Mothers' sense of coherence and oral health related quality of life of preschool children in Udupi Taluk.

OBJECTIVE: To assess the relationship between mothers' Sense of Coherence (SOC) and oral health related quality of life (OHRQoL) of 3-5 year old preschool children in Udupi Taluk. PARTICIPANTS: 388 mothers aged 24-48 years old and their preschool children. BASIC RESEARCH DESIGN: A cross sectional study of mother-child pairs, randomly selected from 8 preschools. METHOD: Information was obtained about mothers' sociodemographic factors along with the short version (SOC 13) of Antonovsky's sense of coherence scale and children's OHRQoL using the early childhood oral health impact scale (ECOHIS). Chi-square tests and multivariate logistic regression were used for analysis. MAIN OUTCOME MEASURES: Mothers' SOC and children's OHRQoL. RESULTS: Mothers' SOC and fathers' education were significantly associated with children's OHRQoL in multivariate analysis. Children of mothers with high SOC were 12.9 times as likely to have high OHRQoL as mothers with low SOC (p < 0.01). Children of fathers with college/university education were twice as likely to have high OHRQoL as those with primary education (p < 0.05). CONCLUSION: Our results suggest that mother's SOC could be a psychosocial determinant of the OHRQoL of their preschool children. Family environment should be considered when designing interventions to promote or improve the oral health as well as OHRQoL of preschool children.

The association of c-reactive protein with arterial compliance in asymptomatic young adults: the Bogalusa heart study.

Atherogeneis is a chronic progressive syndrome caused by endothelial dysfunction, vascular inflammation, vessel wall remodeling and eventual vascular flow compromise. Emerging data suggest that arterial compliance inversely correlates with atherogenesis and cardiovascular (CV) events. However, information is scant on the association of chronic systemic inflammation with arterial elasticity in young asymptomatic adults. The association of hsC-reactive protein (CRP) and central-vascular compliance was studied in 641 individuals (45.2% males; 71.8% whites), aged 31-43 years enrolled in the Bogalusa Heart Study. The measured variables included large-artery compliance (capacitive, C1), representative of the aorta and its major branches; and small-artery compliance (oscillatory, C2), representative of the distal part of the circulation; hsCRP, as a measure of systemic inflammation; along with traditional CV risk factor variables. Significant race and sex differences were noted for C1 (white males>black males P-value <0.0001; males>females P-value 0.04), C2 (whites>blacks P-value 0.0004; males>females P-value<0.0001) and hsCRP (blacks>whites P-value 0.03; females>males P-value 0.002). Mean values of C1 in subjects with high hsCRP levels (>3 mg l(-1)) were significantly lower than those with average (1-3 mg l(-1)) and low levels (<1 mg l(-1)) (14.2 ml per mmHg × 10 versus 15.2 ml per mm Hg × 10 versus 15.7 ml per mmHg × 10, P for trend=0.02), after adjusting for age, race, sex and body surface area (BSA). hsCRP showed a trend toward inverse correlation with C1 (-0.07, P=0.07) but no such trend for C2, after adjusting for race and sex. In the multivariate linear regression model, adding age, race, sex, BSA, mean arterial pressure, insulin resistance, lipoprotein variables and smoking status, the effect persisted between C1 and hsCRP (ß=-0.35, P=0.01). In an asymptomatic population of young adults, hsCRP predicts reduced large-artery compliance (C1). These findings support the role of systemic inflammation in early pathological changes in artery wall in atherogenesis. Small-artery compliance (C2) however did not correlate with hsCRP.

The association of variants in the FTO gene with longitudinal body mass index profiles in non-Hispanic white children and adolescents.

