Modeling and dissection of longitudinal blood pressure and hypertension phenotypes in genetic epidemiological studies

We discuss analyses of the Genetic Analysis Workshop 13 data from the Framingham Heart Study and simulations based on this study. We summarize analyses that investigated measures of systolic blood pressure or hypertension as the main phenotype, with the main focus being the modeling of this complex...

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Bibliographic Details
Published in:Genetic epidemiology 2003, Vol.25 (S1), p.S72-S77
Main Authors: Bickeböller, H., Barrett, J.H., Jacobs, K.B., Rosenberger, A.
Format: Article
Language:English
Subjects:
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Blood Pressure - genetics
Cardiology. Vascular system
Cardiovascular Diseases - epidemiology
Cardiovascular Diseases - genetics
Cell physiology
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Clinical manifestations. Epidemiology. Investigative techniques. Etiology
familial aggregation
Fundamental and applied biological sciences. Psychology
Genetic Linkage
Genetic Predisposition to Disease
Humans
Hypertension - epidemiology
Hypertension - genetics
Longitudinal Studies
Medical sciences
Models, Genetic
Models, Statistical
Molecular and cellular biology
one-stage linkage designs
Phenotype
Systole
two-stage linkage designs
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Summary:We discuss analyses of the Genetic Analysis Workshop 13 data from the Framingham Heart Study and simulations based on this study. We summarize analyses that investigated measures of systolic blood pressure or hypertension as the main phenotype, with the main focus being the modeling of this complex longitudinal phenotype. The approaches include familial aggregation methods and one‐stage and two‐stage linkage methods. For one‐stage linkage methods, phenotype modeling is carried out jointly with the linkage analysis or incorporated in the analysis design. For two‐stage linkage methods, phenotypes are first modeled in order to develop summary measures that are then analyzed in a subsequent linkage analysis. Results depend on phenotype selection and on how analyses account for longitudinality, treatment effects, and heterodasticity. Genet Epidemiol 25 (Suppl. 1):S72–S77, 2003. © 2003 Wiley‐Liss, Inc.
ISSN:0741-0395
1098-2272
DOI:10.1002/gepi.10287