Evidence map›Paper›PMID 9199573›Full record

ArticleAmerican journal of human genetics1997

Heritability of longitudinal changes in coronary-heart-disease risk factors in women twins.

Y Friedlander, M A Austin, B Newman, K Edwards, E I Mayer-Davis, M C King

Abstract readComparative StudyTwin Study
In one paragraph

Article in American journal of human genetics, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed.

  1. A genome-wide association study of monozygotic twin-pairs suggests a locus related to variability of serum high-density lipoprotein cholesterol.Twin research and human genetics : the official journal of the International Society for Twin Studies · 2012
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  3. NIA Long Life Family Study: Objectives, Design, and Heritability of Cross-Sectional and Longitudinal Phenotypes.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Y FriedlanderDepartment of Social Medicine, School of Public Health, Hadassah-University Hospital, Jerusalem, Israel. yfried@vms.huji.ac.il
M A Austin
B Newman
K Edwards
E I Mayer-Davis
M C King

Funding

GENETIC EPIDEMIOLOGY OF CHD RISK FACTORS IN WOMEN TWINSR01HL041830 · NHLBI · KAISER FOUNDATION HOSPITALS · PI SELBY, JOE V · 1989 to 1991
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NHLBI NIH HHS HL-41830
6 · The paper itself

Abstract

Numerous studies have demonstrated genetic influences on levels of coronary heart disease (CHD) risk factors, but there also may be genetic effects on the intraindividual variation in these risk factors over time. Changes in risk factors are likely to reflect genetic-environmental interactions and may have important implications for understanding CHD risk. The present study examines the heritability of changes in CHD risk factors, using data from the two examinations by the Kaiser Permanente Women Twins Study, performed a decade apart. The sample consisted of 348 pairs of women twins who participated in both examinations, including 203 MZ pairs and 145 DZ pairs. Average ages at the two examinations were 41 and 51 years, respectively. By means of three different statistical analytic approaches, moderate heritability estimates were demonstrated for changes in LDL cholesterol (h2 = .25-.36) and in HDL cholesterol (h2 = .23-.58), some of which were statistically significant. Although small to moderate heritability estimates were found for systolic blood pressure (.18-.37; P < .05 for some estimates), no genetic influence on changes in diastolic blood pressure was detected. Based on longitudinal twin data in women, this study demonstrates a genetic influence on changes in both lipoprotein risk factors and systolic blood pressure over a decade. In addition to environmental factors, which clearly are operating, the effect of various "variability genes" may be acting independently of the genetic influences on the absolute levels of these risk factors. Both mapping the gene(s) underlying intraindividual variations in these CHD risk factors and understanding their function(s) could lead to targeted intervention strategies to reduce CHD risk among genetically susceptible individuals.

Indexed as

AdultAnalysis of VarianceBlood PressureCholesterolCholesterol, HDLCholesterol, LDLCoronary DiseaseDiseases in TwinsFemaleHumansLongitudinal StudiesRisk FactorsTime FactorsTriglyceridesTwins, DizygoticTwins, MonozygoticCholesterolCholesterol, HDLCholesterol, LDLTriglycerides

Identifiers

PMID9199573
PMCPMC1716110

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.