Quantitative Genetic Analysis of Lipid Research Clinic Family Data
NCT ID: NCT00005188
Last Updated: 2016-05-13
Study Results
Results pending
The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.
Basic Information
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Recruitment Status
COMPLETED
Study Classification
OBSERVATIONAL
Study Start Date
1986-07-31
Study Completion Date
1991-06-30
Brief Summary
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To assess the mode of inheritance of familial combined hyperlipidemia and familial primary hypoalphalipoproteinemia and to resolve genetic and familial environmental effects on several phenotypes of importance to coronary heart disease.
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Detailed Description
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BACKGROUND:
Although coronary heart disease has long been known to aggregate in families, in 1986 little was known about the relative importance of genetic and environmental factors. This was partly due to the heterogeneous nature of the disease. Instead of analyzing complex endpoints, the tendency had been to focus on the individual risk factors or phenotypes. Plasma lipids and lipoproteins are heterogeneous risk factors that have been analyzed as subgroups from a genetic epidemiological perspective. Attention turned to the familial aggregation of risk factors, particularly the hyperlipidemias, hypertension, and diabetes.
In 1971, the National Heart and Lung Institute began a series of epidemiologic studies at several North American sites under the Lipid Research Clinics Program. The Family Study was designed to investigate the familial association of blood lipids, lipoproteins, and dyslipoproteinemias. This study complemented and did not duplicate ongoing analysis of Lipid Research Clinics data.
DESIGN NARRATIVE:
The study addressed seven phenotypes, all derived from fasting blood samples: total cholesterol, total triglyceride, LDL-cholesterol, HDL-cholesterol, VLDL-cholesterol, uric acid, and glucose levels. The data had already been collected at Lipid Research Clinics in Cincinnati, Iowa, Oklahoma, Minneapolis, and Stanford. Univariate and bivariate segregation analysis were conducted on the mode of inheritance of familial combined hyperlipidemia and familial primary hypoalphalipoproteinemia. Path analysis was used to resolve cultural and biological inheritance for each phenotype within each clinic and for resolution of population heterogeneity among the five Lipid Research Clinics. A general bivariate path model was used to analyze the associations among the various phenotypes. General models were used to analyze temporal trends in family resemblance for the seven phenotypes.
The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.
Although coronary heart disease has long been known to aggregate in families, in 1986 little was known about the relative importance of genetic and environmental factors. This was partly due to the heterogeneous nature of the disease. Instead of analyzing complex endpoints, the tendency had been to focus on the individual risk factors or phenotypes. Plasma lipids and lipoproteins are heterogeneous risk factors that have been analyzed as subgroups from a genetic epidemiological perspective. Attention turned to the familial aggregation of risk factors, particularly the hyperlipidemias, hypertension, and diabetes.
In 1971, the National Heart and Lung Institute began a series of epidemiologic studies at several North American sites under the Lipid Research Clinics Program. The Family Study was designed to investigate the familial association of blood lipids, lipoproteins, and dyslipoproteinemias. This study complemented and did not duplicate ongoing analysis of Lipid Research Clinics data.
DESIGN NARRATIVE:
The study addressed seven phenotypes, all derived from fasting blood samples: total cholesterol, total triglyceride, LDL-cholesterol, HDL-cholesterol, VLDL-cholesterol, uric acid, and glucose levels. The data had already been collected at Lipid Research Clinics in Cincinnati, Iowa, Oklahoma, Minneapolis, and Stanford. Univariate and bivariate segregation analysis were conducted on the mode of inheritance of familial combined hyperlipidemia and familial primary hypoalphalipoproteinemia. Path analysis was used to resolve cultural and biological inheritance for each phenotype within each clinic and for resolution of population heterogeneity among the five Lipid Research Clinics. A general bivariate path model was used to analyze the associations among the various phenotypes. General models were used to analyze temporal trends in family resemblance for the seven phenotypes.
The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.
Conditions
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Cardiovascular Diseases
Heart Diseases
Coronary Disease
Tangier Disease
Atherosclerosis
Eligibility Criteria
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Inclusion Criteria
No eligibility criteria
Maximum Eligible Age
100 Years
Eligible Sex
MALE
Accepts Healthy Volunteers
No
Sponsors
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National Heart, Lung, and Blood Institute (NHLBI)
NIH
Sponsor Role
lead
References
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Rao DC, Wette R. Nonrandom sampling in genetic epidemiology: maximum likelihood methods for multifactorial analysis of quantitative data ascertained through truncation. Genet Epidemiol. 1987;4(5):357-76. doi: 10.1002/gepi.1370040505.
Reference Type
BACKGROUND
Rao DC, Vogler GP, McGue M, Russell JM. Maximum-likelihood estimation of familial correlations from multivariate quantitative data on pedigrees: a general method and examples. Am J Hum Genet. 1987 Dec;41(6):1104-16.
Reference Type
BACKGROUND
Rao DC, Wette R, Ewens WJ. Multifactorial analysis of family data ascertained through truncation: a comparative evaluation of two methods of statistical inference. Am J Hum Genet. 1988 Mar;42(3):506-15.
Reference Type
BACKGROUND
Wette R, McGue MK, Rao DC, Cloninger CR. On the properties of maximum likelihood estimators of familial correlations under variable sibship size. Biometrics. 1988 Sep;44(3):717-25.
Reference Type
BACKGROUND
Province MA, Rao DC. Familial aggregation in the presence of temporal trends. Stat Med. 1988 Jan-Feb;7(1-2):185-98. doi: 10.1002/sim.4780070120.
Reference Type
BACKGROUND
Borecki IB, Laskarzewski P, Rao DC. Genetic factors influencing apolipoprotein AI and AII levels in a kindred with premature coronary heart disease. Genet Epidemiol. 1988;5(6):393-406. doi: 10.1002/gepi.1370050604.
