Effects of household sharing on high density lipoprotein and its subfractions

Sj, Hasstedt; Kuida, Hiroshi; Ko, Ash; Williams, Robert R.

doi:10.1002/gepi.1370020403

Cited by 14 publications

(3 citation statements)

References 40 publications

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“…A young, healthy population will have less environmental variance due to age and lack of disease processes than an older and ill sample; thus, the relative contribution of genetic variance will be larger, resulting in larger heritability estimates. Previous heritability estimates have been higher for HDL 2 than for HDL 3 (32,33). However, a previous study reported highest parent‐offspring correlations for HDL 2b but highest sibling correlations for HDL 3b (34), which agrees well with our result of quite high heritability estimates for both large and small HDL.…”

Section: Discussionmentioning

confidence: 93%

HDL Subspecies in Young Adult Twins: Heritability and Impact of Overweight

Pietiläinen

Söderlund

Rissanen

et al. 2009

Obesity

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The association between abdominal obesity and atherogenic lipid profile emerges from complex interactions of genes and environment. We aimed to explore the heritability and effects of overweight on serum lipid profile (high‐density lipoprotein‐cholesterol (HDL‐C), HDL mean particle size, percentages of HDL2b, 2a, 3a, 3b, and 3c, low‐density lipoprotein‐cholesterol (LDL‐C), LDL peak particle size and triglycerides (TGs)) in healthy, young adults. HDL‐C, LDL‐C, and TG were measured in 52 monozygotic (MZ) and 89 dizygotic (DZ) twin pairs, aged 23–32 years, chosen to represent a wide range of BMIs (17.6–42.9 kg/m2). Of them, 24 MZ and 26 DZ pairs were chosen at random for measurements of HDL mean and LDL peak particle sizes and percentages of HDL subspecies. The heritabilities of the lipid parameters adjusted for BMI were HDL‐C 73%, HDL mean particle size 56%, HDL subspecies 46–63%, LDL‐C 79%, LDL peak particle size 49%, and TG 64%. Genetic and environmental correlations between BMI and HDL‐C, LDL‐C, and TG were modest (0.3–0.4). Abdominal overweight (waist circumference ≥94 cm for males and ≥80 cm for females) associated with decreased HDL‐C, increased LDL‐C, and TG concentrations, smaller HDL mean particle size, lower HDL2b, and higher HDL3c percentages in both genders. Within MZ twins, controlling for genetic influences, within‐pair differences in HDL3c percentage were associated with those in waist (r = 0.46, P = 0.032) and BMI (r = 0.51, P = 0.013). In conclusion, serum lipid parameters, including LDL peak and HDL mean particle sizes and HDL subspecies distribution are under strong genetic control. Overweight associated with significant lipid profile changes, particularly, small HDL3c increased in overweight independent of genetic influences.

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Section: Discussionmentioning

confidence: 93%

HDL Subspecies in Young Adult Twins: Heritability and Impact of Overweight

Pietiläinen

Söderlund

Rissanen

et al. 2009

Obesity

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“…The indices used to measure shared familial environment in these studies, information on smoking and alcohol habits, body mass, and socioeconomic levels, are acknowledged to be crude and inadequate; measures of between-family differences in diet, physical activity patterns, or stress exposure, relevant to individual variation in lipoproteins, have not been attempted, but direct evidence of the influence of shared household experience on HDL-C has been found in the higher correlations of siblings and parent—offspring pairs when the siblings (and offspring) are younger than 20 years of age than when they are older and no longer sharing household experience (Morrison et al, 1982). Household effects shared by juvenile siblings accounted for nearly 20% of the variance in HDL-C in a sample of over 2,000 Utah family members (Hasstedt, Kuida, Ash, & Williams, 1985). Such estimates of environmental effects on HDL-C are in contrast to the negligible estimate (2.9%) yielded by typical MZ—DZ twin data, although the twin estimates were based on a path analytic model similar to those used in the family studies (Coletto, Krieger, & Magalhaes, 1981).…”

Section: Discussionmentioning

confidence: 99%

Shared genes, shared experiences, and similarity of personality: Data from 14,288 adult Finnish co-twins.

Rose¹,

Koskenvuo²,

Kaprio³

et al. 1988

Journal of Personality and Social Psychology

121

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Similarities for Extraversion (E) and Neuroticism (N) scale scores from the Eysenck Personality Inventory were evaluated in 7,144 adult twin pairs, drawn from the population-based Finnish Twin Cohort, as a function of the co-twins' genetic resemblance, gender, age, and the frequency of their social interaction with each other. To separate effects of shared genes from those of shared experience, we performed hierarchical multiple regressions of double-entry data matrices. Results establish the predictive significance of both genetic and experiential influences: Genetic effects remained significant when tested after the effects of social contact were first removed; conversely, for N scores, the effects of social contact remained significant when assessed after genetic influences were first removed. These findings establish genetic variance in major dimensions of adult personality but assign a significant role to common experience as well. The first finding constructively replicates reports by others; the second challenges the widespread assumption that shared experiences have a negligible impact on sibling similarity in adult personality.

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“…GWA studies and Mendelian randomization studies have suggested that genetic mechanisms that raise plasma HDL-C do not seem to lower risk of MI [38]. However, based on family and twin studies, HDL-C levels have shown a heritability ranging from 40 to 60 % [39,40]. Recent GWA studies have shown that only 10-12 % of the heritability is due to common variants [41,42], suggesting that a large proportion of the molecular mechanisms underlying HDL-C functions and metabolism is still unknown.…”

Section: Hdl Metabolism Pathwaymentioning

confidence: 99%

Experimental Biology for the Identification of Causal Pathways in Atherosclerosis

Guo

Garcia-Barrio

Wang

et al. 2016

Cardiovasc Drugs Ther

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More than 60 genomic loci have been implicated by genome-wide association studies (GWAS) and exome-wide association studies as conferring an increased risk of myocardial infarction and coronary artery disease (CAD). However, the causal gene and variant is often unclear. Using the functional analysis of genetic variants in experimental animal models, we anticipate understanding which candidate gene at a specific locus is associated with atherosclerosis and revealing the underlying molecular and cellular mechanisms, ultimately leading to the identification of causal pathways in atherosclerosis and may provide novel therapeutic targets for the treatment of atherosclerotic cardiovascular disease.

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Effects of household sharing on high density lipoprotein and its subfractions

Cited by 14 publications

References 40 publications

HDL Subspecies in Young Adult Twins: Heritability and Impact of Overweight

HDL Subspecies in Young Adult Twins: Heritability and Impact of Overweight

Shared genes, shared experiences, and similarity of personality: Data from 14,288 adult Finnish co-twins.

Experimental Biology for the Identification of Causal Pathways in Atherosclerosis

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