OBJECTIVE: To investigate possible age-related changes in associations between polymorphisms in the fat mass and obesity-associated (FTO) gene and higher body mass index (BMI). DESIGN AND SUBJECTS: Multilevel mixed regression models were used to examine associations between four FTO variants and longitudinal BMI profiles in non-Hispanic white and African American children and adolescents 8-17 years of age from two different longitudinal cohort studies, the Bogalusa Heart Study (BHS) and Project HeartBeat! (PHB). In the BHS, there were 1551 examinations of 478 African Americans and 3210 examinations of 1081 non-Hispanic whites; in PHB, there were 971 examinations of 131 African Americans and 4458 examinations of 505 non-Hispanic whites. RESULTS: In African Americans, no significant FTO associations with BMI were found. In non-Hispanic whites, linkage disequilibrium among all four variants made haplotype analysis superfluous, so we focused on the single-nucleotide polymorphism, rs9939609. In longitudinal multilevel models, the A/A genotype of rs9939609 was associated with higher BMI in non-Hispanic whites in both cohorts at all ages. A significant age-by-genotype interaction found only in the BHS cohort predicted that in those with the A/A genotype, BMI would be ∼0.7 kg m(-2) higher at age 8 and ∼1.6 kg m(-2) higher at age 17 than in those with A/T or T/T genotypes. The design of PHB limited follow-up of any single individual to 4 years, and may have reduced the ability to detect any age-by-genotype interaction in this cohort. CONCLUSIONS: The A/A genotype of rs9939609 in the FTO gene is associated with higher longitudinal BMI profiles in non-Hispanic whites from two different cohorts. The association may change with age, with the A/A genotype being associated with a larger BMI difference in late adolescence than in childhood, though this was observed only in the BHS cohort and requires verification.

Longitudinal versus cross-sectional evaluations of leukocyte telomere length dynamics: age-dependent telomere shortening is the rule.

BACKGROUND: Leukocyte telomere length (LTL) is considered a biomarker of human aging and based on cross-sectional studies it shortens with age. However, longitudinal studies reported that many adults display LTL lengthening. METHODS: Using Southern blots, we compared cross-sectional rates of age-related LTL change across a ∼20 year age range with those based on longitudinal evaluations in three surveys (S1, S2, and S3) with three time intervals: S1-S2 (5.8 years), S2-S3 (6.6 years), and S1-S3 (12.4 years). Hierarchical linear modeling was used to explore LTL dynamics using LTL data from S1, S2, and S3. RESULTS: Cross-sectionally, mean LTL shortenings were 24.6, 25.4, and 23.6 bp/y at S1, S2, and S3, respectively. Longitudinally, more variation was observed in the rate of LTL change during the shorter than longer follow-up periods. Furthermore, using simple differences in LTL, 14.4% and 10.7% of individuals displayed LTL lengthening during S1-S2 and S2-S3, respectively, but only 1.5% during S1-S3 (p < 0.001). The estimated mean rate of LTL shortening based on averaging empirical Bayes' estimates of LTL from a parsimonious hierarchical linear modeling model was 31 bp/y with a range from 23 to 47 bp/y with none of the participants showing LTL lengthening over the average 12.4 years of follow-up. CONCLUSIONS: As aging displays a unidirectional progression, it is unlikely that LTL elongates with age. LTL elongation in longitudinal studies primarily reflects measurement errors of LTL in relation to the duration of follow-up periods.

The contribution of childhood obesity to adult carotid intima-media thickness: the Bogalusa Heart Study.

OBJECTIVE: Although obese children are at increased risk for coronary heart disease in later life, it is not clear if the association results from the persistence of childhood obesity into adulthood. We examined the relation of both childhood and adult levels of body mass index (BMI, kg m(-2)) to carotid intima-media thickness (IMT) measured at the (mean) age of 36 years. DESIGN AND SUBJECTS: Prior to the determination of adult IMT, the 1142 participants had been examined 7 (mean) times in the Bogalusa Heart Study. MEASUREMENTS: In addition to BMI, levels of lipids, lipoproteins and blood pressure were measured at each examination. Cumulative levels of each risk factor were based on the areas under the individual growth curves calculated using multilevel models for repeated (BMI) measurements. We then examined the relation of these cumulative levels to adult IMT. RESULTS: Carotid IMT was associated with cumulative levels of BMI in both childhood and adulthood (P<0.001 for each association). Furthermore, the association between childhood BMI and adult IMT persisted, but was reduced, after controlling for adult BMI. Although childhood levels of lipids, lipoproteins and blood pressure were also associated with adult IMT, these associations were not independent of adult levels of these risk factors. CONCLUSIONS: These results emphasize the adverse effects of elevated childhood BMI levels. In addition to the strong tracking of BMI levels from childhood to adulthood, there appears to be a modest, independent effect of childhood BMI on adult IMT. The prevention of childhood obesity should be emphasized.

