Adolescents who meet the recommended guidelines of nine to 11 hours of sleep per day were shown to have a significantly lower risk of hypertension, according to a new study from UTHealth Houston.
Recently published in the Journal of the American Heart Association, the research revealed that adolescents had a 37% lower risk of developing incidents of high blood pressure by meeting healthy sleep patterns, and underscoring the importance of adequate sleep behaviour. The research further explored the impact of environmental factors potentially impacting sleep.
“Disrupted sleep can lead to changes in the body’s stress response, including elevated levels of stress hormones like cortisol, which in turn can increase blood pressure,” said first author Augusto César Ferreira De Moraes, PhD, assistant professor in the Department of Epidemiology at UTHealth Houston School of Public Health.
De Moraes and his team analysed data from 3320 adolescents across the US to investigate incidents of high blood pressure during nighttime sleep cycles. Scientists identified a rise in hypertension incidents over two data periods, 2018-2020 and 2020-2022, showing an increase from 1.7% to 2.9%. The data included blood pressure readings and Fitbit assessments, which measured total sleep time and REM sleep duration at night. The study’s design analysed covariates such as Fitbit-tracked sleep, blood pressure, and neighbourhood noise by residential geocodes, allowing for a thorough examination of environmental noise exposure for each participant.
Neighbourhood/community noise was not significantly associated with the incidence of hypertension. Environmental factors, such as neighbourhood noise, point to the need for longer-term studies to investigate the relationship between sleep health and hypertension, particularly in relation to socioeconomic status, stress levels, and genetic predispositions.
The study emphasises the importance of improved sleep behaviours and meeting recommendations. “Consistent sleep schedules, minimising screen time before bed, and creating a calm, quiet sleep environment can all contribute to better sleep quality,” advises Martin Ma, MPH, second author of the study and recent graduate of the school. “Although environmental noise didn’t directly affect hypertension in this study, maintaining a quiet and restful sleep environment is still important for overall well-being.”
Research by scientists at the University of Sydney has identified cannabinol (CBN), a constituent in the cannabis plant that improves sleep. Their report is the first to use objective measures to show that (CBN), while not intoxicating, does increase sleep in rats. The study, which has been published in the leading journal Neuropsychopharmacology, found that CBN was comparable in efficacy to zolpidem.
“Our study provides the first objective evidence that CBN increases sleep, at least in rats, by modifying the architecture of sleep in a beneficial way.”
CBN is an end-product of the main intoxicating constituent of cannabis, delta9-tetrahydrocannabinol (THC). THC in cannabis is slowly converted to CBN over time, which means older cannabis contains higher levels of this compound. It has been suggested that the consumption of older cannabis is associated with a sleepier cannabis “high”.
In the United States, highly purified CBN products are being sold as sleep aids, but there has been little high-quality scientific evidence to support this application.
The research team at the Lambert Initiative for Cannabinoid Therapeutics tested the effects of purified CBN on sleep in rats. Using high-tech monitoring, the experiments provided insights into the rats’ sleep patterns including the amount of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep.
NREM is deep sleep that promotes physical recovery and strengthens memories, while REM sleep is associated with dreaming and processing of emotions.
Professor Arnold said: “CBN was found to increase both NREM and REM sleep, leading to increased total sleep time, with a comparable effect to the known sleep drug zolpidem.”
Non-intoxicating
Unlike its parent molecule THC, CBN did not appear to intoxicate rats. THC intoxicates by activating CB1 cannabinoid receptors, which are present in the brain. The study showed that unlike THC, CBN only weakly activates these receptors. To their surprise, the researchers found that a metabolite of CBN had significant effects on cannabinoid CB1 receptors.
A metabolite is a chemical produced via the metabolism of a larger molecule in the body.
They also found that the 11-OH CBN metabolite had some impact on sleep architecture, which might contribute to the overall effects of CBN on sleep.
“This provides the first evidence that CBN indeed increases sleep using objective sleep measures. It was a surprise that CBN metabolism in the body can yield a much greater effect on cannabinoid CB1 receptors than the parent molecule CBN, which has much more limited activity,” Professor Arnold said.
