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Left ventricular (LV) hypertrophy in adults is a recognized risk factor for the subsequent development of cardiovascular morbidity. To make informed preventive health decisions it is important to understand the interaction of genes and environment on LV mass. In both children and adults, weight is a strong correlate of LV mass. We hypothesized that genetic influences common to both of these variables could in part explain the strong relation between weight and LV mass in children. In a population of 341 twins (11 years old), these questions were asked: (1) How much of the total variance of LV mass is under genetic control? (2) After accounting for weight and weight adjusted for sexual maturity, how much of the remaining variance is genetic? (3) Of the total genetic variance, what proportion is specific for LV mass and what proportion is common to both weight and LV mass? (4) How much of the correlation between these 2 variables is explained by genes common to both LV mass and weight? Univariate genetic analyses documented that genes operating at different magnitudes in boys (63%) and girls (71%) explain a significant proportion of the variance of LV mass. After removing the effect of weight and sexual maturity by regression methods, genes remain an important influence. Bivariate genetic analyses confirmed that genes common to LV mass and weight significantly influence the covariation of these variables and that >90% of the correlation of LV mass and weight is due to common genes. (Am J Cardiol 1991;68:661-668), Left ventricular hypertrophy (enlargement) is generally caused by hypertension, and is a good indication that coronary artery disease will develop. Left ventricular (LV) size increases as body weight increases among adults. In order to make effective recommendations about methods for reducing LV mass, it is necessary to understand the mechanisms regulating it. Because of the association between weight and LV mass, it is likely that genetic factors influence both, but the effects of genetics and the environment are difficult to isolate. A total of 341 pubertal (11-year-old) twins were studied to assess the factors affecting LV mass. The children whose blood pressure was in the upper quintile for their sex and age had greater LV mass. Children in the middle and lower quintiles had normal LV mass. In an earlier study of black twins, the differences in LV mass were greater between dizygotic (fraternal) twins than between monozygotic (identical) twins, and it was concluded that both genetic and environmental factors determined LV mass in black children. In this study univariate genetic analyses demonstrated that genetic influences were responsible for 63 percent of the variance in LV mass in boys and 71 percent in girls. After weight and sexual maturity were removed, genetic factors remained significant. Over 90 percent of the strength of the relation between LV mass and weight was explained by genetic influences. (Consumer Summary produced by Reliance Medical Information, Inc.)

Some studies have shown that genetics plays a role in blood pressure and that high-normal infant blood pressure may be the forerunner of adult hypertension. The effects of genetics and environment on blood pressure and heart rate were studied in 251 11-year-old twin pairs. In both sexes, genetic influence could be observed to affect systolic blood pressure, the pressure exerted against the walls of the blood vessels during a heart contraction. Although the amounts of variation of sex-specific genetic effects were the same between the sexes with respect to systolic blood pressure, diastolic pressure (the pressure in between contractions) had a variance of 64 percent among the boys, compared with 51 percent in girls. There were no differences between the sexes with respect to heart rates. There is no firm evidence that a difference in blood pressures exists between boys and girls. No shared environmental effects were noted. (Consumer Summary produced by Reliance Medical Information, Inc.)

Pharmacokinetic variability in drug exposure is a concern for all compounds in development including those for the treatment of asthma and other respiratory disorders. Substantial variability in the oral clearance of GSK2190915, a 5-lipoxygenase-activating protein inhibitor that attenuates the production of leukotriene B4 and cysteinyl leukotrienes, is largely unaccounted for by clinical variables. A study of 41 patients, 78 (3241) of whom were non-Hispanic whites, with mild to moderate asthma identified an association of UGT1A128 and UGT1A32 with the oral clearance of GSK2190915 (P=3.8×10–4and 1.2×10–5, respectively). However, in a subsequent replication study of 403 non-Hispanic white patients with asthma, we failed to observe a statistically significant association between oral clearance of GSK2190915 and either UGT1A128 or UGT1A32 (P>0.05). Therefore, genetic effects that could explain the systemic exposure level variability of GSK2190915 were not identified.

An 18 month prospective study of personality traits (as assessed by Cattell's Children's Personality Questionnaire and Sixteen Personality Factor Questionnaire) was conducted on twin pairs and their parents. The primary personality trait scores for both the adults and children had relatively low stability over the 18 month interval; in addition, in some cases, the inter-factor stability coefficients exceeded the intra-factor coefficients. This finding, coupled with the lack of parent/offspring similarity for the primary personality traits, places in question the predictive power of Cattell's personality questionnaires. A factor analysis on the original items indicated that 5 oblique factors for the children and 6 oblique factors for the adults need be retained. These factors were not only more stable than the primary trait scores, but they also did not have such high inter-factor stability coefficients. Except for Neuroticism and IQ, the adult and juvenile factors do not show structural similarities.

Aortic stiffness, the maximal frequency shift in the descending aorta divided by the Doppler acceleration time, was studied in 384 eleven year old twin children. The extent to which this measurement provided a prediction of systolic blood pressure that was independent of body size, heart rate, cardiac contractility and left ventricular mass was investigated. Aortic stiffness, after adjustment for height and weight, correlated significantly with systolic blood pressure (r = 0.22, p < 0.01), but not with diastolic blood pressure. The short- (r = 0.82) and longer- (r = 0.68) term reproducibility of aortic stiffness was high.