Thank you very much for the high-effort post and the significant findings. I agree this seems to be strong evidence that the DEC2, ADRB1, and GRM1 mutations don’t work as expected in the general population. That is disappointing. A couple of questions:
How do you explain the study results that those mutations do cause shorter sleep in mice? Are those studies flawed? Or is it just luck that we’ve found several mutations that affect mice, but don’t affect humans? (Or maybe they only work in the presence of additional mutations?)
In this Mormon family, a father and 5 of his 8 children (some male, some female) seem to be short sleepers, which looks like an autosomal dominant inheritance pattern… though, looking at the next generation, it seems that the short sleepers Brad and Janice had 8 and 4 children respectively, none of which were short sleepers, while short sleeper Paul had 2 children who are short sleepers. (I hope there is more complete information somewhere. I suspect they’re the ADRB1 family, because of (a) the number of people reported and (b) the names Jones and Fu on the ADRB1 paper, who are also quoted in the article.)
How do we explain this? My brain generates “ADRB1 (or something correlated with it) works, but it requires extra mutations to work (or, similarly, there are some mutations common in the population that stop it from working); Paul married someone with concordant mutations, Brad and Janice married people with discordant mutations”. Does that seem likely, or do you have other explanations in mind?
Thank you very much for the high-effort post and the significant findings. I agree this seems to be strong evidence that the DEC2, ADRB1, and GRM1 mutations don’t work as expected in the general population. That is disappointing. A couple of questions:
How do you explain the study results that those mutations do cause shorter sleep in mice? Are those studies flawed? Or is it just luck that we’ve found several mutations that affect mice, but don’t affect humans? (Or maybe they only work in the presence of additional mutations?)
In this Mormon family, a father and 5 of his 8 children (some male, some female) seem to be short sleepers, which looks like an autosomal dominant inheritance pattern… though, looking at the next generation, it seems that the short sleepers Brad and Janice had 8 and 4 children respectively, none of which were short sleepers, while short sleeper Paul had 2 children who are short sleepers. (I hope there is more complete information somewhere. I suspect they’re the ADRB1 family, because of (a) the number of people reported and (b) the names Jones and Fu on the ADRB1 paper, who are also quoted in the article.)
How do we explain this? My brain generates “ADRB1 (or something correlated with it) works, but it requires extra mutations to work (or, similarly, there are some mutations common in the population that stop it from working); Paul married someone with concordant mutations, Brad and Janice married people with discordant mutations”. Does that seem likely, or do you have other explanations in mind?