“At this stage our results are confined to testing in rats. Further research is needed to see if this translates to humans.”
Further study
In a parallel study, yet to be published, Professor Iain McGregor, Director of Clinical Research at the Lambert Initiative, initiated a placebo-controlled randomised human clinical trial in insomnia patients. This was led by PhD student Isobel Lavender with leading sleep researcher Dr Camilla Hoyos from the Woolcock Institute of Medical Research. The trial has now been completed with very promising results that were recently announced at the International Cannabinoid Research Society and Sleep DownUnder scientific conferences.
“Our research encourages further basic and clinical research on CBN as a new treatment strategy for sleep disorders, including insomnia. Our clinical study only administered CBN on a single occasion. A trial on a larger scale, that includes repeated dosing, is the logical next step,” Professor McGregor said.
Professor Arnold said: “The team has now commenced a preclinical drug discovery program around CBN, as well as observing whether the pro-sleep effects of CBN can be further amplified by other molecules found in cannabis, or by conventional sleep aids, such as melatonin.”
A heart attack can trigger a desire to get more sleep, allowing the heart to heal and reduce inflammation as a result of the heart’s special signals to the brain, according to a new Mount Sinai study. This is the first study showing how the heart and brain communicate via the immune system to promote sleep and recovery after a major cardiovascular event.
The novel findings, published in Nature, highlight the importance of increased sleep after a heart attack, and suggest that sufficient sleep should be a focus of post-heart-attack clinical management and care, including in intensive care, where sleep is frequently disrupted, along with cardiac rehabilitation.
“This study is the first to demonstrate that the heart regulates sleep during cardiovascular injury by using the immune system to signal to the brain. Our data show that after a myocardial infarction (heart attack) the brain undergoes profound changes that augment sleep, and that in the weeks following a myocardial infarction, sleep abundance and drive is increased,” says senior author Cameron McAlpine, PhD, Assistant Professor of Medicine (Cardiology), and Neuroscience, at the Icahn School of Medicine at Mount Sinai. “We found that neuro-inflammation and the recruitment of immune cells called monocytes to the brain after a myocardial infarction is a beneficial and adaptive response that increases sleep to enable heart healing and the reduction of damaging cardiac inflammation.”
The researchers from the Cardiovascular Research Institute at Icahn Mount Sinai first used mouse models to discover this phenomenon. They induced heart attacks in half of the mice and performed high-resolution imaging and cell analysis, and used implantable wireless electroencephalogram devices to record electrical signals from their brains and analyse sleep patterns. After the heart attack, they found a three-fold increase in slow-wave sleep, a deep stage of sleep characterized by slow brain waves and reduced muscle activity. This increase in sleep occurred quickly after the heart attack and lasted one week.
When the researchers studied the brains of the mice with heart attacks, they found that immune cells called monocytes were recruited from the blood to the brain and used a protein called tumour necrosis factor (TNF) to activate neurons in an area of the brain called the thalamus, which caused the increase in sleep. This happened within hours after the cardiac event, and none of this occurred in the mice that did not have heart attacks.
The researchers then used sophisticated approaches to manipulate neuron TNF signaling in the thalamus and uncovered that the sleeping brain uses the nervous system to send signals back to the heart to reduce heart stress, promote healing, and decrease heart inflammation after a heart attack. To further identify the function of increased sleep after a heart attack, the researchers also interrupted the sleep of some of the mice. The mice with sleep disruption after a heart attack had an increase in heart sympathetic stress responses and inflammation, leading to slower recovery and healing when compared to mice with undisrupted sleep.
The research team also performed several human studies. The first studied the brains of patients 1–2 days after a heart attack and found an increase in monocytes compared to people without a heart attack or other CVD, mirroring the mice findings. The next analysed the sleep of more than 80 heart attack patients during the four weeks post-event and followed them for two years. The patients were divided into good sleepers and poor sleepers based on the quality of their sleep during the four weeks post-heart attack. The poor sleepers had a worse prognosis; their risk of having another cardiovascular event was twice as high as good sleepers. Additionally, the good sleepers had a significant improvement in heart function while poor sleepers had no or little improvement.
