Genetics of Sleep – How much do you need?
Whenever I hear a friend talk about how they only sleep 6 hours a night—I feel a combination of pity (that must be rough) and annoyance (how can they do that to themselves), but reading up on the genetics of sleep maybe I should be feeling jealousy (since I need at least 8 solid hours).
Sleep differences are interesting because they affect our day to day lives, but also are associated with metabolic syndrome (coronary heart disease, stroke, and type-2 diabetes), psychiatric diseases, and fatal car accidents. Further, three in ten American women now take some kind of sleeping aid. Also, because sleep is easily quantified it is also amenable to these kinds of studies.
Recently, the first large-scale GWAS study of the genetics of sleep length was released. It found a significant effect of a common variant the gene ABCC9, which codes SUR2 an ATP-dependent K+ channel. SUR2’s role in sleep seems to have been conserved—knocking out the homologous gene in drosophila decreased the length of their sleep-like nighttime rest. Since SUR2 is also expressed in the heart, it calls into question the causality in the correlation between less sleep and heart disease. Is too little sleep contributing to the disease or is this genetic factor influencing both heart disease and sleep? Also possibly of interest, the study’s second most significant association KCNAB1 also codes for a potassium channel. Its interesting to see channels associated with such a distal function as sleep, I tend to think of them just influencing more proximal to membrane excitability such as epilepsy or reflexes.
Previously, a rare familial variant had been found in DEC2, an HDAC-interacting transcriptional repressor that lowered average sleep times of carriers from 8.06 to 6.25 hours, but as the authors noted, these rare variants are not significant to the population at large. Instead genetic differences in need for sleep will likely be regulated by effects of many common variations such as the ones found in ABCC9, gene x gene interactions, and gene x environment interactions.
Personally, I am interested in the influence of genetics not only to psychiatric disease, but also more subtle influences on personality, intelligence, and general individual differences. At the same time I am wary of overly reductionist genetics, and I think it will be important to always remember confounds —from developmental experiences to all-pervading culture. Luckily, the authors of the study include chronopsychologists (I did not know that was a term), interested in further unmasking affects from nicotine use, latitude and season, early rising larks versus night owls, the differences between sleep loss from work and naturally shorter sleep on weekend. Incidentally, if you sleep 6 hours on weekdays and then 12 on weekends, you are not a genetically short sleeper—try to cut down on afternoon caffeine, and manage your sleep cycle and light exposure better!
I hope that studies will follow up with these cohorts: is there any downside to needing less sleep or do these lucky folks simply get more hours in their days? I’ve heard that couples that go to bed at the same time are more likely to stay together–is the same true for couples that need the same amount of sleep? It’s always frustrating when your partner conks out in the middle of your favorite movie, but I digress.
Are you also interested in the neuroscience of dreams? Check out my post: Scientists record lucid dreams with EEG and fMRI simultaneously
Filed under: Channels, Drosophila, Genetics, Human, Metabolic Syndrome, Molecular, Public Health, Sleep | 1 Comment
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I wouldn’t say the relation between channels and sleep is distal as ATP-dependent channels are involved in AMPK activation, respectively eNOS and eHIF-1a (hypoxia), lowered core body temperature, adenosine output. Having in mind recent studies identifying adenosine and melatonin (both with core body temperature lowering effect) as major regulators of sleep behavior, it makes perfect sense.
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