Influence of lipoprotein lipase gene Ser447Stop and beta1-adrenergic receptor gene Arg389Gly polymorphisms and their interaction on obesity from childhood to adulthood: the Bogalusa Heart Study.

OBJECTIVE: To investigate the influence of lipoprotein lipase (LPL) Ser447Stop and beta1-adrenergic receptor (ADRB1) Arg389Gly gene polymorphisms, individually and in combination, on obesity from childhood to adulthood. DESIGN AND SUBJECTS: A community-based cohort of 1331 subjects (30% black and 70% white subjects) was followed over an average period of 23 years from childhood (age range: 4-17 years) to adulthood (age range:18-44 years). MEASUREMENT: Body mass index (BMI, kg/m2) and LPL Ser447Stop and the ADRB1 Arg389Gly genotypes. RESULTS: The frequency of the ADRB1 Gly389 allele was 0.25 in white subjects vs 0.39 in black subjects (P < 0.001); 0.08 vs 0.05 (P = 0.280) for the LPL Stop447 allele. There was no association between the LPL Stop447 allele and BMI among white and black subjects either in childhood and adulthood levels or annual change from childhood to adulthood. The ADRB1 Gly389 allele was associated with lower BMI only in black adults (P = 0.017). Further, the interaction effect of the LPL Stop447 allele and ADRB1 Gly389 allele on adult BMI or its annual change was significant in white subjects and in the total sample (P = 0.03-0.006). Childhood values tended to show a similar trend. Having both ADRB1 Gly389 allele and LPL Stop447 allele was associated with 71% (95% confidence interval: 26-89%) less odds for developing obesity from childhood to adulthood after adjusting for age, race, sex, and childhood BMI. CONCLUSION: While Gly389 allele of the ADRB1 gene lowers obesity in black subjects, this allele in conjunction with Stop447 allele of the LPL gene lowers obesity in adults and attenuates the development of obesity from childhood to adulthood. These findings underscore the importance of gene-gene interaction in the assessment of genetic influences on complex traits such as obesity.

Correlates of carotid artery stiffness in young adults: The Bogalusa Heart Study.

Decreased arterial elasticity, an independent risk factor for cardiovascular (C-V) disease, is associated with C-V risk factors in middle-aged and older individuals. However, information is limited in this regard in young adults. This aspect was examined in a community-based sample of 516 black and white subjects aged 25-38 years (71% white, 39% male). The common carotid artery elasticity was measured from M-mode ultrasonography as Peterson's elastic modulus (Ep) and relative wall thickness-adjusted Young's elastic modulus (YEM). Blacks and males had higher Ep (P < 0.05); males had higher YEM (P < 0.0001); and blacks had higher wall thickness (P < 0.01). For the entire sample adjusted for race and gender both Ep and YEM correlated significantly (P < 0.05-0.0001) with age, BMI, waist, systolic and diastolic blood pressures, heart rate, product of heart rate and pulse pressure, triglycerides, total cholesterol to HDL cholesterol ratio, insulin and glucose. In a multivariate regression model that included hemodynamic variables, systolic blood pressure, product of heart rate and pulse pressure, age, triglycerides, BMI, and male gender (for YEM only) were independent correlates of Ep (R2 = 0.38) and YEM (R2 = 0.25). When the hemodynamic variables were excluded from the model, age, triglycerides, BMI, black race (Ep only), male gender, parental history of hypertension, HDL cholesterol (inverse association), and insulin (marginal significance) remained independent correlates of Ep (R2 = 0.20) and YEM (R2 = 16). Both Ep and YEM increased (P for trend P < 0.0001) with increasing number of independent continuous risk factors (defined as values above or below the age, race, and gender-specific extreme quintiles) that were retained in the regression models. The observed increasing arterial stiffness (or decreased elasticity) with increasing number of risk factors related to insulin resistance syndrome in free-living, asymptomatic young adults has important implications for prevention.

