While several studies have correlated sleep deprivation with weight gain, the underlying cause of increased obesity risk from sleep disruption is unclear, but may relate to changes in appetite, metabolism, motivation, physical activity or a combination of factors. Dr. Christian Benedict from Uppsala University, Sweden and his group have conducted a number of human studies to investigate how sleep loss may affect energy metabolism.
These human studies have measured and imaged behavioral, physiological and biochemical responses to food following acute sleep deprivation. The behavioral data reveal that metabolically healthy, sleep-deprived human subjects prefer larger food portions, seek more calories, exhibit signs of increased food-related impulsivity, experience more pleasure from food, and expend less energy.
Sleep Loss And Weight Gain
The group’s physiological studies indicate that sleep loss shifts the hormonal balance from hormones that promote fullness, such as GLP-1, to those that promote hunger, such as ghrelin. Sleep restriction also increased levels of endocannabinoids, which is known to have appetite-promoting effects. Acute sleep loss also alters the balance of gut bacteria, which has been widely implicated as key for maintaining a healthy metabolism. The same study also found reduced sensitivity to insulin after sleep loss.
“Since perturbed sleep is such a common feature of modern life, these studies show it is no surprise that metabolic disorders such as obesity are also on the rise,” Benedict says. “My studies suggest that sleep loss favors weight gain in humans. It may also be concluded that improving sleep could be a promising lifestyle intervention to reduce the risk of future weight gain.”
Although this work has shed light on how short periods of sleep loss can affect energy metabolism, longer-term studies are needed to validate these findings. The group is now investigating longer-term effects and also whether extending sleep in habitual short sleepers can restore these alterations in appetite and energy metabolism.
Exercise, Sleep Key To Regulating Behavior
Another recent study, published in 2017 in the Journal of Applied Psychology, tracked participants’ sleep patterns and daytime physical movements. It found employees who recorded an average of more than 10,900 steps each day were less likely to perpetuate abuse at home than those recording fewer than 7,000.
“Research shows employees who are mistreated at work are likely to engage in similar behaviors at home,” said University of Central Florida’s College of Business management professor Shannon Taylor, who teamed up with researchers from Illinois and Wisconsin for the study. “If they’ve been belittled or insulted by a supervisor, they tend to vent their frustration on members of their household. Our study shows that happens because they’re too tired to regulate their behavior.”
Study participants included 118 MBA students with full-time jobs who took a survey and then wore activity monitors for a week. A follow-up survey was then sent to the participants’ cohabitants. The study concludes sleep and exercise are intervention points that can be leveraged to prevent the spread of harmful behavior.
The study found that burning an additional 587 calories can reduce the harmful effects of mistreatment and help prevent it from carrying into the home. For the average American man, these gains can be achieved with an hour of swimming or a brisk 90-minute walk. “The findings are particularly compelling given recommendations from the Centers for Disease Control and the American Heart Association to walk between 8,000 and 10,000 steps per day,” Taylor said.
In June 2017, an international team of researchers found – for the first time – seven risk genes for insomnia. The results of the research were published in Nature Genetics. With this finding the researchers have taken an important step towards the unraveling of the biological mechanisms that cause insomnia. In addition, the finding proves that insomnia is not, as is often claimed, a purely psychological condition.
Insomnia is probably the most common health complaint. Even after treatment, poor sleep remains a persistent vulnerability for many people. By having determined the risk genes, professors and lead researchers Danielle Posthuma and Eus Van Someren have come closer to unraveling the biological mechanisms that cause the predisposition for insomnia. Van Someren believes that the findings are the start of a path towards an understanding of insomnia at the level of communication within and between neurons, and thus towards finding new ways of treatment.
He also hopes that the findings will help with the recognition of insomnia. “As compared to the severity, prevalence and risks of insomnia, only few studies targeted its causes. Insomnia is all too often dismissed as being ‘all in your head.’ Our research brings a new perspective. Insomnia is also in the genes.”
In a sample of 113,006 individuals, the researchers found seven genes for insomnia. These genes play a role in the regulation of transcription, the process where DNA is read in order to make an RNA copy of it, and exocytosis, the release of molecules by cells in order to communicate with their environment. One of the identified genes, MEIS1, has previously been related to two other sleep disorders: Periodic Limb Movements of Sleep (PLMS) and Restless Legs Syndrome (RLS).
By collaborating with Konrad Oexle and colleagues from the Institute of Neurogenomics at the Helmholtz Zentrum, München, Germany, the researchers could conclude that the genetic variants in the gene seem to contribute to all three disorders. PLMS and RLS are characterized by restless movement and sensation, respectively, whereas insomnia is characterized mainly by a restless stream of consciousness.
Genetic Overlap With Other Characteristics
The researchers also found a strong genetic overlap with other traits, such as anxiety disorders, depression and neuroticism, and low subjective wellbeing. “This is an interesting finding, because these characteristics tend to go hand in hand with insomnia. We now know that this is partly due to the shared genetic basis,” says neuroscientist Anke Hammerschlag, first author of the study.
