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Debbie A Lawlor

Researcher at University of Bristol

Publications -  1118
Citations -  118183

Debbie A Lawlor is an academic researcher from University of Bristol. The author has contributed to research in topics: Population & Body mass index. The author has an hindex of 147, co-authored 1114 publications receiving 101123 citations. Previous affiliations of Debbie A Lawlor include Southampton General Hospital & University of Vermont.

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Journal ArticleDOI

Genetic Evidence for Causal Relationships Between Maternal Obesity-Related Traits and Birth Weight

Jessica Tyrrell, +89 more
TL;DR: Citing this paper Please note that where the full-text provided on King's Research Portal is the Author Accepted Manuscript or Post-Print version this may differ from the final Published version.
Journal ArticleDOI

Heavier smoking may lead to a relative increase in waist circumference: evidence for a causal relationship from a Mendelian randomisation meta-analysis. The CARTA consortium.

Richard W Morris, +70 more
- 11 Aug 2015 - 
TL;DR: For a given BMI, a gene variant associated with increased cigarette consumption was associated with increase waist circumference, suggesting that smoking in an effort to control weight may lead to accumulation of central adiposity.

GWAS on longitudinal growth traits reveals different genetic factors influencing infant, child, and adult BMI

Alexessander Couto Alves, +90 more
TL;DR: In this paper, the authors combine genome-wide association studies with modeling of longitudinal growth traits to study the genetics of infant and child growth, followed by functional, pathway, genetic correlation, risk score, and colocalization analyses to determine how developmental timings, molecular pathways, and genetic determinants of these traits overlap with those of adult health.
Journal ArticleDOI

Hyperglycemia, Type 2 Diabetes, and Depressive Symptoms: The British Whitehall II study

TL;DR: The U-shaped association between blood glucose and CES-D, with the lowest depression risk seen among those in the normoglycemic range of A1C, did not support the hypothesized protective effect of hyperglycemia.