An autosomal genome scan for loci influencing longitudinal burden of body mass index from childhood to young adulthood in white sibships: The Bogalusa Heart Study.

OBJECTIVE: To examine genetic loci linked to a long-term burden and trend of obesity traits, such as body mass index (BMI), from childhood to adulthood. DESIGN: : Longitudinal study using serial measurements of BMI from childhood. SUBJECTS: A total of 782 unselected white siblings (representing 521 full and 39 half sib-pairs) from 342 families enrolled in the Bogalusa Heart Study. MEASUREMENTS: A total of 357 microsatellite markers with an average spacing of 9.0 cM spanning the 22 autosomal chromosomes were typed. A quadratic growth curve was developed using a random effects model based on serial measurements of BMI from childhood to adulthood. The serial changes in BMI were measured in terms of long-term burden (area under the curve (AUC) divided by follow-up years) and the long-term trend (incremental AUC, calculated as total AUC-baseline AUC). RESULTS: Heritability estimates of long-term measures were 0.78 for total AUC and 0.43 for incremental AUC. In a variance-component-based multipoint linkage analysis with SOLAR, linkage to the long-term measures of BMI was observed on chromosomes 1, 5, 7, 12, 13 and 18. For total AUC, LOD scores were 3.0 at 110 cM on chromosome 12, 2.9 at 26 cM and 2.4 at 52 cM on chromosome 7, and 2.2 at 126 cM on chromosome 5. For incremental AUC, LOD scores were 2.9 at 26 cM, 2.1 at 97 cM and 2.3 at 110 cM on chromosome 12, 2.2 at 69 cM on chromosome 7, 2.2 at 91 cM and 2.5 at 150 cM on chromosome 1, 2.0 at 119 cM on chromosome 5, 2.0 at 54 cM on chromosome 13 and 2.0 at 7 cM on chromosome 18. Several important obesity-related candidate genes are located in the regions or near the markers showing positive linkage. CONCLUSION: Linkage evidence found in this study indicates that regions on these chromosomes might harbor genetic loci that affect the propensity to develop obesity from childhood.

Inter-relationships among childhood BMI, childhood height, and adult obesity: the Bogalusa Heart Study.

OBJECTIVE: Although the body mass index (BMI, mass index, kg/m2) is widely used as a surrogate measure of adiposity, it is moderately associated (r approximately 0.3) with height among children. We examined whether the resulting preferential classification of taller children as overweight is appropriate. DESIGN: Cross-sectional analyses of children (ages, 3-17 y) examined the relation of height to adiposity (as assessed by BMI and skinfold thicknesses) and fasting levels of insulin. Longitudinal analyses examined the relation of childhood height and weight-height indices to adult (mean age, 25 y) levels of adiposity and fasting insulin. SUBJECTS: Children (n=11,406) and adults (n=2911) who had participated in the Bogalusa Heart Study. MEASUREMENTS: We constructed three weight-height indices: BMI, W/H3, and W/Hp. The triceps and subscapular skinfolds, as well as fasting levels of insulin, were also measured. RESULTS: The classification of children as overweight (BMI-for-age > or =95th percentile) varied markedly by height, with a 10-fold difference in the prevalence of overweight across quintiles of height between the ages of 3 and 10 y. Childhood height, however, was also related to skinfold thicknesses and insulin levels, and all associations were modified in a similar manner by age. Furthermore, childhood height was related to adult adiposity, and of the three childhood weight-height indices, BMI showed the strongest associations with adult adiposity. CONCLUSIONS: Because BMI reflects the positive association between height and adiposity among children, it is a better weight-height index than is either W/H3 or W/Hp.

Longitudinal changes in risk variables underlying metabolic Syndrome X from childhood to young adulthood in female subjects with a history of early menarche: the Bogalusa Heart Study.

