title: Impact of dietary intervention, sex, and apolipoprotein E phenotype on tracking of serum lipids and apolipoproteins in 1- to 5-year-old children: the Special Turku Coronary Risk Factor Intervention Project (STRIP).
abstract: The effects of dietary intervention, sex, and apolipoprotein E phenotype on tracking of serum lipid values in young children have remained poorly characterized. We investigated these associations in 1062 infants who were randomized into control and intervention groups (n=522 and n=540, respectively) at age 7 months; the intervention group received counseling aimed at maintaining a low-saturated fat, low-cholesterol diet. In 519 children in the control (n=254) and intervention (n=265) groups, serum lipid values were studied annually between 13 months and 5 years of age. In all children, tracking was strongest for the ratio of high density lipoprotein (HDL) cholesterol to total cholesterol; when a 13-month-old child belonged to the lowest quartile of the distribution, the odds ratio for belonging to the same quartile at older ages was 39.0 (95% CI 23.1 to 66.0). Dietary intervention did not influence the tracking of serum lipids. Tracking of HDL cholesterol was stronger in the boys than in the girls (P=0.018). Tracking of non-HDL cholesterol and apolipoprotein B in the children with phenotypes E2/3 or E3/3 was stronger than that in the other children (P=0.031 and P=0.014, respectively). In conclusion, the apolipoprotein E phenotype strongly influences tracking of non-HDL cholesterol and apolipoprotein B values in early childhood, whereas dietary intervention had no effect on tracking of any of the lipids. A child's sex influenced tracking only of HDL cholesterol, with boys showing stronger tracking.
authors.affiliation: Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Turku, Finland. leena.rask-nissila@utu.fi
authors.forename: Leena
authors.initials: L
authors.lastname: Rask-Nissilä
authors.forename: Eero
authors.initials: E
authors.lastname: Jokinen
authors.forename: Jorma
authors.initials: J
authors.lastname: Viikari
authors.forename: Anne
authors.initials: A
authors.lastname: Tammi
authors.forename: Tapani
authors.initials: T
authors.lastname: Rönnemaa
authors.forename: Jukka
authors.initials: J
authors.lastname: Marniemi
authors.forename: Pia
authors.initials: P
authors.lastname: Salo
authors.forename: Taina
authors.initials: T
authors.lastname: Routi
authors.forename: Hans
authors.initials: H
authors.lastname: Helenius
authors.forename: Ilkka
authors.initials: I
authors.lastname: Välimäki
authors.forename: Olli
authors.initials: O
authors.lastname: Simell
mesh_terms: D001053:Apolipoproteins / Q000097:blood*; D001057:Apolipoproteins E / Q000235:genetics*; D002675:Child, Preschool; D003327:Coronary Disease / Q000097:blood / Q000209:etiology / Q000517:prevention & control*; D018752:Diet, Fat-Restricted; D005260:Female; D006801:Humans; D007223:Infant; D007700:Kinetics; D008055:Lipids / Q000097:blood*; D008297:Male; D016017:Odds Ratio; D010641:Phenotype; D011110:Polymorphism, Genetic; D012307:Risk Factors; D012737:Sex Factors
chemical_list: D001053:Apolipoproteins; D001057:Apolipoproteins E; D008055:Lipids