EMADS

Welcome! This is an informational page devoted to EMADS, the exome meta-analysis of drinking and smoking. This page has a description of the project and standard documents related to the effort.

Description and Rationale

EMADS is a collaborative effort of many studies to investigate the potential role of rare exomic variation on drinking and smoking phenotypes. Through the effort we hope to extend results of previous GWAS meta-analyses of drinking and smoking, as well as identify novel genetic associations. We use the exome chip as the primary genotyping technology, largely because larger samples have been genotyped on the exome chip (compared to sequencing). However, some studies also have whole genome or exome sequences, and these will be included in analysis.

Projects

The current primary goal of the EMADS consortium is a genome-wide exomic analysis of nonsynonymous variation in smoking and drinking phenotypes.

We hope to expand the list of possible projects using the data available through our consortium. These may include a project headed by Nancy Saccone and Laura Beirut on detailed analysis of the chromosome 15 region and smoking.

Guidelines for participation

While we have no strict policies or procedures, there are a few best practices guidelines to consider.

• 1. We by no means restrict the activities of participating studies, but we believe it’s best if participants refrain from contribution to similar meta-anlayses that duplicate our efforts. Ideally, similar meta-analyses would join efforts.
• 2. Any work that uses data from EMADS should, at the very least, include the consortium name in the list of authors. Depending on the extent of involvement of individuals in EMADS, individual contributors should also be included in the author list.

Authorship

While authorship is decided on an individual basis for each paper (depending on contribution), typically, authorship is arranged in groups. Papers typically might include:

1. A group of 6 or fewer junior investigators who strongly led the efforts, usually starred to denote equal contribution, followed by additional junior investigators who played key, central roles.

2. In alphabetical order, junior investigators who had substantial individual contributions but not as much as those in Group 1. Typically, these might be lead analysts or other junior investigators who made a sizable contribution such as GWA analyses performed specifically for the paper.

3. In alphabetical order, junior investigators who had notable individual contributions but not as much as those in Groups 1 or 2. Typically, these might be lead analysts for replication cohorts, providing results for a group of top hits.

4. In alphabetical order, junior and senior investigators who had contributions worthy of authorship (participating in analysis, phenotype collection, genotyping, oversight of cohorts, etc. that was specific to the paper) but not as much as those in the other groups.

5. In alphabetical order, senior investigators who had contributions worthy of authorship and contributed more than those in group 4. Typically, these might be a lead PI of a participating cohort who did not participate as strongly in EMADS activities as those in group 6.

6. In alphabetical order, senior investigators who participated strongly in EMADS activities but did not strongly lead/oversee the writing and/or analysis for the paper. Typically, these might be members of the EMADS steering committee or leaders of other key EMADS activities.

7. The senior investigators who strongly led/oversaw the writing and/or analysis of the paper, including a subset that are co-corresponding authors (usually 6 or fewer).