OBJECTIVES: To examine the longitudinal changes in adiposity and related risk variables of Syndrome X from childhood to young adulthood with respect to early onset of menarche. DESIGN: Community-based longitudinal cohort of female subject (65% white, 35% blacks subjects) who participated in two or more surveys from childhood to young adulthood and had reported their menarcheal age (<12 y, n=437 vs > or =12 y, n=1042). RESULTS: In childhood (5-11 y), adolescence (12-18 y), and young adulthood (19-37 y), females with early menarche displayed significantly higher body mass index (BMI) and triceps skinfold thickness; higher stature in childhood and adolescence; higher fasting insulin and homeostasis model assessment index of insulin resistance (HOMA-IR) in childhood and adulthood; and higher fasting glucose in adulthood. Blood pressure and lipoprotein variables showed no early menarche-related differences. Longitudinal rates of change in BMI (P=0.002), triceps skinfold thickness (P=0.05), insulin (P=0.09), and HOMA-IR (P=0.05) were positive and faster among female subjects with early menarche; fasting glucose decreased slowly in this group (P=0.006). In a multivariate analysis, body fatness and insulin related independently to early menarche (P<0.001). This association was stronger in white subjects (P=0.0008). In adulthood, the prevalence of clustering of three to four risk factors of syndrome X (highest quartile of: (1) BMI, (2) fasting insulin, (3) systolic or mean arterial pressure, and (4) total cholesterol to HDL cholesterol or triglycerides to HDL cholesterol ratio specific for age, race, and study year) was higher among those with early menarche (10.7 vs 6.2%, P=0.002). The odds for developing such clustering in adulthood among those with early menarche was 1.54 (95% CI=1.14-2.07), regardless of race. CONCLUSION: Early menarche is characterized by excess body fatness and insulin beginning in early childhood and higher prevalence of clustering of adverse levels of risk variables of metabolic Syndrome X in young adulthood.

Differences in body shape representations among young adults from a biracial (Black-White), semirural community: the Bogalusa Heart Study.

In this study, the authors examined body image perception and body mass index (weight (kg)/height (m)(2)) among race-gender groups in a biracial (Black-White) population of young adults in Bogalusa, Louisiana. A mail-out survey was completed in 1994 by 3,698 (65%) participants aged 18.5-35 years in the Bogalusa Heart Study (mean age = 27.6 years). As part of the survey, body image perception was determined in terms of body shape representations from a figure rating scale. A body image discrepancy score was calculated from the difference between z-standardized values of body image perception and body mass index. A stepwise proportional odds model including the covariates income, employment, education, and physical activity was used to identify factors influencing lower perception of body shape. Mean body mass index was highest among Black females (p < 0.001). The odds of having a lower perception of body shape (vs. body mass index) were 1.72 times higher in Blacks (p < 0.001), 0.80 times lower in persons who were currently employed (p < 0.001), and 0.86 times lower in persons with a higher education (p = 0.032). Gender, income, and physical activity were not found to be significant predictors of body image perception (p > 0.05). The authors conclude that significant differences exist within racial groups concerning body image perception in relation to overweight status among young adults. This has implications for prevention and education programs.

Influence of the beta2-adrenergic receptor Arg16Gly polymorphism on longitudinal changes in obesity from childhood through young adulthood in a biracial cohort: the Bogalusa Heart Study.

BACKGROUND: The beta2-adrenergic receptor (ADRB2) plays a major role in regulating energy expenditure by stimulating lipid metabolism in human adipose tissue. Polymorphisms in the ADRB2 gene have been associated with obesity and various weight-related traits in cross-sectional studies of adults, but little is known about the effects of the ADRB2 gene on childhood obesity or the propensity to gain weight over time. OBJECTIVE: To assess the effects of a polymorphism in codon 16 (Arg16-->Gly) of the ADRB2 gene, which has been associated with a decrease in beta2-receptor density and efficiency, on longitudinal changes in obesity from childhood to young adulthood in a biracial cohort. DESIGN: Seven cross-sectional screenings of children and five cross-sectional screenings of young adults who were previously examined as children produced longitudinal data from childhood to young adulthood. METHODS: Height, weight and subscapular and triceps skinfolds were measured by trained examiners following identical protocols over the course of the study. Gender- and age-stratified analyses using random coefficients models were used to examine longitudinal genetic effects on obesity in 1151 African-American and Caucasian males and females who attended an average of six examinations over a 24 y period from childhood to young adulthood. RESULTS: Age-stratified analyses showed no clear genetic relationships with changes in obesity measures over time in females, but an age-dependent association was observed in males, where the relationship between the Arg16Gly polymorphism and obesity became stronger with age. In males who were 4-9 y of age at the beginning of the study in 1973, body mass index (BMI) was 4% higher in Gly/Gly and Arg/Gly males compared to those with Arg/Arg by 26 y of age. Subscapular skinfold measurements in Gly/Gly males became significantly different from Arg/Arg males (20% higher) by age 20. In the oldest male cohort (10-14 y of age in 1973), BMI increased at a significantly greater rate (0.4%/y) in males carrying the Gly16 form of the receptor relative to Arg/Arg males. BMI was significantly different between homozygous genotypes by approximately 26 y of age, and reached 8% higher in Gly/Gly males by age 32. Subscapular skinfolds also increased at a significantly greater rate (2%/y) in Gly/Gly males compared to Arg/Arg males, becoming significantly different (27%) by approximately 22 y of age and reaching a maximum difference of 50% by age 32. CONCLUSIONS: Our data suggest that the beta2-adrenergic receptor is associated with the propensity to gain weight from childhood to young adulthood in males. An increased understanding of genetic influences on the development of obesity may improve the effectiveness of interventions designed to reduce excess body weight and help define the role of genetic factors in diabetes and cardiovascular disease.

