@article {7375,
	title = {A DNA methylation biomarker of alcohol consumption.},
	journal = {Mol Psychiatry},
	year = {2016},
	month = {2016 Nov 15},
	abstract = {<p>The lack of reliable measures of alcohol intake is a major obstacle to the diagnosis and treatment of alcohol-related diseases. Epigenetic modifications such as DNA methylation may provide novel biomarkers of alcohol use. To examine this possibility, we performed an epigenome-wide association study of methylation of cytosine-phosphate-guanine dinucleotide (CpG) sites in relation to alcohol intake in 13 population-based cohorts (ntotal=13 317; 54\% women; mean age across cohorts 42-76 years) using whole blood (9643 European and 2423 African ancestries) or monocyte-derived DNA (588 European, 263 African and 400 Hispanic ancestry) samples. We performed meta-analysis and variable selection in whole-blood samples of people of European ancestry (n=6926) and identified 144 CpGs that provided substantial discrimination (area under the curve=0.90-0.99) for current heavy alcohol intake (⩾42 g per day in men and ⩾28 g per day in women) in four replication cohorts. The ancestry-stratified meta-analysis in whole blood identified 328 (9643 European ancestry samples) and 165 (2423 African ancestry samples) alcohol-related CpGs at Bonferroni-adjusted P<1 {\texttimes} 10(-7). Analysis of the monocyte-derived DNA (n=1251) identified 62 alcohol-related CpGs at P<1 {\texttimes} 10(-7). In whole-blood samples of people of European ancestry, we detected differential methylation in two neurotransmitter receptor genes, the γ-Aminobutyric acid-A receptor delta and γ-aminobutyric acid B receptor subunit 1; their differential methylation was associated with expression levels of a number of genes involved in immune function. In conclusion, we have identified a robust alcohol-related DNA methylation signature and shown the potential utility of DNA methylation as a clinically useful diagnostic test to detect current heavy alcohol consumption.Molecular Psychiatry advance online publication, 15 November 2016; doi:10.1038/mp.2016.192.</p>},
	issn = {1476-5578},
	doi = {10.1038/mp.2016.192},
	author = {Liu, C and Marioni, R E and Hedman, {\r A} K and Pfeiffer, L and Tsai, P-C and Reynolds, L M and Just, A C and Duan, Q and Boer, C G and Tanaka, T and Elks, C E and Aslibekyan, S and Brody, J A and K{\"u}hnel, B and Herder, C and Almli, L M and Zhi, D and Wang, Y and Huan, T and Yao, C and Mendelson, M M and Joehanes, R and Liang, L and Love, S-A and Guan, W and Shah, S and McRae, A F and Kretschmer, A and Prokisch, H and Strauch, K and Peters, A and Visscher, P M and Wray, N R and Guo, X and Wiggins, K L and Smith, A K and Binder, E B and Ressler, K J and Irvin, M R and Absher, D M and Hernandez, D and Ferrucci, L and Bandinelli, S and Lohman, K and Ding, J and Trevisi, L and Gustafsson, S and Sandling, J H and Stolk, L and Uitterlinden, A G and Yet, I and Castillo-Fernandez, J E and Spector, T D and Schwartz, J D and Vokonas, P and Lind, L and Li, Y and Fornage, M and Arnett, D K and Wareham, N J and Sotoodehnia, N and Ong, K K and van Meurs, J B J and Conneely, K N and Baccarelli, A A and Deary, I J and Bell, J T and North, K E and Liu, Y and Waldenberger, M and London, S J and Ingelsson, E and Levy, D}
}