In another human study, the researchers analysed the impact of five weeks of restricted sleep in 20 healthy adults. Sleep was monitored using electronic devices and the participants kept a sleep diary. During the five-week study period, half the participants slept for the recommended seven to eight hours a night uninterrupted, while the other half restricted their sleep by 1.5 hours each night – either delaying bedtime or waking up early. After the study period, researchers analysed blood monocytes and found similar sympathetic stress signaling and inflammatory responses in the sleep-restricted group as those that were identified in mice.
The British Sleep Society has released a position statement in the Journal of Sleep Research advocating for the abolition of the twice-yearly clock changes in the UK and the restoration of permanent Standard Time (Greenwich Mean Time). This recommendation is based on scientific evidence highlighting the adverse effects of the clock change and Daylight Saving Time (DST) on sleep and circadian health.
The British Sleep Society emphasises that sleep is central to health and well-being and the enforced changes of clock time to DST can interfere negatively with sleep regulation. “What we often don’t realise is that DST changes our schedules, moving them forward by one hour while daylight remains the same. DST forces us all to get up and go to work or school one hour earlier, often in the dark,” said co-author Eva Winnebeck, PhD, of the University of Surrey. The Society stresses that natural daylight in the morning is crucial for maintaining an alignment of our body clocks with day and night, which is essential for optimal sleep and overall health.
“Some people even advocate switching to DST all year around. We think this is misguided, because it would leave us with dark mornings during the winter, and morning light is critically important for keeping our body clocks synchronized,” says coauthor Malcolm von Schantz, PhD, of Northumbria University.
Other sleep societies have also argued against year-round DST and advocate for the return to year-round Standard Time, but this position statement is the first published UK perspective. “The unique location and orientation of our UK landmass needs to be considered because permanent DST would over-disadvantage people west and north of London,” said first author Megan Crawford, PhD, of the University of Strathclyde.
A team of scientists in Singapore and the US uncovered how a protein that controls our biological clock modifies its own function, offering new ways for treating jet lag and seasonal adjustments
Scientists from Duke-NUS Medical School and the University of California, Santa Cruz, have discovered the secret to regulating our internal clock. They identified that this regulator sits right at the tail end of Casein Kinase 1 delta (CK1δ), a protein which acts as a pace setter for our internal biological clock or the natural 24-hour cycles that control sleep-wake patterns and other daily functions, known as circadian rhythm.
Published in the journal PNAS, their findings could lead to new treatments for circadian rhythm disorders.
CK1δ regulates circadian rhythms by tagging other proteins involved in circadian rhythm to fine-tune the timing of these rhythms. In addition to modifying other proteins, CK1δ itself can be tagged, thereby altering its own ability to regulate the proteins involved in running the body’s internal clock.
Previous research identified two distinct versions of CK1δ, known as isoforms δ1 and δ2, which vary by just 16 building blocks or amino acids right at the end of the protein in a part called the C-terminal tail. Yet these small differences significantly impact CK1δ’s function. While it was known that when these proteins are tagged, their ability to regulate the body clock decreases, no one knew exactly how this happened.
Using advanced spectroscopy and spectrometry techniques to zoom in on the tails, the researchers found that how the proteins are tagged is determined by their distinct tail sequences.
Professor Carrie Partch at the University of California, Santa Cruzand corresponding author of the study explained:
“Our findings pinpoint to three specific sites on CK1δ’s tail where phosphate groups can attach, and these sites are crucial for controlling the protein’s activity. When these spots get tagged with a phosphate group, CK1δ becomes less active, which means it doesn’t influence our circadian rhythms as effectively. Using high-resolution analysis, we were able to pinpoint the exact sites involved—and that’s really exciting.”
Having first studied this protein more than 30 years ago while investigating its role in cell division, Professor David Virshup, the director of the Cancer and Stem Cell Biology Programme at Duke-NUS and co-corresponding author of the study, elaborated:
“With the technology we have available now, we were finally able to get to the bottom of a question that has gone unanswered for more than 25 years. We found that the δ1 tail interacts more extensively with the main part of the protein, leading to greater self-inhibition compared to δ2. This means that δ1 is more tightly regulated by its tail than δ2. When these sites are mutated or removed, δ1 becomes more active, which leads to changes in circadian rhythms. In contrast, δ2 does not have the same regulatory effect from its tail region.”