Influence of lipoprotein lipase serine 447 stop polymorphism on tracking of triglycerides and HDL cholesterol from childhood to adulthood and familial risk of coronary artery disease: the Bogalusa heart study.

The effects of the lipoprotein lipase (LPL) Serine 447 Stop (S447X) polymorphism on high-density lipoprotein cholesterol (HDLC) and triglycerides (TG) have been demonstrated. However, little is known about its effect on the tracking of HDLC and TG over time and familial risk of coronary artery disease (CAD). This aspect was examined in black and white individuals (n=829) aged 5-18 year at baseline, followed on average 18.8 yr. The frequency of the X447 allele was lower in Blacks than Whites (0.043 vs. 0.087, P=0.002). Carriers vs. noncarriers of the X447 allele had lower TG (99.3 vs 122.1 mg/dl, P<0.01) and higher HDLC (51.1 vs. 49.7 mg/dl, P<0.05) in adulthood, but not in childhood. The trends in genotype-specific means of childhood and adulthood levels of HDLC and TG in sex or race subgroups were similar to those in the total sample. With respect to tracking over time, of those in the bottom quartile of HDLC in childhood, 46.1% of the noncarriers vs. 23.1% of the carriers remained in this lowest quartile into adulthood (P=0.03); corresponding values for the top quartile of HDLC were 37.5% for the noncarriers vs. 57.1% for the carriers (P=0.03). Although TG tended to track better among the carriers in the bottom quartile and among the noncarriers in the top quartile, this trend was not significant. Carriers showed lower prevalence of parental history of CAD than noncarriers (6.9% vs. 14.1%, P=0.02) independently of lipoprotein variables, adiposity, blood pressure, age, sex and race. Thus, the X447 allele of the LPL gene is associated with an increase in HDLC and a decrease in TG in adults, tracking of HDLC since childhood, and a lower family history of CAD.

Distribution and correlates of lipoproteins and their subclasses in black and white young adults. The Bogalusa Heart Study.

Lipoprotein subclasses vary in CAD risk potential, but their distribution and correlates are not well documented in black and white young adults. A subsample of 449 (32%) young adults (67% white, 58% female) aged 20-37 years examined in the Bogalusa Heart Study had lipoprotein subclasses measured in terms of cholesterol by vertical spin density-gradient ultracentrifugation. LDL subclass pattern was characterized as either predominantly LDL(1) (large, buoyant), LDL(2) (intermediate) or LDL(3) (small, dense). Whites had significantly higher levels of VLDL, VLDL(3), and LDL and lower levels of HDL(2) and HDL(3) than blacks. White females had significantly higher levels of HDL(2) than white males. Visceral fatness, measured as waist circumference, and race were the major contributors to the explained variance (6-22%) of these lipoproteins, with adverse trends seen among whites and persons with large waist circumferences. Sex (males>females), waist circumference (positive), HDL(2) (negative), and HDL(3) (positive) were the predictor variables for the likelihood of having the LDL(3) pattern. When glucose and insulin were included in the multivariate analysis, insulin (positive), sex (males>females), HDL(2) (negative) and HDL(3) (positive) became significant predictors of LDL(3) pattern. Positive parental history of CAD was associated with LDL (P=0.009) in white males, and HDL(2) (P=0.008) and LDL(3) subclass pattern (P=0.038) in white females; whereas none in blacks. The observed correlates of lipoprotein subclasses and patterns need to be considered in estimating CAD risk in young adults.

