Trouble falling asleep at night? Chase that daytime light, study shows
IMAGE: AN OVERCAST DECEMBER DAY ON THE UNIVERSITY OF WASHINGTON CAMPUS IN SEATTLE. view more
CREDIT: UNIVERSITY OF WASHINGTON
(Note: researcher contact information at the end)
A study measuring the sleep patterns of students at the University of Washington has turned up some surprises about how and when our bodies tell us to sleep — and illustrates the importance of getting outside during the day, even when it’s cloudy.
Published online Dec. 7 in the Journal of Pineal Research, the study found that UW students fell asleep later in the evening and woke up later in the morning during — of all seasons — winter, when daylight hours on the UW’s Seattle campus are limited and the skies are notoriously overcast.
The team behind this study believes it has an explanation: The data showed that in winter students received less light exposure during the day. Other research has indicated that getting insufficient light during the day leads to problems at night, when it’s time for bed.
“Our bodies have a natural circadian clock that tells us when to go to sleep at night,” said senior author Horacio de la Iglesia, a UW professor of biology. “If you do not get enough exposure to light during the day when the sun is out, that ‘delays’ your clock and pushes back the onset of sleep at night.”
The study used wrist monitors to measure sleep patterns and light exposure for 507 UW undergraduate students from 2015 to 2018. Data indicated that students were getting roughly the same amount of sleep each night regardless of season. But, on school days during the winter, students were going to bed on average 35 minutes later and waking up 27 minutes later than summer school days. This finding surprised the team, since Seattle — a high-latitude city — receives nearly 16 hours of sunlight on the summer solstice, with plenty evening light for social life, and just over eight hours of sunlight on the winter solstice.
“We were expecting that in the summer students would be up later due to all the light that’s available during that season,” said de la Iglesia.
Based on student sleep data, the researchers hypothesized that something in winter was “pushing back” the students’ circadian cycles. For most humans, including college students, the innate circadian cycle governing when we’re awake and asleep runs at about 24 hours and 20 minutes — and is “calibrated” daily by input from our environment. For UW students in the study, sleep data indicated that their circadian cycles were running up to 40 minutes later in winter compared to summer.
The team focused on light as a potential explanation for this winter delay. But light has different impacts on circadian rhythms at different times of the day.
“Light during the day — especially in the morning — advances your clock, so you get tired earlier in the evening, but light exposure late in the day or early night will delay your clock, pushing back the time that you will feel tired,” said de la Iglesia. “Ultimately, the time that you fall asleep is a result of the push and pull between these opposite effects of light exposure at different times of the day.”
Data showed that daytime light exposure had a greater impact than evening light exposure in the UW study. Each hour of daytime light “moved up” the students’ circadian phases by 30 minutes. Even outdoor light exposure on cloudy or overcast winter days in Seattle had this effect, since that light is still significantly brighter than artificial indoor lighting, said de la Iglesia. Each hour of evening light — light from indoor sources like lamps and computer screens — delayed circadian phases by an average of 15 minutes.
“It’s that push-and-pull effect,” said de la Iglesia. “And what we found here is that since students weren’t getting enough daytime light exposure in the winter, their circadian clocks were delayed compared to summer.”
The study offers lessons not just for college students.
“Many of us live in cities and towns with lots of artificial light and lifestyles that keep us indoors during the day,” said de la Iglesia. “What this study shows is that we need to get out — even for a little while and especially in the morning — to get that natural light exposure. In the evening, minimize screen time and artificial lighting to help us fall asleep.”
Lead author on the paper is Gideon Dunster, an associate manager with the Allen Institute for Cell Science, who conducted the study as a UW doctoral student. Co-authors are UW undergraduate alum Isabelle Hua, now a researcher at the National Institute of Neurological Disorders and Stroke; Alex Grahe in the UW Department of Biology; Jason Fleischer and Satchidananda Panda of the Salk Institute; Kenneth Wright and Céline Vetter of the University of Colorado, Boulder; and UW teaching professor of biology Jennifer Doherty. The research was funded by the National Science Foundation. Dunster was supported by the Riddiford-Truman Fellowship and the Hoag Endowed Graduate Fellowship through the UW Department of Biology.
###
For more information, contact Horacio de la Iglesia at horaciod@uw.edu.