This discovery highlights how a small part of CK1δ can greatly influence its overall activity. This self-regulation is vital for keeping CK1δ activity balanced, which, in turn, helps regulate our circadian rhythms.
The study also addressed the wider implications of these findings. CK1δ plays a role in several important processes beyond circadian rhythms, including cell division, cancer development, and certain neurodegenerative diseases. By better understanding how CK1δ’s activity is regulated, scientists could open new avenues for treating not just circadian rhythm disorders but also a range of conditions.
The researchers plan to further investigate how real-world factors, such as diet and environmental changes, affect the tagging sites on CK1δ. This could provide insights into how these factors affect circadian rhythms and might lead to practical solutions for managing disruptions.
The demands of the working week, often influenced by school or work schedules, can lead to sleep disruption and deprivation. Fortunately, new research presented at ESC Congress 2024 shows that people that ‘catch up’ on their sleep by sleeping in at weekends may see their risk of heart disease fall by one-fifth.
“Sufficient compensatory sleep is linked to a lower risk of heart disease,” said study co-author Mr Yanjun Song of the State Key Laboratory of Infectious Disease, Fuwai Hospital, National Centre for Cardiovascular Disease, Beijing, China. “The association becomes even more pronounced among individuals who regularly experience inadequate sleep on weekdays.”
It is well known that people who suffer sleep deprivation ‘sleep in’ on days off to mitigate the effects of sleep deprivation. However, there is a lack of research on whether this compensatory sleep helps heart health.
The authors used data from 90 903 subjects involved in the UK Biobank project, and to evaluate the relationship between compensated weekend sleep and heart disease, sleep data was recorded using accelerometers and grouped by quartiles (divided into four approximately equal groups from most compensated sleep to least). Q1 (n = 22 475 was the least compensated, having -16.05 hours to -0.26 hours (ie, having even less sleep); Q2 (n = 22 901) had -0.26 to +0.45 hours; Q3 (n=22 692) had +0.45 to +1.28 hours, and Q4 (n=22 695) had the most compensatory sleep (1.28 to 16.06 hours).
Sleep deprivation was self-reported, with those self-reporting less than 7 hours sleep per night defined as having sleep deprivation. A total of 19 816 (21.8%) of participants were defined as sleep deprived. The rest of the cohort may have experienced occasional inadequate sleep, but on average, their daily hours of sleep did not meet the criteria for sleep deprivation – the authors recognise this a limitation to their data.
Hospitalisation records and cause of death registry information were used to diagnose various cardiac diseases including ischaemic heart disease (IHD), heart failure (HF), atrial fibrillation (AF), and stroke.
With a median follow-up of almost 14 years, participants in the group with the most compensatory sleep (quartile 4) were 19% less likely to develop heart disease than those with the least (quartile 1). In the subgroup of patients with daily sleep deprivation those with the most compensatory sleep had a 20% lower risk of developing heart disease than those with the least. The analysis did not show any differences between men and women.
Co-author Mr Zechen Liu, also of State Key Laboratory of Infectious Disease, Fuwai Hospital, National Centre for Cardiovascular Disease, Beijing, China, added: “Our results show that for the significant proportion of the population in modern society that suffers from sleep deprivation, those who have the most ‘catch-up’ sleep at weekends have significantly lower rates of heart disease than those with the least.”
A good night’s sleep is essential for children’s health and development, but childhood sleep patterns may also be linked to future substance use. A new study, led by a team of Penn State researchers, found that adolescents were more likely to have consumed alcohol or tried marijuana by age 15 if they went to bed later and slept fewer hours during childhood and adolescence. The team published their findings in Annals of Epidemiology.
“The study suggests that there might be some critical ages when sleep can be a target for intervention,” said Anne-Marie Chang, associate professor of biobehavioural health at Penn State and senior author of the paper. “If we improve sleep in the school-age population, not only could that show improvements in sleep health but in other aspects like the decision to engage in risky behaviours like alcohol and other substance use.”
