Abstract
Sleeping 7 to 8 hours per night appears to be optimal, since both shorter and longer sleep times are related to increased morbidity and mortality. Depressive disorder is almost invariably accompanied by disturbed sleep, leading to decreased sleep duration, and disturbed sleep may be a precipitating factor in the initiation of depressive illness. Here, we examined whether, in healthy individuals, sleep duration is associated with genes that we earlier found to be associated with depressive disorder. Population-based molecular genetic study. Regression analysis of 23 risk variants for depressive disorder from 12 genes to sleep duration in healthy individuals. Three thousand, one hundred, forty-seven individuals (25-75 y) from population-based Health 2000 and FINRISK 2007 samples. We found a significant association of rs687577 from GRIA3 on the X-chromosome with sleep duration in women (permutation-based corrected empirical P=0.00001, β=0.27; Bonferroni corrected P=0.0052; f=0.11). The frequency of C/C genotype previously found to increase risk for depression in women was highest among those who slept for 8 hours or less in all age groups younger than 70 years. Its frequency decreased with the lengthening of sleep duration, and those who slept for 9 to 10 hours showed a higher frequency of C/A or A/A genotypes, when compared with the midrange sleepers (7-8 hours) (permutation-based corrected empirical P=0.0003, OR=1.81). The GRIA3 polymorphism that was previously found to be associated with depressive disorder in women showed an association with sleep duration in healthy women. Mood disorders and short sleep may share a common genetic background and biologic mechanisms that involve glutamatergic neurotransmission.
Highlights
Sleep is an important contributor to our general health and well-being
We examined 23 single nucleotide polymorphisms (SNPs) (Supplementary Table S1) from 12 genes; tryptophan hydroxylase 2 (TPH2), solute carrier family 6, member 4 (SLC6A4), GRIA3, disrupted in schizophrenia 1 (DISC1), brain-derived neurotrophic factor (BDNF), corticotropin releasing hormone receptor 1 (CRHR1), neuronal PAS domain protein 2 (NPAS2), nuclear factor, interleukin 3 regulated (NFIL3), aryl hydrocarbon receptor nuclear translocator-like (ARNTL), aryl hydrocarbon receptor nuclear translocator-like 2 (ARNTL2), TIMELESS, and RAR-related orphan receptor A (RORA)
Out of variants from the 12 candidate genes that had been identified in our previous studies,[26,27] GRIA3, encoding for inotorphic glutamatergic receptor, associated strongly with sleep duration in healthy females
Summary
Sleeping from 7 to 8 hours per night is considered optimal for health, since, in cross-sectional studies, both shorter and longer sleep have been related to poor health outcomes, including obesity, heart disease, neuroticism, anxiety, and death,[1,2,3,4,5,6,7] as well as, in prospective studies, to increased morbidity and mortality.[8,9,10] Both short and long sleep are common; according to a crosssectional population-based study conducted in the United States, 28.3% of the respondents reported having a sleep duration of 6 hours or less, whereas 8.5% reported sleep durations of 9 hours or more.[11] The prevalence of short sleepers (≤ 6 hours) in the Finnish adult population has been estimated to be 14.5% (16.7% of men and 12.5% of women) and that of long sleepers (≥ 9 hours) to be 13.5% (10.5% of men and 16.1% of women).[12] The proportion of both long and short sleepers appears to be relatively stable, even when the average sleep. Many of these features have a strong genetic component; for example, the heritability of EEG power spectrum in non-rapid eye movement (NREM) sleep has been found to be as high as 96%.17 According to twin studies in Finland and Australia, even self-reported sleep duration has a relatively high heritability estimate: 44% and 33%, respectively.[18,19]
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