IJE Advance Access originally published online on May 27, 2004
International Journal of Epidemiology 2004 33(5):953-954; doi:10.1093/ije/dyh217
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
IJE vol.33 no.5 © International Epidemiological Association 2004; all rights reserved.
Commentary |
Commentary: Twins, low birthweight and type 2 diabetes
MRC Unit, Southampton General Hospital, Tremona Road, Southampton SO16 4YD, UK. E-mail: diwp@mrc.soton.ac.uk
| The first 10% of the full text of this article appears below. |
One of the important issues raised by the fetal origins hypothesis is the extent to which the associations between birthweight and adult health outcomes, such as type 2 diabetes, are explained by common genetic factors, or are a result of fetal programming by the early environment. Indeed, a genetic explanation has been specifically proposed for the association between birthweight and type 2 diabetes.1 In pathophysiological terms this is logical. Since insulin has a central role in controlling fetal growth, genetic factors which impair insulin secretion
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
G. D. Smith Epidemiological Freudianism Int. J. Epidemiol., February 1, 2005; 34(1): 1 - 2. [Full Text] [PDF] |
||||
![]() |
G. Davey Smith Genetic epidemiology: an 'enlightened narrative'? Int. J. Epidemiol., October 1, 2004; 33(5): 923 - 924. [Full Text] [PDF] |
||||