The research team explored childhood sleep at different developmental stages within the same sample of children to see if there’s an impact on later substance use, which few studies have investigated. They focused on two different facets of sleep health – total duration of sleep and time of sleep or bedtime. The researchers explained that if children, especially school-aged children, go to bed later, it could affect their ability to sleep well.
“Sleep is multifaceted. It’s important for children because it helps with growth and development. The brain is more plastic during younger ages and you want healthy sleep to support neural development,” said David Reichenberger, co-lead author and who earned his doctoral degree in biobehavioural health at Penn State during the time of the research. “Poor sleep health could have downstream effects on their physical health as well as decision making, which could in turn be related to their decision to engage in substance use.”
The study drew on data from 1514 children in the Future of Families and Child Wellbeing Study, a diverse longitudinal birth cohort of children from 20 cities across the United States. Parents reported their child’s regular weekday bedtime at ages three, five and nine. They also reported their child’s sleep duration at ages five and nine.
When the research team evaluated the relationship between childhood bedtime and sleep duration with future alcohol and marijuana use as teens, they found a longitudinal association. Teens were 45% more likely to try alcohol by age 15 if they had a later bedtime at age nine when compared to other children with earlier bedtimes at age nine. However, bedtime at age five wasn’t associated with future alcohol use, nor was sleep duration at ages five or nine. When it came to marijuana use, later bedtime at age five was associated with 26% increased odds of trying marijuana by age 15, while sleeping an hour less at age nine was associated with 19% increased odds of trying marijuana by age 15.
The research team also examined data from adolescents at age 15, who self-reported their bedtime, sleep duration and alcohol and marijuana use. They found that teens with a later bedtime had a 39% greater chance of drinking alcohol and a 34% greater chance of trying marijuana. Sleeping one hour less was associated with 28% increased odds of ever trying alcohol but wasn’t associated with marijuana use.
“Sleep at ages closer to adolescence is the most crucial in terms of future substance use risk. It’s that stage of development when children are rapidly changing and their brain is maturing,” Reichenberger said, noting that previous research by other groups suggests that shorter sleep duration and later bedtimes may increase impulsivity and impair decision making, which could influence substance use choices.
The findings highlight the critical role of sleep across multiple aspects of long-term health and wellbeing, researchers said. For school-age children, creating an environment that’s conducive for sleep and establishing an age-appropriate bedtime are key elements for cultivating good sleep.
“Exploring the connection between sleep and substance use is a critical area of research because we continue to struggle with an epidemic of opioid addiction and substance use,” Chang said. “It’s an important area to continue to research and to disseminate our research findings to the broader population, families and health care professionals.”
Adequate sleep can help prevent osteoporosis, according to a growing body of research. As part of the University of Colorado Department of Medicine’s annual Research Day, held on April 23, faculty member Christine Swanson, MD, MCR, described her clinical research on how sleep interacts with osteoporosis.
“Osteoporosis can occur for many reasons such as hormonal changes, aging, and lifestyle factors,” said Swanson, an associate professor in the Division of Endocrinology, Metabolism, and Diabetes. “But some patients I see don’t have an explanation for their osteoporosis.
“Therefore, it’s important to look for novel risk factors and consider what else changes across the lifespan like bone does – sleep is one of those,” she added.
How bone density and sleep change over time
In people’s early- to mid-20s, they reach what is called peak bone mineral density, which is higher for men than it is for women, Swanson said. This peak is one of the main determinants of fracture risk later in life.
Bone density mostly plateaus for a couple of decades. Then, when women enter the menopausal transition, they experience accelerated bone loss. Men also experience bone density decline as they age.
Sleep patterns also evolve over time. As people get older, their total sleep time decreases, and their sleep composition changes. For instance, sleep latency, which is the time it takes to fall asleep, increases with age. On the other hand, slow wave sleep, which is deep restorative sleep, decreases as we age.
“And it’s not just sleep duration and composition that change. Circadian phase preference also changes across the lifespan in both men and women,” Swanson said, referring to people’s preference for when they go to sleep and when they wake up.
