
- Kannel WB, Vasan RS: Triglycerides as vascular risk factors: new epidemiologic insights. Curr Opin Cardiol. 2009, 24: 345-350. 10.1097/HCO.0b013e32832c1284.PubMed CentralView ArticlePubMedGoogle Scholar
- Onat A, Sari I, Yazici M, Can G, Hergenc G, Avci GS: Plasma triglycerides, an independent predictor of cardiovascular disease in men: a prospective study based on a population with prevalent metabolic syndrome. Int J Cardiol. 2006, 108: 89-95. 10.1016/j.ijcard.2005.06.056.View ArticlePubMedGoogle Scholar
- Varbo A, Nordestgaard BG, Tybjaerg-Hansen A, Schnohr P, Jensen GB, Benn M: Nonfasting triglycerides, cholesterol, and ischemic stroke in the general population. Ann Neurol. 2011, 69: 628-634. 10.1002/ana.22384.View ArticlePubMedGoogle Scholar
- Mahoney LT, Burns TL, Stanford W, Thompson BH, Witt JD, Rost CA, Lauer RM: Coronary risk factors measured in childhood and young adult life are associated with coronary artery calcification in young adults: the Muscatine Study. J Am Coll Cardiol. 1996, 27: 277-284.View ArticlePubMedGoogle Scholar
- Berenson GS, Wattigney WA, Tracy RE, Newman WP, Srinivasan SR, Webber LS, Dalferes ER, Strong JP: Atherosclerosis of the aorta and coronary arteries and cardiovascular risk factors in persons aged 6 to 30 years and studied at necropsy (The Bogalusa Heart Study). Am J Cardiol. 1992, 70: 851-858. 10.1016/0002-9149(92)90726-F.View ArticlePubMedGoogle Scholar
- Newman WP, Freedman DS, Voors AW, Gard PD, Srinivasan SR, Cresanta JL, Williamson GD, Webber LS, Berenson GS: Relation of serum lipoprotein levels and systolic blood pressure to early atherosclerosis. The Bogalusa Heart Study. N Engl J Med. 1986, 314: 138-144. 10.1056/NEJM198601163140302.View ArticlePubMedGoogle Scholar
- Relationship of atherosclerosis in young men to serum lipoprotein cholesterol concentrations and smoking. A preliminary report from the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) Research Group. JAMA. 1990, 264: 3018-3024.
- Chen W, Srinivasan SR, Li S, Xu J, Berenson GS: Metabolic syndrome variables at low levels in childhood are beneficially associated with adulthood cardiovascular risk: the Bogalusa Heart Study. Diabetes Care. 2005, 28: 126-131. 10.2337/diacare.28.1.126.View ArticlePubMedGoogle Scholar
- Nguyen QM, Srinivasan SR, Xu JH, Chen W, Berenson GS: Fasting plasma glucose levels within the normoglycemic range in childhood as a predictor of prediabetes and type 2 diabetes in adulthood: the Bogalusa Heart Study. Arch Pediatr Adolesc Med. 2010, 164: 124-128. 10.1001/archpediatrics.2009.268.View ArticlePubMedGoogle Scholar
- Thearle MS, Bunt JC, Knowler WC, Krakoff J: Childhood predictors of adult acute insulin response and insulin action. Diabetes Care. 2009, 32: 938-943. 10.2337/dc08-1833.PubMed CentralView ArticlePubMedGoogle Scholar
- Nicklas TA, von Duvillard SP, Berenson GS: Tracking of serum lipids and lipoproteins from childhood to dyslipidemia in adults: the Bogalusa Heart Study. Int J Sports Med. 2002, 23 (Suppl 1): S39-S43.View ArticlePubMedGoogle Scholar
- Eisenmann JC, Welk GJ, Wickel EE, Blair SN: Stability of variables associated with the metabolic syndrome from adolescence to adulthood: the Aerobics Center Longitudinal Study. Am J Hum Biol. 2004, 16: 690-696. 10.1002/ajhb.20079.View ArticlePubMedGoogle Scholar
- Webber LS, Srinivasan SR, Wattigney WA, Berenson GS: Tracking of serum lipids and lipoproteins from childhood to adulthood. The Bogalusa Heart Study. Am J Epidemiol. 1991, 133: 884-899.PubMedGoogle Scholar
- Nadeau KJ, Maahs DM, Daniels SR, Eckel RH: Childhood obesity and cardiovascular disease: links and prevention strategies. Nat Rev Cardiol. 2011, 8: 513-525. 10.1038/nrcardio.2011.86.PubMed CentralView ArticlePubMedGoogle Scholar
- Manlhiot C, Larsson P, Gurofsky RC, Smith RW, Fillingham C, Clarizia NA, Chahal N, Clarke JT, McCrindle BW: Spectrum and management of hypertriglyceridemia among children in clinical practice. Pediatrics. 2009, 123: 458-465. 10.1542/peds.2008-0367.View ArticlePubMedGoogle Scholar
- McCrindle BW, Urbina EM, Dennison BA, Jacobson MS, Steinberger J, Rocchini AP, Hayman LL, Daniels SR: Drug therapy of high-risk lipid abnormalities in children and adolescents: a scientific statement from the American Heart Association Atherosclerosis, Hypertension, and Obesity in Youth Committee, Council of Cardiovascular Disease in the Young, with the Council on Cardiovascular Nursing. Circulation. 2007, 115: 1948-1967. 10.1161/CIRCULATIONAHA.107.181946.View ArticlePubMedGoogle Scholar
- Schwandt P, Haas GM, Liepold E: Lifestyle and cardiovascular risk factors in 2001 child–parent pairs: the PEP Family Heart Study. Atherosclerosis. 2010, 213: 642-648. 10.1016/j.atherosclerosis.2010.09.032.View ArticlePubMedGoogle Scholar
- Dennison BA, Kikuchi DA, Srinivasan SR, Webber LS, Berenson GS: Parental history of cardiovascular disease as an indication for screening for lipoprotein abnormalities in children. J Pediatr. 1989, 115: 186-194. 10.1016/S0022-3476(89)80063-0.View ArticlePubMedGoogle Scholar
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.