Context. - Although the association between parental coronary artery disease (CAD) and its risk factors in the offspring is known, the timing and the course of development of risk factors from childhood to adulthood in the offspring is not known.
- To examine the association between parental CAD and longitudinal changes in risk factor profile from childhood to young adulthood in offspring.
- Cohort study.
- Bogalusa, La, a semirural, biracial community.
- Individuals with clinically verified parental history of CAD (n=271) vs those without such a history (n=1253) Mean age at first CAD event was 50 years for fathers and 52 years for mothers.
- Body mass index, subscapular skinfolds, blood pressure, and triglyceride, cholesterol (total, very low-density lipoprotein [VLDL-C], low-density lipoprotein [LDL-C], and high-density lipoprotein [HDL-C] cholesterols), glucose, and insulin levels.
- The offspring of parents with CAD were consistently overweight beginning in childhood.
Their levels of total serum cholesterol, LDL-C, plasma glucose, and insulin became significantly higher at older ages, because of a higher rate of increase in these risk factors over time.
In adulthood, the offspring with a positive parental history had a higher prevalence of obesity (body mass index>85th percentile in the National Health and Nutrition Examination Survey 1,35% vs 26%, P=01), elevated total cholesterol (>6. (...)
Mots-clés Pascal : Cardiopathie coronaire, Déterminisme génétique, Transmission, Descendance, Evolution, Facteur risque, Obésité, Décalage, Age apparition, Etude comparative, Homme, Etat nutritionnel, Appareil circulatoire pathologie, Génétique, Trouble nutrition
Mots-clés Pascal anglais : Coronary heart disease, Genetic determinism, Transmission, Progeny, Evolution, Risk factor, Obesity, Shift, Age of onset, Comparative study, Human, Nutritional status, Cardiovascular disease, Genetics, Nutrition disorder
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 98-0042810
Code Inist : 002B30A01A2. Création : 17/04/1998.