Thanks for posting this! I think this topic is extremely neglected and the lack of side effects among natural short-sleepers strongly suggests that there could be interventions with no obvious downsides.
My main concern with your drug-centered approach is: what if the causal path from short-sleeper genes to a short-sleeper phenotype flows through nerodevelopmental pathways, such that once neural structures are locked-in in adulthood it’s not possible to induce the desired phenotype by mimicking the direct effects of the genes? If this is true, then reaping the benefits of short-sleeper genes would seem to require genetic engineering (I doubt embryo selection would scale given the low frequency of the target alleles). This would obviously be politically problematic and I’m not sure it’d be technically feasible right away (last time I checked, CRISPR people were worried about off-target mutations, but I’m not up to date with that literature so this may not be an issue anymore).
Thanks for posting this! I think this topic is extremely neglected and the lack of side effects among natural short-sleepers strongly suggests that there could be interventions with no obvious downsides.
My main concern with your drug-centered approach is: what if the causal path from short-sleeper genes to a short-sleeper phenotype flows through nerodevelopmental pathways, such that once neural structures are locked-in in adulthood it’s not possible to induce the desired phenotype by mimicking the direct effects of the genes? If this is true, then reaping the benefits of short-sleeper genes would seem to require genetic engineering (I doubt embryo selection would scale given the low frequency of the target alleles). This would obviously be politically problematic and I’m not sure it’d be technically feasible right away (last time I checked, CRISPR people were worried about off-target mutations, but I’m not up to date with that literature so this may not be an issue anymore).