Trends of lipoprotein variables from childhood to adulthood in offspring of parents with coronary heart disease: the Bogalusa Heart Study.

Although dyslipidemia among offspring of parents with coronary heart disease (CHD) has been known, the development of this adverse relationship with respect to specific lipoprotein variables from childhood to young adulthood has not been elucidated. This aspect was examined in a young adult cohort with (n = 271) and without (n = 805) a parental history of CHD followed longitudinally since childhood by repeated surveys from 1973 to 1991. Trends in fasting lipoprotein variables by parental CHD status were assessed by Lowess smoothing curve and Generalized Estimating Equations (GEE). In multivariate analyses adjusted for race and sex, parental CHD associated positively with low-density lipoprotein cholesterol (LDL-C, P <.01) and triglycerides (P <.05) mainly at the young adulthood age, whereas a positive association was noted with very-low-density lipoprotein cholesterol (VLDL-C) during both childhood and young adulthood (P <.05). The positive association between parental CHD and LDL-C in young adulthood persisted independently of body mass index (BMI) and fasting insulin, but disappeared when fasting glucose was added to the model. With respect to triglycerides and VLDL-C, inclusion of BMI, insulin, and/or glucose eliminated the adverse association with parental CHD. These observations suggest that parental CHD is just one more explanatory variable that loses its partial contribution to lipoprotein profiles in their offspring when other strongly interrelated contributory variables such as age, body fatness, and measures of glucose homeostasis are taken into account. Information on these risk variables in conjunction with parental or family history of CHD may enhance the potential of CHD risk assessment in youth.

The magnitude of familial associations of cardiovascular risk factor variables between parents and offspring are influenced by age: the Bogalusa Heart Study.

PURPOSE: Although parent-offspring associations of cardiovascular risk factor variables are known, the age-specific nature of this familial relationship is not clear. METHODS: This aspect was examined in 727 unrelated children (mean age: 11.2 years) and their parents who participated in the Bogalusa Heart Study during their childhood (mean age: 11.3 years) and adulthood (mean age: 25.5 years). RESULTS: After adjusting for covariates, the mothers' childhood-offspring correlations were consistently higher than mothers' adulthood-offspring correlations for body mass index (BMI) [r = 0.45 vs. 0.32], systolic blood pressure (SBP) [r = 0.30 vs. 0.10], diastolic blood pressure (DPB) [r = 0.22 vs. 0.13] and low-density lipoprotein cholesterol (LDLC) [r = 0.20 vs. 0.11]. In contrast, high-density lipoprotein cholesterol (HDLC) and triglycerides did not show such age-specific trends in mother-offspring correlations. Corresponding father-offspring correlations showed similar patterns, but the differences were of lesser magnitude. Multiple regression analyses using offspring's risk factor variables as dependent variables revealed that parents' childhood obesity, blood pressure and LDLC levels were better predictors of the corresponding variables in the young offspring than parents' adulthood values. Further, sex of either parents or offspring made no difference in the above findings. CONCLUSIONS: The magnitude of the familial associations of cardiovascular risk factor variables between parents and offspring are influenced by age. Intrinsic genetic make-up, duration of exposure to environment and gene-environment interactions may play a role in this association.

Combined effects of endothelial nitric oxide synthase gene polymorphism (G894T) and insulin resistance status on blood pressure and familial risk of hypertension in young adults: the Bogalusa Heart Study.

