Evidence for gene-environmental interactions in Utah familes with hypertension, dyslipidaemia and early coronary heart disease

R. R. Williams, Steven Hunt, P. N. Hopkins, L. L. Wu, M. C. Schumacher, B. M. Stults, L. Ball, J. Ware, S. J. Hasstedt, J. M. Lalouel

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Abstract

Among 45258 Utah families surveyed, about 4% have a strong aggregation of early coronary disease. In detailed clinical evaluation, about 21% of such high risk coronary families were found to have familial dyslipidaemic hypertension (FDH) and about 3% were found to have heterozygous familial hypercholesterolaemia (hFH). Common and potentially modifiable environmental factors seem to play an important role in these high risk families. Non-genetic obesity promotes the expression of FDH. A high fat diet promotes the expression of FH. Cigarette smoking promotes earlier death in all coronary prone families. Practical approaches are suggested for helping coronary prone pedigrees by applying our understanding of genetic and environmental factors that promote earlier coronary disease onset.

Original languageEnglish
Pages (from-to)1-6
Number of pages6
JournalClinical and Experimental Pharmacology and Physiology
Volume19
Issue numberSUPPL. 20
Publication statusPublished - 1992
Externally publishedYes

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Keywords

  • atherosclerosis
  • epidemiology
  • genetics
  • hypertension
  • lipid abnormalities
  • nutrition
  • pathophysiology

ASJC Scopus subject areas

  • Physiology
  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Medicine(all)

Cite this

Williams, R. R., Hunt, S., Hopkins, P. N., Wu, L. L., Schumacher, M. C., Stults, B. M., Ball, L., Ware, J., Hasstedt, S. J., & Lalouel, J. M. (1992). Evidence for gene-environmental interactions in Utah familes with hypertension, dyslipidaemia and early coronary heart disease. Clinical and Experimental Pharmacology and Physiology, 19(SUPPL. 20), 1-6.