Personally I think nyssos's explanation (that disease is a complex function of the joint distribution of genotype and environment) is still more convincing, and that the reason environment temporarily got more attention is simply that our ability to understand causality of disease in non-mendelian contexts is still very limited (it being an extremely complex function).

I've worked in this field for a while and continuously get into arguments with geneticists, part of that is because I simply don't understand the explanations genetics gives (I'm a molecular biologist and computer scientist; the difference is that genenticists treat genotype to phenotype as a black box, while molecular biologists see it as an event system), but another part of it is that most scientists are highly susceptible to the streelight effect, and genetics is something tangible you can easily measure in the lab, while environment is... much more complicated.

I agree with your perspective, but would add a little nuance. I think the molecularly-mediated version of genetics is promising (e.g., Transcriptome Wide Association Studies, or TWAS). It breaks out of the black box a little, but still enriches for causal associations that purely mechanistic approaches miss. Pure molecular mechanism has a hard time tracing from cells to organismal phenotype at age 60 in a varied environment.

Do you do computational biology? I think that field is fascinating. I’m working on human biomolecular data viz tools in a consortium of academic labs (Harvard, CMU, etc.) funded by the NIH. Really enjoy working with computational biologist.

How much better could you predict if you sequence both DNA and samples of expressed RNA from various parts of the body?