Familial and Individual Influences on Blood Pressure

1986 ◽  
Vol 35 (1-2) ◽  
pp. 7-21 ◽  
Author(s):  
J. Sims ◽  
J.K. Hewitt ◽  
K.A. Kelly ◽  
D. Carroll ◽  
J.R. Turner

AbstractAlthough familial aggregation of blood pressure is well documented, few studies have considered the changing contribution of genetic and environmental influences during adulthood. Applying maximum likelihood model fitting to blood pressure covariation in balanced pedigrees including both parents and their young adult twin offsprings (25 MZ, 32 DZ, aged between 16 and 24 years), it is shown that the increased variation in parents is explained by such developmental changes. For DBP, an apparent reduction in heritability from 68% to 38% from young adulthood to middle age results from the increasing impact of individual environmental experience (E1), with little or no influence from shared family environmental (E2). For SBP, shared environmental effects may play a part. Given the relatively small size of the present sample, the conclusions are to be seen as tentative. An augmented family study, incorporating middle aged twins and their young adult offspring, will clarify the causation of these developmental changes.

1987 ◽  
Vol 36 (4) ◽  
pp. 467-473 ◽  
Author(s):  
J. Sims ◽  
D. Carroll ◽  
J.K. Hewitt ◽  
J.R. Turner

AbstractIn an earlier study of blood pressure variation in middle aged parents and their young adult twin offspring, the greater blood pressure variation observed in the parent sample was accounted for in terms of an increasing influence of individual environmental experiences with increasing age and a commensurate reduction in the impact of heredity. In the present study, the sample size was enlarged to provide a more powerful test of these effects. Maximum likelihood model-fitting techniques were applied to blood pressure covariation in balanced pedigrees, consisting of 85 families (40 MZ and 45 DZ twin pairs). As before, our analysis indicated that a developmental effect was a salient factor in the older age group.


2000 ◽  
Vol 14 (7) ◽  
pp. 441-445 ◽  
Author(s):  
RM Fuentes ◽  
I-L Notkola ◽  
S Shemeikka ◽  
J Tuomilehto ◽  
A Nissinen

2018 ◽  
Vol 21 (5) ◽  
pp. 378-383 ◽  
Author(s):  
Yoon-Mi Hur ◽  
Eun-ji Choi ◽  
Jong-Woo Kim ◽  
Hee-Jeong Jin ◽  
Siwoo Lee

The present study aimed to estimate heritability of Hwabyung (HB) symptoms in adolescent and young adult twins in South Korea. The sample included 1,601 twins consisting of 143 pairs of monozygotic male (MZM), 67 pairs of dizygotic male (DZM), 295 pairs of monozygotic female (MZF), 114 pairs of dizygotic female (DZF), and 117 pairs of opposite-sex dizygotic (OSDZ) twins and 129 twins with non-participating co-twins (mean age = 19.1 ± 3.1 years; range: 12–29 years). An HB symptom questionnaire was given to twins via a telephone interview. Consistent with the literature of HB, the mean level of HB was significantly higher in females than in males. Maximum likelihood twin correlations for HB were 0.31 (95% CI [0.16, 0.45]) for MZM, 0.19 (95% CI [-0.05, 0.41]) for DZM, 0.50 (95% CI [0.41, 0.58]) for MZF, 0.28 (95% CI [0.11, 0.44]) for DZF, and 0.23 (95% CI [0.05, 0.40]) for OSDZ twins. These patterns of twin correlations suggested the presence of additive genetic influences on HB. Model-fitting analysis showed that additive genetic and individual-specific environmental influences on HB were 44% (95% CI [37, 51]) and 56% (95% CI [49, 63]), respectively. Shared environmental influences were not significant. These parameter estimates were not significantly different between two sexes, and did not change significantly with age in the present sample, suggesting that genetic and environmental influences on HB in both sexes are stable across adolescence and young adulthood.


Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Amber L Fyfe-Johnson ◽  
Julia Steinberger ◽  
Alan R Sinaiko ◽  
Alvaro Alonso ◽  
Donald R Dengel ◽  
...  

Introduction: Cardiovascular (CV) risk factors measured in childhood and adulthood are positively associated with increased carotid intima-media thickness (cIMT) later in life. In particular, body mass index (BMI), systolic blood pressure (SBP), and lipids are implicated. However, questions remain regarding prediction of cIMT from adolescent and young adult CV risk factors. Hypothesis: CV risk factors are positively associated with young adult and early middle age cIMT thickening, both cross-sectionally and longitudinally. Methods: CV risk factors (BMI, SBP, metabolic syndrome [MetS, mean of CV risk factor z-scores]) were measured in two pediatric cohort studies. The Insulin Study measured CV risk factors in 305 adolescents at mean ages 15 and 22 years, with cIMT measured at mean age 22 years. The Prevention of High Blood Pressure in Children Study measured CV risk factors in 444 individuals at mean ages 24 and 38 years, with cIMT measured at mean age 38 years. Predictors were categorized into quartiles; cIMT was measured by ultrasonography. Linear regression models were used to predict cIMT and adjust for potential confounding variables. Differences between risk factor quartile 4 and quartile 1 (Q4-Q1) were used in analyses, with a p -test for trend based on continuous predictors. Results: Positive cross sectional associations were found between CV risk factors at ages 24 and 38 and cIMT at 38 (Table). Positive longitudinal associations were found between BMI (Q4-Q1: 0.024 mm, p=0.0001) and MetS score (Q4-Q1: 0.019 mm, p=0.004) at age 15 and cIMT at age 22, and between BMI (Q4-Q1: 0.045 mm, p=0.01) and MetS score (Q4-Q1: 0.048 mm, p<0.0001) at age 24 and cIMT at age 38 (Table). SBP at ages 24 and 38 was predictive of cIMT at age 38. Conclusions: These findings suggest that CV risk factors beginning in adolescence predict cIMT thickening in young adulthood, and this predictive association continues into middle age. This supports early identification of CV risk, and initiation of preventive strategies to reduce early CV disease.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
D Kim ◽  
H Jung ◽  
P.S Yang ◽  
H.T Yu ◽  
T.H Kim ◽  
...  

