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Invited commentary: Gene x lifestyle interactions and complex disease traits--inferring cause and effect from observational data, sine qua non.

Franks, Paul LU and Nettleton, J A (2010) In American Journal of Epidemiology 172(9). p.992-997
Abstract
Observational epidemiology has made outstanding contributions to the discovery and elucidation of relations between lifestyle factors and common complex diseases such as type 2 diabetes. Recent major advances in the understanding of the human genetics of this disease have inspired studies that seek to determine whether the risk conveyed by bona fide risk loci might be modified by lifestyle factors such as diet composition and physical activity levels. A major challenge is to determine which of the reported findings are likely to represent causal interactions and which might be explained by other factors. The authors of this commentary use the Bradford-Hill criteria, a set of tried-and-tested guidelines for causal inference, to evaluate the... (More)
Observational epidemiology has made outstanding contributions to the discovery and elucidation of relations between lifestyle factors and common complex diseases such as type 2 diabetes. Recent major advances in the understanding of the human genetics of this disease have inspired studies that seek to determine whether the risk conveyed by bona fide risk loci might be modified by lifestyle factors such as diet composition and physical activity levels. A major challenge is to determine which of the reported findings are likely to represent causal interactions and which might be explained by other factors. The authors of this commentary use the Bradford-Hill criteria, a set of tried-and-tested guidelines for causal inference, to evaluate the findings of a recent study on interaction between variation at the cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like 1 (CDKAL1) locus and total energy intake with respect to prevalent metabolic syndrome and hemoglobin A₁(c) levels in a cohort of 313 Japanese men. The current authors conclude that the study, while useful for hypothesis generation, does not provide overwhelming evidence of causal interactions. They overview ways in which future studies of gene × lifestyle interactions might overcome the limitations that motivated this conclusion. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
human, CDKAL1 protein, energy intake, hemoglobin A1c protein, Japan, metabolic syndrome X
in
American Journal of Epidemiology
volume
172
issue
9
pages
992 - 997
publisher
Oxford University Press
external identifiers
  • wos:000283660500002
  • scopus:77958548114
ISSN
0002-9262
DOI
10.1093/aje/kwq280
language
English
LU publication?
yes
id
567b25ad-1b48-4f0e-a600-29366a6da657 (old id 1715821)
date added to LUP
2010-11-11 11:49:09
date last changed
2018-05-29 09:23:25
@article{567b25ad-1b48-4f0e-a600-29366a6da657,
  abstract     = {Observational epidemiology has made outstanding contributions to the discovery and elucidation of relations between lifestyle factors and common complex diseases such as type 2 diabetes. Recent major advances in the understanding of the human genetics of this disease have inspired studies that seek to determine whether the risk conveyed by bona fide risk loci might be modified by lifestyle factors such as diet composition and physical activity levels. A major challenge is to determine which of the reported findings are likely to represent causal interactions and which might be explained by other factors. The authors of this commentary use the Bradford-Hill criteria, a set of tried-and-tested guidelines for causal inference, to evaluate the findings of a recent study on interaction between variation at the cyclin-dependent kinase 5 regulatory subunit-associated protein 1-like 1 (CDKAL1) locus and total energy intake with respect to prevalent metabolic syndrome and hemoglobin A₁(c) levels in a cohort of 313 Japanese men. The current authors conclude that the study, while useful for hypothesis generation, does not provide overwhelming evidence of causal interactions. They overview ways in which future studies of gene × lifestyle interactions might overcome the limitations that motivated this conclusion.},
  author       = {Franks, Paul and Nettleton, J A},
  issn         = {0002-9262},
  keyword      = {human,CDKAL1 protein,energy intake,hemoglobin A1c protein,Japan,metabolic syndrome X},
  language     = {eng},
  number       = {9},
  pages        = {992--997},
  publisher    = {Oxford University Press},
  series       = {American Journal of Epidemiology},
  title        = {Invited commentary: Gene x lifestyle interactions and complex disease traits--inferring cause and effect from observational data, sine qua non.},
  url          = {http://dx.doi.org/10.1093/aje/kwq280},
  volume       = {172},
  year         = {2010},
}