Asset Details
Do you wish to reserve the book?
Carnitine palmitoyltransferase 1A P479L and infant death: policy implications of emerging data
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Carnitine palmitoyltransferase 1A P479L and infant death: policy implications of emerging data
Do you wish to request the book?
Carnitine palmitoyltransferase 1A P479L and infant death: policy implications of emerging data
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Carnitine palmitoyltransferase 1A P479L and infant death: policy implications of emerging data
2017
Overview
Carnitine palmitoyltransferase 1 isoform A (CPT1A) is a crucial enzyme for the transport of long-chain fatty acids into the mitochondria. The
CPT1A
p.P479L variant is found in high frequencies among indigenous populations residing on the west and north coasts of Alaska and Canada and in northeast Siberia and Greenland. Epidemiological studies have reported a statistical association between P479L homozygosity and infant death in Alaska Native and Canadian Inuit populations. Here, we review the available evidence about the P479L variant and apply to these data the epidemiological criteria for assessing causal associations. We found insufficient evidence to support a causal association with infant death and, further, that if a causal association is present, then the genotype is likely to be only one of a complex set of factors contributing to an increased risk of infant death. We conclude that additional research is needed to clarify the observed association and to inform effective preventative measures for infant death. In light of these findings, we discuss the policy implications for public health efforts because policies based on the observed association between P479L homozygosity and infant death data are premature.
Genet Med
advance online publication 26 January 2017
Publisher
Nature Publishing Group US,Elsevier Limited
Subject
