Article

A genetic study of hyper-alpha-lipoproteinemia

  1. Dr. D. C. Rao Director1,3,*,
  2. J. M. Lalouel1,4,
  3. B. K. Suarez3,
  4. G. Schonfeld2,
  5. C. J. Glueck5,
  6. R. M. Siervogel6,
  7. John M. Opitz Editor

Article first published online: 2 JUN 2005

DOI: 10.1002/ajmg.1320150203

Issue

American Journal of Medical Genetics

American Journal of Medical Genetics

Volume 15, Issue 2, pages 195–203, June 1983

Additional Information

How to Cite

Rao, D. C., Lalouel, J. M., Suarez, B. K., Schonfeld, G., Glueck, C. J., Siervogel, R. M. and Opitz, J. M. (1983), A genetic study of hyper-alpha-lipoproteinemia. Am. J. Med. Genet., 15: 195–203. doi: 10.1002/ajmg.1320150203

Author Information

  1. 1

    Division of Biostatistics, Washington University School of Medicine, St. Louis, Missouri

  2. 2

    Lipid Research Center, Washington University School of Medicine, St. Louis, Missouri

  3. 3

    Departments of Psychiatry and Genetics, Washington University School of Medicine, St. Louis, Missouri

  4. 4

    Laboratoire D'Anthropologie Biologique, University of Paris, 75005 Paris, France

  5. 5

    The Lipid Research Clinic, The General Clinical Research Center, the CLINFO Center, University of Cincinnati, College of Medicine, Cincinnati, Ohio

  6. 6

    Department of Pediatrics, Fels Research Institute, Wright State University School of Medicine, Yellow Springs, Ohio

*Division of Biostatistics, Washington University School of Medicine, Campus Box 8067, 4566 Scott Avenue, St. Louis, MO 63110

Publication History

  1. Issue published online: 2 JUN 2005
  2. Article first published online: 2 JUN 2005
  3. Manuscript Revised: 17 JAN 1983
  4. Manuscript Received: 25 NOV 1981

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Keywords:

  • hyper-alpha-lipoproteinemia;
  • HDL-cholesterol

Abstract

Because of its association with longevity and reduced incidence of coronary heart disease, it becomes important to find out how elevated HDL-cholesterol levels are determined. Analyses of family data from Cincinnati initially suggested environmental factors common to sibs; however, some form of dominant inheritance could not be ruled out. Reanalysis of the Cincinnati data by Iselius and Lalouel concluded against a major locus, but did identify three families as possibly segregating for a major locus. Analysis of an additional 26 kindreds from the same population in Cincinnati by Siervogel and associates concluded that a major gene could be causing familial aggregation of high density lipoprotein in white kindreds. In this analysis, we pooled all the white Cincinnati kindreds (n = 31), and investigated the familial transmission using complex segregation analysis. We failed to obtain clear evidence for major locus determination. Under the parsimonious hypothesis of no major locus, the polygenic heritability and common sibling environmental correlation were estimated as 0.531 and 0.263, respectively, consistent with other evidence.

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