The researchers also studied whether the same genetic variants were important for men and women. “Part of the genetic variants turned out to be different. This suggests that, for some part, different biological mechanisms may lead to insomnia in men and women,” says professor Posthuma. “We also found a difference between men and women in terms of prevalence: in the sample we studied, including mainly people older than 50 years, 33% of the women reported to suffer from insomnia. For men this was 24%.”
The risk genes could be tracked down in cohorts with the DNA and diagnoses of many thousands of people. The UK Biobank – a large cohort from England that has DNA available – did not have information as such about the diagnosis of insomnia, but they had asked their participants whether they found it difficult to fall asleep or to have uninterrupted sleep. By making good use of information from the Dutch Sleep Registry, the UK Biobank was able, for the first time, to determine which of them met the insomnia profile. Linking the knowledge from these two cohorts is what made the difference.
Deep Sleep A Fountain Of Youth?
As we grow old, our nights are frequently plagued by bouts of wakefulness, bathroom trips and other nuisances as we lose our ability to generate the deep, restorative slumber we enjoyed in youth. But does that mean older people just need less sleep? Not according to UC Berkeley researchers, who argue in an article published in the journal Neuron that the unmet sleep needs of the elderly elevate their risk of memory loss and a wide range of mental and physical disorders.
“Nearly every disease killing us in later life has a causal link to lack of sleep,” said senior author, Matthew Walker, a UC Berkeley professor of psychology and neuroscience. “We’ve done a good job of extending life span, but a poor job of extending our health span. We now see sleep, and improving sleep, as a new pathway for helping remedy that.”
Sleep deterioration has been linked to Alzheimer’s disease, heart disease, obesity, diabetes and stroke. Though older people are less likely to notice or report mental fogginess and other symptoms of sleep deprivation, numerous brain studies reveal how poor sleep leaves them cognitively worse off. Moreover, the shift from deep, consolidated sleep in youth to fitful, dissatisfying sleep can start as early as the thirties, paving the way for sleep-related cognitive and physical ailments in middle age.
While the pharmaceutical industry is raking in billions by catering to insomniacs, Walker warns that the pills designed to help us doze off are a poor substitute for the natural sleep cycles that the brain needs in order to function well. “Don’t be fooled into thinking sedation is real sleep. It’s not,” he said.
Slow Wave Sleep
For their review of sleep research, Walker – along with researchers Bryce Mander and Joseph Winer – cite studies, including some of their own, that show the aging brain has trouble generating the kind of slow brain waves that promote deep curative sleep, as well as the neurochemicals that help us switch stably from sleep to wakefulness. “The parts of the brain deteriorating earliest are the same regions that give us deep sleep,” said Mander, a postdoctoral researcher in Walker’s Sleep and Neuroimaging Laboratory at UC Berkeley.
Aging typically brings on a decline in deep, non-rapid eye movement (NREM) or “slow wave sleep,” and the characteristic brain waves associated with it, including both slow waves and faster bursts of brain waves known as “sleep spindles.” Youthful, healthy slow waves and spindles help transfer memories and information from the hippocampus, which provides the brain’s short-term storage, to the prefrontal cortex, which consolidates the information, acting as the brain’s long-term storage.
“Sadly, both these types of sleep brain waves diminish markedly as we grow old, and we are now discovering that this sleep decline is related to memory decline in later life,” said Winer. Another deficiency in later life is the inability to regulate neurochemicals that stabilize our sleep and help us transition from sleep to waking states. These neurochemicals include galanin, which promotes sleep, and orexin, which promotes wakefulness. A disruption to the sleep-wake rhythm commonly leaves older adults fatigued during the day but frustratingly restless at night.
Of course, not everyone is vulnerable to sleep changes in later life: “Just as some people age more successfully than others, some people sleep better than others as they get older, and that’s another line of research we’ll be exploring,” Mander said.
Quantity Vs. Quality Sleep
Meanwhile, non-pharmaceutical interventions are being explored to boost the quality of sleep, such as electrical stimulation to amplify brain waves during sleep and acoustic tones that act like a metronome to slow brain rhythms. However, promoting alternatives to prescription and over-the-counter sleep aids is sure to be challenging.
“The American College of Physicians has acknowledged that sleeping pills should not be the first-line kneejerk response to sleep problems,” Walker said. “Sleeping pills sedate the brain, rather than help it sleep naturally. We must find better treatments for restoring healthy sleep in older adults, and that is now one of our dedicated research missions.”
Also important to consider in changing the culture of sleep is the question of quantity versus quality. “Previously, the conversation has focused on how many hours you need to sleep,” Mander said. “However, you can sleep for a sufficient number of hours, but not obtain the right quality of sleep. We also need to appreciate the importance of sleep quality. Indeed, we need both quantity and quality.”