Reference Type
BACKGROUND
Province MA, Tishler P, Rao DC. Repeated-measures model for the investigation of temporal trends using longitudinal family studies: application to systolic blood pressure. Genet Epidemiol. 1989;6(2):333-47. doi: 10.1002/gepi.1370060204.
Reference Type
BACKGROUND
McGue M, Wette R, Rao DC. Path analysis under generalized marital resemblance: evaluation of the assumptions underlying the mixed homogamy model by the Monte Carlo method. Genet Epidemiol. 1989;6(2):373-88. doi: 10.1002/gepi.1370060207.
Reference Type
BACKGROUND
Reddy BM, Rao DC. Phenylthiocarbamide taste sensitivity revisited: complete sorting test supports residual family resemblance. Genet Epidemiol. 1989;6(3):413-21. doi: 10.1002/gepi.1370060304.
Reference Type
BACKGROUND
Rao DC, Wette R. Nonrandom sampling in genetic epidemiology: an implementation of the Hanis-Chakraborty method for multifactorial analysis. Genet Epidemiol. 1989;6(3):461-70. doi: 10.1002/gepi.1370060308.
Reference Type
BACKGROUND
Perusse L, Rice T, Bouchard C, Vogler GP, Rao DC. Cardiovascular risk factors in a French-Canadian population: resolution of genetic and familial environmental effects on blood pressure by using extensive information on environmental correlates. Am J Hum Genet. 1989 Aug;45(2):240-51.
Reference Type
BACKGROUND
Byard PJ, Mukherjee BN, Bhattacharya SK, Russell JM, Rao DC. Familial aggregation of blood pressure and anthropometric variables in patrilocal households. Am J Phys Anthropol. 1989 Jul;79(3):305-11. doi: 10.1002/ajpa.1330790306.
Reference Type
BACKGROUND
McGue M, Gerrard JW, Lebowitz MD, Rao DC. Commingling in the distributions of immunoglobulin levels. Hum Hered. 1989;39(4):196-201. doi: 10.1159/000153860.
Reference Type
BACKGROUND
Rao DC, Wette R. Environmental index in genetic epidemiology: an investigation of its role, adequacy, and limitations. Am J Hum Genet. 1990 Jan;46(1):168-78.
Reference Type
BACKGROUND
Vogler GP, Wette R, Laskarzewski PM, Perry TS, Rice T, Province MA, Rao DC. Heterogeneity in the biological and cultural determinants of high-density lipoprotein cholesterol in five North American populations: the Lipid Research Clinics Family Study. Hum Hered. 1989;39(5):249-57. doi: 10.1159/000153868.
Reference Type
BACKGROUND
Rice T, Vogler GP, Perry TS, Laskarzewski PM, Province MA, Rao DC. Heterogeneity in the familial aggregation of fasting serum uric acid level in five North American populations: the Lipid Research Clinics Family Study. Am J Med Genet. 1990 Jun;36(2):219-25. doi: 10.1002/ajmg.1320360216.
Reference Type
BACKGROUND
Rice T, Vogler GP, Perry TS, Laskarzewski PM, Province MA, Rao DC. Heterogeneity in the familial aggregation of fasting plasma glucose in five North American populations: the Lipid Research Clinics Family Study. Int J Epidemiol. 1990 Jun;19(2):290-6. doi: 10.1093/ije/19.2.290.
Reference Type
BACKGROUND
Rice T, Laskarzewski PM, Rao DC. Commingling and complex segregation analysis of fasting plasma glucose in the Lipid Research Clinics family study. Am J Med Genet. 1992 Nov 1;44(4):399-404. doi: 10.1002/ajmg.1320440402.
Reference Type
BACKGROUND
Rice T, Laskarzewski PM, Perry TS, Rao DC. Commingling and segregation analysis of serum uric acid in five North American populations: the Lipid Research Clinics family study. Hum Genet. 1992 Sep-Oct;90(1-2):133-8. doi: 10.1007/BF00210757.
Reference Type
BACKGROUND
Rice T, Vogler GP, Laskarzewski PM, Perry TS, Rao DC. Familial aggregation of lipids and lipoproteins in families ascertained through random and nonrandom probands in the Minnesota Lipid Research Clinic Family Study. Hum Biol. 1991 Aug;63(4):419-39.
Reference Type
BACKGROUND
Rice T, Vogler GP, Laskarzewski PM, Perry TS, Rao DC. Familial aggregation of lipids and lipoproteins in families ascertained through random and nonrandom probands in the Stanford Lipid Research Clinics Family Study. Am J Med Genet. 1991 Jun 1;39(3):270-7. doi: 10.1002/ajmg.1320390306.
Reference Type
BACKGROUND
Rice T, Vogler GP, Perry TS, Laskarzewski PM, Rao DC. Familial aggregation of lipids and lipoproteins in families ascertained through random and nonrandom probands in the Iowa Lipid Research Clinics family study. Hum Hered. 1991;41(2):107-21. doi: 10.1159/000153987.
Reference Type
BACKGROUND
Borecki IB, Rao DC, Yaouanq J, Lalouel JM. Serum ferritin as a marker of affection for genetic hemochromatosis. Hum Hered. 1990;40(3):159-66. doi: 10.1159/000153924.
Reference Type
BACKGROUND
Vogler GP, Wette R, McGue MK, Rao DC. Properties of alternative estimators of familial correlations under variable sibship size. Biometrics. 1995 Mar;51(1):276-83.
Reference Type
BACKGROUND
Other Identifiers
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1066
Identifier Type: -
Identifier Source: org_study_id
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