How is sleep linked to bone health?
Genes that control our internal clock are present in all of our bone cells, Swanson said.
“When these cells resorb and form bone, they release certain substances into the blood that let us estimate how much bone turnover is going on at a given time,” she said.
These markers of bone resorption and formation follow a daily rhythm. The amplitude of this rhythm is larger for markers of bone resorption than it is for markers of bone formation, she said.
“This rhythmicity is likely important for normal bone metabolism and suggests that sleep and circadian disturbance could directly affect bone health,” she said.
Researching the connection between sleep and bone health
To further understand this relationship, Swanson and colleagues researched how markers of bone turnover responded to cumulative sleep restriction and circadian disruption.
For this study, participants lived in a completely controlled inpatient environment. The participants did not know what time it was, and they were put on a 28-hour schedule instead of a 24-hour day.
“This circadian disruption is designed to simulate the stresses endured during rotating night shift work and is roughly equivalent to flying four time zones west every day for three weeks,” she said. “The protocol also caused participants to get less sleep.”
The research team measured bone turnover markers at the beginning and end of this intervention and found significant detrimental changes in bone turnover in both men and women in response to the sleep and circadian disruption. The detrimental changes included declines in markers of bone formation that were significantly greater in younger individuals in both sexes compared to the older individuals.
In addition, young women showed significant increases in the bone resorption marker.
If a person is forming less bone while still resorbing the same amount – or even more – then, over time, that could lead to bone loss, osteoporosis, and increased fracture risk, Swanson said.
“And sex and age may play an important role, with younger women potentially being the most susceptible to the detrimental impact of poor sleep on bone health,” she said.
During a night’s sleep, the brain weakens the new connections between neurons that had been forged while awake – but only during the first half, according to a new study in fish by UCL scientists.
The researchers say that their findings, published in Nature, provide insight into the role of sleep, but still leave an open question around what function the latter half of a night’s sleep serves.
The researchers say the study supports the Synaptic Homeostasis Hypothesis, a key theory on the purpose of sleep which proposes that sleeping acts as a reset for the brain.
Lead author Professor Jason Rihel (UCL Cell & Developmental Biology) said: “When we are awake, the connections between brain cells get stronger and more complex. If this activity were to continue unabated, it would be energetically unsustainable. Too many active connections between brain cells could prevent new connections from being made the following day.
“While the function of sleep remains mysterious, it may be serving as an ‘off-line’ period when those connections can be weakened across the brain, in preparation for us to learn new things the following day.”
For the study, the scientists used optically translucent zebrafish, with genes enabling synapses to be easily imaged. The research team monitored the fish over several sleep-wake cycles.
The researchers found that brain cells gain more connections during waking hours, and then lose them during sleep. They found that this was dependent on how much sleep pressure (need for sleep) the animal had built up before being allowed to rest; if the scientists deprived the fish from sleeping for a few extra hours, the connections continued to increase until the animal was able to sleep.
Professor Rihel added: “If the patterns we observed hold true in humans, our findings suggest that this remodelling of synapses might be less effective during a mid-day nap, when sleep pressure is still low, rather than at night, when we really need the sleep.”
The researchers also found that these rearrangements of connections between neurons mostly happened in the first half of the animal’s nightly sleep. This mirrors the pattern of slow-wave activity, which is part of the sleep cycle that is strongest at the beginning of the night.
First author Dr Anya Suppermpool (UCL Cell & Developmental Biology and UCL Ear Institute) said: “Our findings add weight to the theory that sleep serves to dampen connections within the brain, preparing for more learning and new connections again the next day. But our study doesn’t tell us anything about what happens in the second half of the night. There are other theories around sleep being a time for clearance of waste in the brain, or repair for damaged cells – perhaps other functions kick in for the second half of the night.”
A new review of research evidence has explored the key differences in how women and men sleep, variations in their body clocks, and how this affects their metabolism. Published in Sleep Medicine Reviews, the paper highlights the crucial role sex plays in understanding these factors and suggests a person’s biological sex should be considered when treating sleep, circadian rhythm and metabolic disorders.
