proposed as an EP for MD—measured over a comparable time period. The major point here is that the relative ‘performance’ of EPs versus PD in assessing a ‘genetic signal’ cannot be divorced from the problems of measurement. It is perfectly possible for us to study an EP that is ‘truly’ closer to gene action than our PD. But if our measures of EP are less reliable than those of our PD, unless we account for this unreliability in our models, we would get the wrong answer—that EP cannot be sitting in the causal path to our PD.