Impaired endothelial function with decreased nitric oxide production is shared by insulin resistance and essential hypertension. Although there are limited data on the association between the endothelial nitric oxide synthase (eNOS) G894T polymorphism and hypertension, information is absent on the combined effects of eNOS G894T genotype and insulin resistance status on blood pressure (BP) levels and the familial risk of hypertension. This aspect was examined in a community-based sample of 1021 unrelated African American and white young adults aged 19 to 38 years. African Americans displayed a lower frequency of the T894 allele than whites (0.105 v 0.324, P < .001). After adjusting for sex, age, and body mass index (BMI), noncarriers versus carriers of the T894 allele had significantly higher systolic (SBP), diastolic (DBP) BP and mean arterial pressure (MAP) levels (111.7 v 109.2 mm Hg for SBP; 73.6 v 72.3 mm Hg for DBP; 86.3 v 84.6 mm Hg for MAP), with both African Americans and whites showing similar trends. This association was modulated by insulin resistance status, measured by the homeostasis model assessment of insulin resistance (HOMA IR) using fasting insulin and glucose. Subjects with high insulin resistance (above the median HOMA IR) showed significantly greater differences in BP levels between noncarriers and carriers of the T894 allele. Furthermore, the G894T genotype and insulin resistance also showed a combined effect on the prevalence of parental hypertension, a measure of familial risk, with noncarriers versus carriers in the high insulin resistance group showing higher prevalence (70.5% v 51.3%, P = .006, adjusted for race). Thus, the allelic variation (G894T) in the eNOS gene locus in conjunction with insulin resistance may be one factor contributing to the predisposition to hypertension.

Relationship of childhood obesity to coronary heart disease risk factors in adulthood: the Bogalusa Heart Study.

BACKGROUND: Childhood obesity is related to adult levels of lipids, lipoproteins, blood pressure, and insulin and to morbidity from coronary heart disease (CHD). However, the importance of the age at which obesity develops in these associations remains uncertain. OBJECTIVE AND DESIGN: We assessed the longitudinal relationship of childhood body mass index (BMI, kg/m(2)) to adult levels of lipids, insulin, and blood pressure among 2617 participants. All participants were initially examined at ages 2 to 17 years and were reexamined at ages 18 to 37 years; the mean follow-up was 17 years. RESULTS: Of the overweight children (BMI >/=95th percentile), 77% remained obese (>/=30 kg/m(2)) as adults. Childhood overweight was related to adverse risk factor levels among adults, but associations were weak (r ~ 0.1-0.3) and were attributable to the strong persistence of weight status between childhood and adulthood. Although obese adults had adverse levels of lipids, insulin, and blood pressure, levels of these risk factors did not vary with childhood weight status or with the age (/=18 years) of obesity onset. CONCLUSIONS: Additional data are needed to assess the independent relationship of childhood weight status to CHD morbidity. Because normal-weight children who become obese adults have adverse risk factor levels and probably will be at increased risk for adult morbidity, our results emphasize the need for both primary and secondary prevention.

The Ser(447)-Stop polymorphism of lipoprotein lipase is associated with variation in longitudinal serum high-density lipoprotein-cholesterol profiles: the Bogalusa Heart Study.

The Ser(447)-Stop polymorphism of lipoprotein lipase (LPL) has been associated with altered high-density lipoprotein-cholesterol (HDL-C) and triglyceride (TG) levels at individual measurements, but nothing is known of its associations with lipid profiles derived from serial measurements. We used multilevel statistical models to study effects of this polymorphism on longitudinal lipid profiles in 1,006 Bogalusa Heart Study subjects examined 4 to 9 times between the ages of 4 and 38 years. Stop(447) allele frequencies in African Americans (0.053 +/- 0.011) and whites (0.091 +/- 0.009) differed significantly (chi(2) = 7.595, 1 df, P =.006; Stop(447) homozygotes and heterozygotes combined). Overall, TG levels were lower and HDL-C levels higher in blacks than in whites of the same age and sex. Longitudinal TG profiles were lower in Stop(447) carriers at all ages. However, longitudinal HDL-C profiles differed among genotype groups with age: the Stop(447) allele was associated with higher HDL-C only in subjects above approximately 10 years of age. Genotype-specific HDL-C profiles also differed significantly among race/sex groups. Thus, we found evidence of LPL genotype effects that vary within individuals with age. Possible mechanisms, which could account for age-related changes in the effects of LPL variants, are discussed.