6 research outputs found
Habitual sleep disturbances and migraine: a Mendelian randomization study
OBJECTIVE: Sleep disturbances are associated with increased risk of migraine, however the extent of shared underlying biology and the direction of causal relationships between these traits is unclear. Delineating causality between sleep patterns and migraine may offer new pathophysiologic insights and inform subsequent intervention studies. Here, we used genetic approaches to test for shared genetic influences between sleep patterns and migraine, and to test whether habitual sleep patterns may be causal risk factors for migraine and vice versa. METHODS: To quantify genetic overlap, we performed genome-wide genetic correlation analyses using genome-wide association studies of nine sleep traits in the UK Biobank (n ≥ 237,627), and migraine from the International Headache Genetics Consortium (59,674 cases and 316,078 controls). We then tested for potential causal effects between sleep traits and migraine using bidirectional, two-sample Mendelian randomization. RESULTS: Seven sleep traits demonstrated genetic overlap with migraine, including insomnia symptoms (rg = 0.29, P < 10-31 ) and difficulty awakening (rg = 0.11, P < 10-4 ). Mendelian randomization analyses provided evidence for potential causal effects of difficulty awakening on risk of migraine (OR [95% CI] = 1.37 [1.12-1.68], P = 0.002), and nominal evidence that liability to insomnia symptoms increased the risk of migraine (1.09 [1.02-1.16], P = 0.02). In contrast, there was minimal evidence for an effect of migraine liability on sleep patterns or disturbances. INTERPRETATION: These data support a shared genetic basis between several sleep traits and migraine, and support potential causal effects of difficulty awakening and insomnia symptoms on migraine risk. Treatment of sleep disturbances may therefore be a promising clinical intervention in the management of migraine
Leptin and hunger levels in young healthy adults after one night of sleep loss
P>Short-term sleep curtailment associated with activation of the stress
system in healthy, young adults has been shown to be associated with
decreased leptin levels, impaired insulin sensitivity, and increased
hunger and appetite. To assess the effects of one night of sleep loss in
a less stressful environment on hunger, leptin, adiponectin, cortisol
and blood pressure/heart rate, and whether a 2-h mid-afternoon nap
reverses the changes associated with sleep loss, 21 young healthy
individuals (10 men, 11 women) participated in a 7-day sleep deprivation
experiment (four consecutive nights followed by one night of sleep loss
and two recovery nights). Half of the subjects were randomly assigned to
take a mid-afternoon nap (14:00-16:00 hours) the day following the night
of total sleep loss. Serial 24-h blood sampling and hunger scales were
completed on the fourth (predeprivation) and sixth day
(postdeprivation). Leptin levels were significantly increased after one
night of total sleep loss, whereas adiponectin, cortisol levels, blood
pressure/heart rate, and hunger were not affected. Daytime napping did
not influence the effects of sleep loss on leptin, adiponectin, or
hunger. Acute sleep loss, in a less stressful environment, influences
leptin levels in an opposite manner from that of short-term sleep
curtailment associated with activation of the stress system. It appears
that sleep loss associated with activation of the stress system but not
sleep loss per se may lead to increased hunger and appetite and hormonal
changes, which ultimately may lead to increased consumption of ‘comfort’
food and obesity
Habitual sleep disturbances and migraine : a Mendelian randomization study
OBJECTIVE: Sleep disturbances are associated with increased risk of migraine, however the extent of shared underlying biology and the direction of causal relationships between these traits is unclear. Delineating causality between sleep patterns and migraine may offer new pathophysiologic insights and inform subsequent intervention studies. Here, we used genetic approaches to test for shared genetic influences between sleep patterns and migraine, and to test whether habitual sleep patterns may be causal risk factors for migraine and vice versa. METHODS: To quantify genetic overlap, we performed genome-wide genetic correlation analyses using genome-wide association studies of nine sleep traits in the UK Biobank (n ≥ 237,627), and migraine from the International Headache Genetics Consortium (59,674 cases and 316,078 controls). We then tested for potential causal effects between sleep traits and migraine using bidirectional, two-sample Mendelian randomization. RESULTS: Seven sleep traits demonstrated genetic overlap with migraine, including insomnia symptoms (rg = 0.29, P < 10-31 ) and difficulty awakening (rg = 0.11, P < 10-4 ). Mendelian randomization analyses provided evidence for potential causal effects of difficulty awakening on risk of migraine (OR [95% CI] = 1.37 [1.12-1.68], P = 0.002), and nominal evidence that liability to insomnia symptoms increased the risk of migraine (1.09 [1.02-1.16], P = 0.02). In contrast, there was minimal evidence for an effect of migraine liability on sleep patterns or disturbances. INTERPRETATION: These data support a shared genetic basis between several sleep traits and migraine, and support potential causal effects of difficulty awakening and insomnia symptoms on migraine risk. Treatment of sleep disturbances may therefore be a promising clinical intervention in the management of migraine.publishedVersionPeer reviewe
Habitual sleep disturbances and migraine : a Mendelian randomization study
Ville Artto työryhmän jäsenenäObjective Sleep disturbances are associated with increased risk of migraine, however the extent of shared underlying biology and the direction of causal relationships between these traits is unclear. Delineating causality between sleep patterns and migraine may offer new pathophysiologic insights and inform subsequent intervention studies. Here, we used genetic approaches to test for shared genetic influences between sleep patterns and migraine, and to test whether habitual sleep patterns may be causal risk factors for migraine and vice versa. Methods To quantify genetic overlap, we performed genome-wide genetic correlation analyses using genome-wide association studies of nine sleep traits in the UK Biobank (n >= 237,627), and migraine from the International Headache Genetics Consortium (59,674 cases and 316,078 controls). We then tested for potential causal effects between sleep traits and migraine using bidirectional, two-sample Mendelian randomization. Results Seven sleep traits demonstrated genetic overlap with migraine, including insomnia symptoms (rg = 0.29, P <10(-31)) and difficulty awakening (rg = 0.11, P <10(-4)). Mendelian randomization analyses provided evidence for potential causal effects of difficulty awakening on risk of migraine (OR [95% CI] = 1.37 [1.12-1.68], P = 0.002), and nominal evidence that liability to insomnia symptoms increased the risk of migraine (1.09 [1.02-1.16], P = 0.02). In contrast, there was minimal evidence for an effect of migraine liability on sleep patterns or disturbances. Interpretation These data support a shared genetic basis between several sleep traits and migraine, and support potential causal effects of difficulty awakening and insomnia symptoms on migraine risk. Treatment of sleep disturbances may therefore be a promising clinical intervention in the management of migraine.Peer reviewe