Our Research Findings
Our Research Findings
Asthma and Mental Health Disorders. European Respiratory Journal 2019; 54: 1901507
- This study was based on UK Biobank application 45052. GWAS single SNP summary statistics generated from this study. Citation: Zhu Z, Zhu X, Liu CL, Shi H, Shen S, Yang Y, Hasegawa K, Camargo CA Jr, Liang L. (2019) Shared genetics of asthma and mental health disorders: a large-scale genome-wide cross-trait analysis. Eur Respir J. 2019 Dec 19;54(6). pii: 1901507. doi: 10.1183/13993003.01507-2019. Print 2019 Dec.
Asthma and allergy cross-trait heritability. Nature Genetics. 2018; 50(6): 857-864.
- Cross-trait heritability for asthma and allergy. We used UK Biobank (UKBB) data field 6152 as our doctor diagnosed asthma and allergic disease (hay fever, allergic rhinitis or eczema) phenotypes. This data is generated from UKBB application #16549.
- Data field 6152 contains a question from touchscreen for the participants to answer: “has a doctor ever told you that you have had any of the following conditions? (You can select more than one answer): Blood clot in the leg (DVT); blood clot in the lung; emphysema/chronic bronchitis; asthma; hayfever, allergic rhinitis or eczema; none of the above; prefer not to answer.
- Citation: Zhaozhong Zhu, Phil H. Lee, Mark D. Chaffin, Wonil Chung, Po-Ru Loh, Quan Lu, David C. Christiani, Liming Liang (2018) A genome-wide cross trait analysis from UK Biobank highlights the shared genetic architecture of asthma and allergic diseases. Nature Genetics. 2018 June ; 50(6): 857–864.
GWAS single SNP summary statistics for asthma
GWAS single SNP summary statistics for allergic diseases
Obesity and asthma cross-trait heritability. Journal of Allergy and Clinical Immunology. 2020; 145(2):537-549.
- This study was based on UK Biobank application 45052
- UKB GWAS summary statistics for BMI
- UKB GWAS summary statistics for BMI-adjusted WHR
- UKB GWAS summary statistics for BMI-adjusted WC
- UKB GWAS summary statistics for childhood-onset asthma
- UKB GWAS summary statistics for adult-onset asthma
- UKB GWAS summary statistics for atopic asthma
- UKB GWAS summary statistics for non-atopic asthma
- Citation: Zhu Z, Guo Y, Shi H, Liu CL, Panganiban RA, Chung W, O’Connor LJ, Himes BE, Gazal S, Hasegawa K, Camargo CA Jr., Qi L, Moffatt MF, Hu FB, Lu Q, Cookson WOC, Liang L. Shared genetic and experimental links between obesity-related traits and asthma subtypes in UK Biobank. J Allergy Clin Immunol 2020;145(2):537-549 PMID: 31669095
Cross-trait polygenic risk model. Nature Communications. 10(1), 569
- All Predictors for human height by aid of BMI with 437K training samples from UK Biobank using PRS, LDpred, MCP, Lasso, PRS+MTAG, LDpred+MTAG, MCP+CTPR and Lasso+CTPR are available from the following link: Link
- Citation: Wonil Chung, Jun Chen, Constance Chen, Sara Lindstroem, Zhaozhong Zhu, Po-Ru Loh, Peter Kraft and Liming Liang (2019), Efficient Cross-Trait Penalized Regression Increases Prediction Accuracy in Large Cohorts using Secondary Phenotypes, Nature Communications, 10(1), 569: Link
- Wonil Chung at Harvard T.H. Chan School of Public Health
Cell type specific effect for EWAS
- See notes here:
DNA methylation patterns across cord blood and placenta. Epigenetics. 2019 Apr;14(4):405-420.
- Citation: Baoshan Ma, Catherine Allard, Luigi Bouchard, Patrice Perron, Murray Mittleman, Marie-France Hivert, Liming Liang. Locus-specific Methylation Prediction in Cord Blood and Placenta (Epigenetics, 2019).
- DNA methylation is known to be responsive to prenatal exposures, which may be a part of the mechanism linking early developmental exposures to future chronic diseases. Many studies use blood to measure DNA methylation, yet we know that DNA methylation is tissue specific. Placenta is central to fetal growth and development, but it is rarely feasible to collect this tissue in large epidemiological studies; on the other hand, cord blood samples are more accessible. Our previous research suggested that large scale epidemiology studies using easy-to-access surrogate tissues (e.g. blood) could be recalibrated to improve the understanding of epigenetics in hard-to-access tissues (e.g. atrium and artery) and might enable non-invasive disease screening using epigenetic profiles. In this study, based on paired samples of both placenta and cord blood tissues from 169 individuals, we investigated the methylation concordance between placenta and cord blood. We then employed a machine-learning-based model to predict locus-specific DNA methylation levels in placenta using DNA methylation levels in cord blood. We found that methylation correlation between placenta and cord blood is lower than other tissue pairs, consistent with existing observations that placenta methylation has a distinct pattern. Nonetheless, there are still a number of CpG sites showing robust association between the two tissues. We built prediction models for placenta methylation based on cord blood data and documented a subset of 1,012 CpG sites with high correlation between measured and predicted placenta methylation levels. The resulting list of CpG sites and prediction models could help to reveal the loci where internal or external influences may affect DNA methylation in both placenta and cord blood, and provide a reference data to predict the effects on placenta in future study even when the tissue is not available in an epidemiological study.
