ABSTRACT
To describe the time course of the early development genetic variance for blood pressure, a cohort of twins is being followed from birth to 1 year of age. The present interim report describes systolic and diastolic blood pressure measurements for 102 twin pairs (39 monozygotic (MZ) and 63 dizygotic (DZ) in the newborn period and at 1, 3 and 6 months of age. Mean values for both systolic and diastolic blood pressure were similar regardless of race, sex, zygosity, or chorionicity. Statistically significant genetic variance was detected for systolic blood pressure at 6 months of age but not for diastolic blood pressure at any data point. The data are consistent with the hypothesis that genetic factors that determine within-family similarities of blood pressure may be detected early in life, and support the need for further investigation of both genetic and environmental determinants of blood pressure in young populations.
Subject(s)
Blood Pressure , Genetics , Twins , Diastole , Environment , Ethnicity , Female , Humans , Infant , Infant, Newborn , Male , Pregnancy , Systole , Twins, Dizygotic , Twins, MonozygoticSubject(s)
Cholesterol/blood , Myocardial Infarction/genetics , Adult , Child , Environment , Female , Humans , Male , Middle Aged , Myocardial Infarction/blood , RiskABSTRACT
Plasma cholesterol levels were obtained on 90 children of 39 men with premature myocardial infarction and 86 children of 39 healthy men. The mean cholesterol among children of affected men (195.1 mg/100 ml) was higher than among children of healthy men (176.6 mg/100 ml) (P equal to .009). Higher mean levels were demonstrable at each of nine age groups from 1 to 21 years(P equal to .004). Levels greater than 230 mg/100 ml were found in 16.7% of children of affected fathers and 4.7% of children of healthy fathers, a ratio of 3.6 to 1 (P equal to .01). These findings are compatible with the hypothesis that elevated childhood cholesterol level offers a mechanism whereby family history predicts coronary disease. A dip in cholesterol during adolescence, a finding that varies with population studied, was demonstratable among children of both affected healthy men.
Subject(s)
Cholesterol/blood , Family , Myocardial Infarction/genetics , Adolescent , Adult , Child , Child, Preschool , Female , Humans , Hypercholesterolemia/diagnosis , Infant , Male , Sex FactorsABSTRACT
Sibling aggregation of blood pressure has been shown in children 2 to 14 years of age. To determine the earliest age at which this finding is detectable, blood pressures were evaluated in 98 siblings from 43 black families with newborns. Variances of blood pressure scores were significantly greater among families than within families for systolic (p less than .025) but not diastolic pressures. Sib-sib intraclass correlation coefficients were .26 (95% two-sided confidence limits .05 to .47) for systolic and .16 (-.06 to .38) for diastolic pressures. When 1-month-old infant pressures were added, significant aggregation was present for systolic (p less than .01) and diastolic (p less than .025) pressures. The intraclass correlation coefficients were .21 (.02 to .38) and .17 (.03 to .34), respectively. When newborn scores were substituted, aggregation was not demonstrable. These data demonstrate a familial influence on blood pressure in infancy by 1 month of age.
Subject(s)
Blood Pressure , Family , Infant, Newborn , Adolescent , Child , Child, Preschool , Female , Humans , Hypertension/genetics , Infant , MaleSubject(s)
Blood Pressure , Family , Child , Child, Preschool , Female , Genotype , Humans , Infant , Infant, Newborn , Pregnancy , Social Environment , TwinsABSTRACT
Risk factors for coronary artery disease were present to a greater degree in children of men who had experienced premature myocardial infarction when compared to children of unaffected male parents. Levels of cholesterol and body weight, as well as family history of premature CAD, differed significantly between the groups of children. The chance of identifying a child with hyperlipidemia was three times greater if the father had premature CAD. Data regarding familial aggregation of risk factors for CAD are reviewed and their significance discussed.