Grant number: 1743364
JOURNAL
Journal of Pineal Research
METHOD OF RESEARCH
Observational study
SUBJECT OF RESEARCH
People
ARTICLE TITLE
Daytime light exposure is a strong predictor of seasonal variation in sleep and circadian timing of university students
ARTICLE PUBLICATION DATE
7-Dec-2022
COI STATEMENT
Co-author Kenneth P. Wright (University of Colorado, Boulder) reports research support/donated materials: DuPont Nutrition & Biosciences, Grain Processing Corporation, and Friesland Campina Innovation Centre and being a consultant to and/or receiving personal fees from Circadian Therapeutics, Inc., Circadian Biotherapies, Inc., Philips, Inc, and U.S. Army Medical Research and Materiel Command - Walter Reed Army Institute of Research, outside the submitted work.
Unravelling the secrets of a good night's sleep
Researchers from the University of Tsukuba identify a signaling pathway within brain cells that regulates how long and how deeply we sleep
Peer-Reviewed PublicationTsukuba, Japan—A good night's sleep can work wonders for both mind and body. But what is it that determines how much we need to sleep, and what can cause us to sleep more deeply?
In a new study, researchers from the University of Tsukuba have now provided some answers, revealing a signaling pathway within brain cells that regulates the length and depth of sleep.
"We examined genetic mutations in mice and how these affect their patterns of sleep," says senior author of the study, Professor Hiromasa Funato. "We identified a mutation that led to the mice sleeping much longer and more deeply than usual." The researchers found that this was caused by low levels of an enzyme called histone deacetylase 4 (HDAC4), which is known to suppress the expression of target genes.
Previous studies on HDAC4 have shown that it is greatly affected by the attachment of phosphate molecules in a process known as phosphorylation. When this occurs, HDAC4 tends to move away from the cell nucleus, and the suppression of certain proteins is reduced. The researchers were interested in whether this phosphorylation of HDAC4 would affect sleep.
"We focused on a protein called salt-inducible kinase 3, otherwise known as SIK3, which phosphorylates HDAC4," says Professor Funato. "We previously found that this protein has strong effects on sleep." The team found that when there was a lack of SIK3 or when HDAC4 was modified to prevent phosphorylation, the mice slept less. In contrast, when the mice had a more active version of SIK3, which increased the phosphorylation of HDAC4, they slept a lot more. They also identified a further protein, LKB1, which phosphorylates SIK3, and has similar sleep-suppressing effects when deficient.
"Our findings indicate that there is a signaling pathway within brain cells from LKB1 to SIK3 and then to HDAC4," says study co-senior author, Professor Masashi Yanagisawa. "This pathway leads to the phosphorylation of HDAC4, which promotes sleep, most probably because it affects the expression of sleep-promoting genes."
The team carried out further experiments to identify the brain cells in which these pathways regulate sleep. This involved altering the amounts of SIK3 and HDAC4 in different cell types and brain regions. The results indicated that signaling within the cells of the cortex regulates the depth of sleep, while signaling within the hypothalamus regulates the amount of deep sleep. For both brain regions, the excitatory neurons, which can activate other neurons, were identified as playing a key role.
These results provide an important insight into how sleep is regulated, which could potentially lead to a greater understanding of sleep disorders as well as the development of new treatments.
###
This work was supported by the World Premier International Research Center Initiative from MEXT, JSPS KAKENHI, JST CREST, AMED, JSPS DC2, University of Tsukuba Basic Research Support Program Type A, Funding Program for World-Leading Innovative R&D on Science and Technology (FIRST Program).
Original Paper
The article, "Kinase signalling in excitatory neurons regulates sleep quantity and depth," was published in Nature at DOI: 10.1038/s41586-022-05450-1
Correspondence
Professor and Director YANAGISAWA Masashi
International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba
Professor / Visiting Professor FUNATO Hiromasa
Department of Anatomy, Graduate School of Medicine, Toho University / International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba
Related Link
International Institute for Integrative Sleep Medicine (WPI-IIIS)
JOURNAL
Nature
ARTICLE TITLE
Kinase signalling in excitatory neurons regulates sleep quantity and depth
ARTICLE PUBLICATION DATE
7-Dec-2022
No comments:
Post a Comment