- This method is easily applicable to other samples and tissues. In order for the investigators to use our method, we have developed an R package which can be used to build the prediction model based on a training dataset with paired surrogate and target tissues, and generate predicted target tissue methylation with only surrogate tissue methylation. The program, detailed instruction and example datasets, as well as supplementary files can be found in the below links. If you find our method and program useful, please cite the above reference.
- Download: Package with R function and instructions prediction-software-package-20190218.zip.
- Supplementary figures:
- Supplementary tables:
Host and gut microbial tryptophan metabolism and type 2 diabetes: an integrative analysis of host genetics, diet, gut microbiome and circulating metabolites in cohort studies. Gut. 2022;71(6):1095-1105.
- Summary statistics here are the GWAS data derived in this paper
- GWAS summary statistics for serotonin
- GWAS summary statistics for tryptophan
- GWAS summary statistics for kynurenine
- GWAS summary statistics for indolepropionate
- GWAS summary statistics for indoxylsulfate
- GWAS summary statistics for xanthurenate
- GWAS summary statistics for kynurenate
- GWAS summary statistics for quinolinate
- GWAS summary statistics for indoleacetate
- GWAS summary statistics for indolelactate
- GWAS summary statistics for picolinate
- Qi Q, Li J, Yu B, Moon JY, Chai JC, Merino J, Hu J, Ruiz-Canela M, Rebholz C, Wang Z, Usyk M, Chen GC, Porneala BC, Wang W, Nguyen NQ, Feofanova EV, Grove ML, Wang TJ, Gerszten RE, Dupuis J, Salas-Salvadó J, Bao W, Perkins DL, Daviglus ML, Thyagarajan B, Cai J, Wang T, Manson JE, Martínez-González MA, Selvin E, Rexrode KM, Clish CB, Hu FB, Meigs JB, Knight R, Burk RD, Boerwinkle E, Kaplan RC. Host and gut microbial tryptophan metabolism and type 2 diabetes: an integrative analysis of host genetics, diet, gut microbiome and circulating metabolites in cohort studies. Gut. 2022 Jun;71(6):1095-1105. PMID: 34127525
The Mediterranean diet, plasma metabolome, and cardiovascular disease risk. Eur Heart J. 2020;41(28):2645-2656.
- Summary statistics here are the GWAS for the Medi-Diet metabolic signature (n=1,925) SNPs only
- Li J, Guasch-Ferré M, Chung W, Ruiz-Canela M, Toledo E, Corella D, Bhupathiraju SN, Tobias DK, Tabung FK, Hu J, Zhao T, Turman C, Feng YA, Clish CB, Mucci L, Eliassen AH, Costenbader KH, Karlson EW, Wolpin BM, Ascherio A, Rimm EB, Manson JE, Qi L, Martínez-González MÁ, Salas-Salvadó J, Hu FB, Liang L. The Mediterranean diet, plasma metabolome, and cardiovascular disease risk. Eur Heart J. 2020;41(28):2645-2656. PMID: 32406924.
Epigenome-wide association analysis of infant bronchiolitis severity: a multicenter prospective cohort study. Nature Communications. 2023;14(1):5495.
- This study was based on 35th Multicenter Airway Research Collaboration (MARC-35) cohort
- MARC-35 EWAS summary statistics for bronchiolitis severity
- Citation: Zhu Z, Li Y, Freishtat RJ, Celedón JC, Espinola JA, Harmon B, Hahn A, Camargo CA Jr, Liang L, Hasegawa K. Epigenome-wide association analysis of infant bronchiolitis severity: a multicenter prospective cohort study. Nature Communications. 2023;14(1):5495. PMID: 37679381.
- Contact: Please contact Dr. Zhaozhong Zhu (zzhu5@mgh.harvard.edu) for any questions related to this study
Cross omics risk scores of inflammation markers are associated with all-cause mortality: The Canadian Longitudinal Study on Aging.
- R example code for 1- 2- and 3-way CRP risk scores
- Citation: Anat Yaskolka Meir, Huan Yun, Jie Hu, Jun Li, Jiaxuan Liu, Alaina Bever, Andrew Ratanatharathorn, Mingyang Song, A. Heather Eliassen, Lori Chibnik, Karestan Koenen, Guillaume Pare, Meir J Stampfer, Liming Liang. Cross omics risk scores of inflammation markers are associated with all-cause mortality: The Canadian Longitudinal Study on Aging. PMID: XXXXXXXX (the issue number and PMID are to be determined)
- Contact: Please contact Dr. Liming Liang for any questions related to this study