Daylight savings time ends November 4 unless you have CLOCK gene polymorphism rs1801260

For 2007, November 4 is when we (in the US ) set our clocks back an hour so we get an extra hour sleep. But, whether or not you actually go to sleep is another matter. One genetic polymorphism correlates with being a “night owl” as well as other conditions.

Partial eclipse of the moon

As far as standard time, the U.S. Navy Astronomical Applications has an explanation:

Starting in 2007, daylight time begins in the United States on the second Sunday in March and ends on the first Sunday in November. On the second Sunday in March, clocks are set ahead one hour at 2:00 a.m. local standard time, which becomes 3:00 a.m. local daylight time. On the first Sunday in November, clocks are set back one hour at 2:00 a.m. local daylight time, which becomes 1:00 a.m. local standard time. These dates were established by the Energy Policy Act of 2005, Pub. L. no. 109-58, 119 Stat 594 (2005).

Circadian rhythm is pretty much correlated with genetics. (Howard Hughes Medical Institute has a great page of biological clock animations for more explanation.) The CLOCK gene — “Circadian Locomotor Output Cycles Kaput- is one of a number of genes involved with regulating both how long you sleep, but also when you go to sleep, as well as what time of year that happens, and even if you gain weight.

People with a particular polymorphism in one of the genes related to circadian rhythm are more likely to be “night owls” — and one particular polymorphism (rs1801260) is correlated with ADHD, bipolar and moral decision-making in depressed patients. Abstracts below the jump.

Am J Med Genet B Neuropsychiatr Genet. 2007 Oct 18; [Epub ahead of print]
A polymorphism at the 3′-untranslated region of the CLOCK gene is associated with adult attention-deficit hyperactivity disorder.

Kissling C, Retz W, Wiemann S, Coogan AN, Clement RM, Hünnerkopf R, Conner AC, Freitag CM, Rösler M, Thome J.

Department of Psychiatry, Institute of Life Sciences, Swansea University, Swansea, United Kingdom.

Attention-deficit hyperactivity disorder (ADHD) is frequently found in childhood and persists in about 50% of cases into adulthood. Several studies demonstrate a relationship between ADHD, circadian rhythmicity and sleeping disturbances in unmedicated ADHD patients. Since ADHD is a very complex disease with a high genetic load involving multiple genes of moderate effect, we hypothesized a link between adult ADHD and genes involved in the circadian timekeeping system. A 3′-UTR polymorphism of the circadian locomotor output cycles protein kaput (CLOCK) gene, rs1801260, has been linked to disturbed sleep patterns, although both the C-allele and more controversially the T-allele have been proposed as risk factors for different measures of evening preference. This study compared self-rating and interview based measures of ADHD psychopathology of 143 subjects with and without ADHD with their rs1801260 genotype to test the hypothesis that ADHD is linked to one of the alleles of the CLOCK polymorphism. The T > C single nucleotide polymorphism rs1801260 was genotyped in DNA isolated from blood samples. The associations between genotype and ADHD-scores were compared using non-parametric ANCOVA with post hoc pairwise comparisons. There was a strong, significant association (P < 0.001) between each of the adult ADHD assessments and the rs1801260 polymorphism with at least one T-mutation being the risk allele. This is the first study suggesting that a polymorphism of a gene within the circadian “clock” mechanism is a direct or linked contributing factor in adult ADHD. (c) 2007 Wiley-Liss, Inc.

PMID: 17948273 [PubMed - as supplied by publisher]

Genes Brain Behav. 2007 Mar 26; [Epub ahead of print]

Clock genes beyond the clock: CLOCK genotype biases neural correlates of moral valence decision in depressed patients.

Benedetti F, Radaelli D, Bernasconi A, Dallaspezia S, Falini A, Scotti G, Lorenzi C, Colombo C, Smeraldi E.

Department of Neuropsychiatric Sciences, Scientific Institute and University Vita-Salute San Raffaele, Milan, and C.E.R.M.A.C. (Centro di Eccellenza Risonanza Magnetica ad Alto Campo), University Vita-Salute San Raffaele, Milan, Italy.

Gene polymorphisms in the mammalian biological clock system influence individual rhythms. A single nucleotide polymorphism (SNP) in the 3′ flanking region of CLOCK (3111 T/C; rs1801260) influenced diurnal preference in healthy humans and caused sleep phase delay and insomnia in patients affected by bipolar disorder. Genes of the biological clock are expressed in many brain structures other than in the ‘master clock’ suprachiasmatic nuclei. These areas, such as cingulate cortex, are involved in the control of many human behaviors. Clock genes could then bias ‘nonclock’ functions such as information processing and decision making. Thirty inpatients affected by a major depressive episode underwent blood oxygen-level dependent (BOLD) functional magnetic resonance imaging (fMRI). The cognitive activation paradigm was based on a go/no-go task. Morally connoted words were presented. Genotyping of CLOCK was performed for each patients. We measured activity levels through actimetry during the day before the fMRI study. CLOCK 3111 T/C SNP was associated with activity levels in the second part of the day, neuropsychological performance and BOLD fMRI correlates (interaction of genotype and moral valence of the stimuli). Our results support the hypothesis that individual clock genotype may influence several variables linked with human behaviors in normal and psychopathological conditions.

PMID: 17428266 [PubMed - as supplied by publisher]

Am J Med Genet B Neuropsychiatr Genet. 2007 Jul 5;144(5):631-5.

Actimetric evidence that CLOCK 3111 T/C SNP influences sleep and activity patterns in patients affected by bipolar depression.

Benedetti F, Dallaspezia S, Fulgosi MC, Lorenzi C, Serretti A, Barbini B, Colombo C, Smeraldi E.

Department of Neuropsychiatric Sciences, Scientific Institute and University Vita-Salute San Raffaele, Milan, Italy.

Depressive insomnia and diurnal fluctuations of mood and activity are core clinical features of mood disorders. Here we studied the effect of CLOCK 3111 T/C SNP (rs1801260) on the actimetric recorded diurnal activity and nocturnal sleep of 39 bipolar depressed inpatients. Compared to T/T homozygotes, carriers of the C allele had a similar degree of severity of depression, but showed higher activity levels in the evening, a delayed sleep onset (mean 79 min later), and a reduced amount of sleep during the night (mean 75 min less). Ongoing lithium treatment significantly interacted with rs1801260 by enhancing activity levels in the evening and reducing the differences among genotype groups. Individual characteristics of the molecular clock can influence sleep symptoms in mood disorders.

PMID: 17221848 [PubMed - indexed for MEDLINE]