Differences in sleep
The review found women rate their sleep quality lower than men’s and report more fluctuations in their quality of sleep, corresponding to changes throughout the menstrual cycle.
“Lower sleep quality is associated with anxiety and depressive disorders, which are twice as common in women as in men,” says senior author Dr Sarah L. Chellappa from the University of Southampton. “Women are also more likely than men to be diagnosed with insomnia, although the reasons are not entirely clear. Recognising and comprehending sex differences in sleep and circadian rhythms is essential for tailoring approaches and treatment strategies for sleep disorders and associated mental health conditions.”
The paper’s authors also found women have a 25 to 50% higher likelihood of developing restless legs syndrome and are up to four times as likely to develop sleep-related eating disorder, where people eat repeatedly during the night.
Meanwhile, men are three times more likely to be diagnosed with obstructive sleep apnoea (OSA). OSA manifests differently in women and men, which might explain this disparity. OSA is associated with a heightened risk of heart failure in women, but not men.
Sleep lab studies found women sleep more than men, spending around 8 minutes longer in non-REM (Rapid Eye Movement) sleep, where brain activity slows down. While the time we spend in NREM declines with age, this decline is more substantial in older men. Women also entered REM sleep, characterised by high levels of brain activity and vivid dreaming, earlier than men.
Variations in body clocks
The all-woman research ream from the University of Southampton in the UK, and Stanford University and Harvard University in the United States, found differences between the sexes are also present in our circadian rhythms.
They found melatonin, a hormone that helps with the timing of circadian rhythms and sleep, is secreted earlier in women than men. Core body temperature, which is at its highest before sleep and its lowest a few hours before waking, follows a similar pattern, reaching its peak earlier in women than in men.
Corresponding to these findings, other studies suggest women’s intrinsic circadian periods are shorter than men’s by around six minutes.
Dr Renske Lok from Stanford University, who led the review, says: “While this difference may be small, it is significant. The misalignment between the central body clock and the sleep/wake cycle is approximately five times larger in women than in men. Imagine if someone’s watch was consistently running six minutes faster or slower. Over the course of days, weeks, and months, this difference can lead to a noticeable misalignment between the internal clock and external cues, such as light and darkness.
“Disruptions in circadian rhythms have been linked to various health problems, including sleep disorders, mood disorders and impaired cognitive function. Even minor differences in circadian periods can have significant implications for overall health and well-being.”
Men tend to be later chronotypes, preferring to go to bed and wake up later than women. This may lead to social jet lag, where their circadian rhythm doesn’t align with social demands, like work. They also have less consistent rest-activity schedules than women on a day-to-day basis.
Impact on metabolism
The research team also investigated if the global increase in obesity might be partially related to people not getting enough sleep – with 30% of 30- to 64-year-olds sleeping less than six hours a night in the United States, with similar numbers in Europe.
There were big differences between how women’s and men’s brains responded to pictures of food after sleep deprivation. Brain networks associated with cognitive (decision making) and affective (emotional) processes were twice as active in women than in men. Another study found women had a 1.5 times higher activation in the limbic region (involved in emotion processing, memory formation, and behavioural regulation) in response to images of sweet food compared to men.
Despite this difference in brain activity, men tend to overeat more than women in response to sleep loss. Another study found more fragmented sleep, taking longer to get to sleep, and spending more time in bed trying to get to sleep were only associated with more hunger in men.
Both women and men nightshift workers are more likely to develop type 2 diabetes, but this risk is higher in men. Sixty-six per cent of women nightshift workers experienced emotional eating and another study suggests they are around 1.5 times more likely to be overweight or obese compared to women working day shifts.
The researchers also found emerging evidence on how women and men respond differently to treatments for sleep and circadian disorders. For example, weight loss was more successful in treating women with OSA than men, while women prescribed zolpidem may require a lower dosage than men to avoid lingering sleepiness the next morning.
Dr Chellappa added: “Most of sleep and circadian interventions are a newly emerging field with limited research on sex differences. As we understand more about how women and men sleep, differences in their circadian rhythms and how these affect their metabolism, we can move towards more precise and personalised healthcare which enhances the likelihood of positive outcomes.”
