Menu
GWAS Study

Genome-wide associations for birth weight and correlations with adult disease.

Horikoshi M, Beaumont RN, Day FR et al.

27680694 PubMed ID
GWAS Study Type
160295 Participants
Scroll to explore
Chapter I

Publication Details

Comprehensive information about this research publication

Authors

HM
Horikoshi M
BR
Beaumont RN
DF
Day FR
WN
Warrington NM
KM
Kooijman MN
FJ
Fernandez-Tajes J
FB
Feenstra B
VZ
van Zuydam NR
GK
Gaulton KJ
GN
Grarup N
BJ
Bradfield JP
SD
Strachan DP
LR
Li-Gao R
AT
Ahluwalia TS
KE
Kreiner E
RR
Rueedi R
LL
Lyytikäinen LP
CD
Cousminer DL
WY
Wu Y
TE
Thiering E
WC
Wang CA
HC
Have CT
HJ
Hottenga JJ
VN
Vilor-Tejedor N
JP
Joshi PK
BE
Boh ETH
NI
Ntalla I
PN
Pitkänen N
MA
Mahajan A
VL
van Leeuwen EM
JR
Joro R
LV
Lagou V
NM
Nodzenski M
DL
Diver LA
ZK
Zondervan KT
BM
Bustamante M
MP
Marques-Vidal P
MJ
Mercader JM
BA
Bennett AJ
RN
Rahmioglu N
ND
Nyholt DR
MR
Ma RCW
TC
Tam CHT
TW
Tam WH
GS
Ganesh SK
VR
van Rooij FJ
JS
Jones SE
LP
Loh PR
RK
Ruth KS
TM
Tuke MA
TJ
Tyrrell J
WA
Wood AR
YH
Yaghootkar H
SD
Scholtens DM
PL
Paternoster L
PI
Prokopenko I
KP
Kovacs P
AM
Atalay M
WS
Willems SM
PK
Panoutsopoulou K
WX
Wang X
CL
Carstensen L
GF
Geller F
SK
Schraut KE
MM
Murcia M
VB
van Beijsterveldt CE
WG
Willemsen G
AE
Appel EVR
FC
Fonvig CE
TC
Trier C
TC
Tiesler CM
SM
Standl M
KZ
Kutalik Z
BS
Bonas-Guarch S
HD
Hougaard DM
SF
Sánchez F
TD
Torrents D
WJ
Waage J
HM
Hollegaard MV
DH
de Haan HG
RF
Rosendaal FR
MC
Medina-Gomez C
RS
Ring SM
HG
Hemani G
MG
McMahon G
RN
Robertson NR
GC
Groves CJ
LC
Langenberg C
LJ
Luan J
SR
Scott RA
ZJ
Zhao JH
MF
Mentch FD
MS
MacKenzie SM
RR
Reynolds RM
LW
Lowe WL
TA
Tönjes A
SM
Stumvoll M
LV
Lindi V
LT
Lakka TA
VD
van Duijn CM
KW
Kiess W
KA
Körner A
ST
Sørensen TI
NH
Niinikoski H
PK
Pahkala K
RO
Raitakari OT
ZE
Zeggini E
DG
Dedoussis GV
TY
Teo YY
SS
Saw SM
MM
Melbye M
CH
Campbell H
WJ
Wilson JF
VM
Vrijheid M
DG
de Geus EJ
BD
Boomsma DI
KH
Kadarmideen HN
HJ
Holm JC
HT
Hansen T
SS
Sebert S
HA
Hattersley AT
BL
Beilin LJ
NJ
Newnham JP
PC
Pennell CE
HJ
Heinrich J
AL
Adair LS
BJ
Borja JB
MK
Mohlke KL
EJ
Eriksson JG
WE
Widén EE
KM
Kähönen M
VJ
Viikari JS
LT
Lehtimäki T
VP
Vollenweider P
BK
Bønnelykke K
BH
Bisgaard H
MD
Mook-Kanamori DO
HA
Hofman A
RF
Rivadeneira F
UA
Uitterlinden AG
PC
Pisinger C
PO
Pedersen O
PC
Power C
HE
Hyppönen E
WN
Wareham NJ
HH
Hakonarson H
DE
Davies E
WB
Walker BR
JV
Jaddoe VW
JM
Jarvelin MR
GS
Grant SF
VA
Vaag AA
LD
Lawlor DA
FT
Frayling TM
DS
Davey Smith G
MA
Morris AP
OK
Ong KK
FJ
Felix JF
TN
Timpson NJ
PJ
Perry JR
ED
Evans DM
MM
McCarthy MI
FR
Freathy RM
Chapter II

Abstract

Summary of the research findings

Birth weight (BW) has been shown to be influenced by both fetal and maternal factors and in observational studies is reproducibly associated with future risk of adult metabolic diseases including type 2 diabetes (T2D) and cardiovascular disease. These life-course associations have often been attributed to the impact of an adverse early life environment. Here, we performed a multi-ancestry genome-wide association study (GWAS) meta-analysis of BW in 153,781 individuals, identifying 60 loci where fetal genotype was associated with BW (P < 5 × 10-8). Overall, approximately 15% of variance in BW was captured by assays of fetal genetic variation. Using genetic association alone, we found strong inverse genetic correlations between BW and systolic blood pressure (Rg = -0.22, P = 5.5 × 10-13), T2D (Rg = -0.27, P = 1.1 × 10-6) and coronary artery disease (Rg = -0.30, P = 6.5 × 10-9). In addition, using large -cohort datasets, we demonstrated that genetic factors were the major contributor to the negative covariance between BW and future cardiometabolic risk. Pathway analyses indicated that the protein products of genes within BW-associated regions were enriched for diverse processes including insulin signalling, glucose homeostasis, glycogen biosynthesis and chromatin remodelling. There was also enrichment of associations with BW in known imprinted regions (P = 1.9 × 10-4). We demonstrate that life-course associations between early growth phenotypes and adult cardiometabolic disease are in part the result of shared genetic effects and identify some of the pathways through which these causal genetic effects are mediated.

133,903 European ancestry individuals, 6,635 African American individuals, 420 Turkish ancestry individuals, 365 Moroccan ancestry individuals, 395 Surinamese ancestry individuals, 840 Chinese ancestry individuals.

Chapter III

Study Statistics

Key metrics and study information

160295
Total Participants
GWAS
Study Type
Yes
Replicated
9,799 European ancestry individuals, 1,449 Filipino ancestry individuals.
Replication Participants
Other admixed ancestry, East Asian, Asian unspecified, Other, European, African American or Afro-Caribbean, Greater Middle Eastern (Middle Eastern, North African or Persian)
Ancestry
Netherlands, Singapore, Philippines, U.S., Australia, Germany, Switzerland, Denmark, Finland, U.K., Greece, Spain
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

Important Disclaimer: This review has been performed semi-automatically and is provided for informational purposes only. While we strive for accuracy, this analysis may contain errors, omissions, or misinterpretations of the original research. DNA Genics disclaims all liability for any inaccuracies, errors, or consequences arising from the use of this information. Users should independently verify all information and consult original research publications before making any decisions based on this content. This analysis is not intended as a substitute for professional scientific review or medical advice.

Analysis In Progress

Our analysis of this publication is currently being prepared. Please check back soon for comprehensive insights into the health and genetic findings discussed in this research.