David Goldstein
razib | January 26, 2010Update: Also see p-ter at Gene Expression Classic.
Follow up on yesterday's post on the new Dickson et al. paper from David Goldstein's lab, A New Way to Look for Diseases' Genetic Roots:
The Icelandic gene-hunting firm deCODE genetics, which emerged last week from bankruptcy, has long led in detecting SNPs associated with common disease. Dr. Kari Stefansson, the company's founder and research director, agreed that whole genome sequencing would "give us a lot of extremely exciting data." But he disputed Dr. Goldstein's view that rare variants carried most of the missing heritability. Both…
razib | January 25, 2010David Goldstein, a geneticist at Duke, has critiqued the current focus on large-scale genomwide associations before. Now he is taking to the next step, as his group has a paper out which suggests that the reason that association studies have been relatively unfruitful in terms of bang-for-buck is due to the fact that they're picking up "synthetic associations." Rare Variants Create Synthetic Genome-Wide Associations:
It has long been assumed that common genetic variants of modest effect make an important contribution to common human diseases, such as most forms of cardiovascular disease,…
razib | April 20, 2009In response to the NEJM issue on personal genomics and the CDCV hypothesis, p-ter offers a proposal:
Let's follow Goldstein's back-of-the-envelope calculations: assume there are ~100K polymorphisms (assuming Goldstein isn't making the mistake I attribute to him, this includes polymorphisms both common and rare) that contribute to human height, that we've found the ones that account for the largest fractions of the variance, and that these fractions of variance follow an exponential distribution.
Now, assume you have assembled a cohort of 5000 individuals and done a genome-wide association…