Abstract Aims Pulse pressure (PP) is a well-known risk factor for cardiovascular disease. However, the association between the PP and dementia is not well identified. This study aimed to determine the effect of PP on the risk of dementia development in different age subgroups using a longitudinal, population-based, and stroke-free cohort from the general population. Methods The association of PP with the development of incident dementia was assessed from January 1, 2005, to December 31, 2013, in 433,154 participants without a history of dementia or stroke from the Korea National Health Insurance Service-Health Screening cohort. The diagnosis of dementia was defined using the 10th revision of the International Classification of Disease codes. Results The mean age of the cohort was 55.7±9.2 years, 45.7% were women. Hypertension was 23.6%. The mean systolic and diastolic blood pressure of the entire cohort were 125.9±16.6 and 78.4±10.7 mmHg, respectively. Mean PP was 47.5±10.9 mmHg. In the middle-age group (40 to 50 year-old), increasing of 10 mmHg of PP was associated with incident dementia after adjusting mean blood pressure and clinical variables with a hazard ratio (HR) of 1.21 (95% confidence interval [CI]: 1.19–1.23, p&lt;0.001). The association was still significant even after censoring for stroke (HR: 1.16, 95% CI: 1.08–1.22, p&lt;0.001). In the older population, elevation of PP was not associated with dementia development (HR: 0.98, 95% CI: 0.95–1.01, p=0.247) Conclusion PP was associated with increased risk of dementia only in middle-aged population beyond that of mean arterial pressure. Funding Acknowledgement Type of funding source: None


2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Jia Y. Wan ◽  
Deborah L. Goodman ◽  
Emileigh L. Willems ◽  
Alexis R. Freedland ◽  
Trina M. Norden-Krichmar ◽  
...  

Abstract Background To identify genetic associations of quantitative metabolic syndrome (MetS) traits and characterize heterogeneity across ethnic groups. Methods Data was collected from GENetics of Noninsulin dependent Diabetes Mellitus (GENNID), a multiethnic resource of Type 2 diabetic families and included 1520 subjects in 259 African-American, European-American, Japanese-Americans, and Mexican-American families. We focused on eight MetS traits: weight, waist circumference, systolic and diastolic blood pressure, high-density lipoprotein, triglycerides, fasting glucose, and insulin. Using genotyped and imputed data from Illumina’s Multiethnic array, we conducted genome-wide association analyses with linear mixed models for all ethnicities, except for the smaller Japanese-American group, where we used additive genetic models with gene-dropping. Results Findings included ethnic-specific genetic associations and heterogeneity across ethnicities. Most significant associations were outside our candidate linkage regions and were coincident within a gene or intergenic region, with two exceptions in European-American families: (a) within previously identified linkage region on chromosome 2, two significant GLI2-TFCP2L1 associations with weight, and (b) one chromosome 11 variant near CADM1-LINC00900 with pleiotropic blood pressure effects. Conclusions This multiethnic family study found genetic heterogeneity and coincident associations (with one case of pleiotropy), highlighting the importance of including diverse populations in genetic research and illustrating the complex genetic architecture underlying MetS.


Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3568
Author(s):  
Bernardita Cayupe ◽  
Carlos Morgan ◽  
Gustavo Puentes ◽  
Luis Valladares ◽  
Héctor Burgos ◽  
...  

Prenatally malnourished rats develop hypertension in adulthood, in part through increased α1-adrenoceptor-mediated outflow from the paraventricular nucleus (PVN) to the sympathetic system. We studied whether both α1-adrenoceptor-mediated noradrenergic excitatory pathways from the locus coeruleus (LC) to the PVN and their reciprocal excitatory CRFergic connections contribute to prenatal undernutrition-induced hypertension. For that purpose, we microinjected either α1-adrenoceptor or CRH receptor agonists and/or antagonists in the PVN or the LC, respectively. We also determined the α1-adrenoceptor density in whole hypothalamus and the expression levels of α1A-adrenoceptor mRNA in the PVN. The results showed that: (i) agonists microinjection increased systolic blood pressure and heart rate in normotensive eutrophic rats, but not in prenatally malnourished subjects; (ii) antagonists microinjection reduced hypertension and tachycardia in undernourished rats, but not in eutrophic controls; (iii) in undernourished animals, antagonist administration to one nuclei allowed the agonists recover full efficacy in the complementary nucleus, inducing hypertension and tachycardia; (iv) early undernutrition did not modify the number of α1-adrenoceptor binding sites in hypothalamus, but reduced the number of cells expressing α1A-adrenoceptor mRNA in the PVN. These results support the hypothesis that systolic pressure and heart rate are increased by tonic reciprocal paraventricular–coerulear excitatory interactions in prenatally undernourished young-adult rats.


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