If you have ever wondered if your lack of sleep is killing you slowly, you are not likely alone. More than a third of all American adults do not get the recommended seven hours of sleep at night, according to the U.S. Centers for Disease Control and Prevention.
A predilection for afternoon naps does not necessarily mean you need to worry about your own mortality, but the scientific evidence is increasingly clear: The timing and quality of your sleep play an integral role in your body and brain health. And according to new research, there may be a link between sleep and longevity, too.
The new findings suggest that a condition called Excessive Daytime Sleepiness is linked to one of the most important genetic markers for longevity, a little section of DNA found on the end of chromosomes called a telomere.
“Sleep isn't a luxury,” Joshua Bock tells Inverse. Bock is a postdoctoral research fellow at the Mayo Clinic in Rochester, Minnesota, and the lead author on the new paper. “It's something that you should do every day, like eating healthy and exercising. Sleep needs to be in that conversation.”
The new findings will be presented by Bock and his colleagues in a poster at the annual Experimental Biology conference, which is taking place virtually this week.
Here's the background — Telomeres are often compared to the little piece of plastic on the end of your shoelace that keeps it from fraying. They sit on the ends of chromosomes and serve to protect the other DNA strands in the chromosomes that replicate each time a cell divides. Every time this happens, the telomeres get a little shorter. In turn, telomeres have been described as an “indicator of biological age,” because shorter telomeres are linked to risk for cardiovascular disease, cognitive decline, and even bone loss. Longer telomeres, meanwhile, are tied to the early stages of life and increased physical activity.
Sleepiness has also been linked to increased risk for cardiovascular problems too. Yet whether there might be a thread tying sleepiness, telomere length, and cardiovascular issues was more obscure. Obstructive sleep apnea, a condition that can be clearly identified with a sleep test and which is often characterized by daytime sleepiness, has actually been linked to longer telomeres, for example.
What they did — Using blood samples taken from 210 people in 2017 for another study, Bock’s research group originally set out to find potential DNA markers for sleep apnea, a sleep disorder that affects at least 25 million people in the United States and which often necessitates a mask to help them breathe as they sleep.
The 2017 study found that people with sleep apnea had longer than expected telomeres. But Bock knew from other research that sleepiness is linked to cardiovascular risk, and that short telomeres are, too. The question he sought to answer was: What was the nature of the relationship between sleepiness, telomere length, and cardiovascular problems?
Bock and his team divided 169 of the blood samples into four clinical groups:
- Samples from people with daytime sleepiness and sleep apnea
- Samples from people with daytime sleepiness and no sleep apnea
- Samples from people with no daytime sleepiness, but who did have sleep apnea
- Samples from people with no daytime sleepiness or sleep apnea
Back in 2017, these participants were also asked to answer yes or no to a question regarding excessive daytime sleepiness. The researchers then compared the different groups’ telomere lengths.
What they discovered — Initially, the researchers found that there was no difference in telomere length between those who said they experienced excessive daytime sleepiness and those who did not. But when participants with sleep apnea were removed from the equation — that is, when people with only daytime sleepiness and those without both conditions were compared, daytime sleepiness was linked with shorter telomeres.
Why it matters — This study lays the groundwork for taking daytime sleepiness seriously — it may be a marker for long-term health risks, rather than a mere byproduct of bad habits or a dutiful commitment to a culture that celebrates long work hours. In this case, sleepiness relates to your chromosomes and, by extension, your heart.
“We typically think of sleepiness as a symptom of something, whether that's narcolepsy or like sleep apnea, or just, you know, staying up too late doing whatever it is you were doing,” Bock says. “But now we're looking at it through the lens of its own cardiovascular risk factor.”
The new research also draws a line between daytime sleepiness and sleep apnea, which is linked to the opposite effect on telomeres: lengthening. Telomere lengthening is often associated with biological “youth” and healthfulness, while the shortening observed in this study is associated with aging and cell damage. But it’s not so straightforward. In fact, longer-than-average telomeres can be linked to more serious diseases.
“You need to find a happy medium there, because telomere lengthening, or going too far in the opposite direction, is going to predispose you to cancer,” Bock says. “So you really need to find a, quote-unquote, ‘ideal’ telomere length.”
What's next — Bock says that this study is just the beginning, and points out that it’s limited by a couple of factors. For one, sleepiness is subjective, and in the questionnaire, the participants answered only “yes” or “no” as to whether they experienced excessive daytime sleepiness. In future sleep studies, Bock says, the questions could be more in-depth, but in this case, the initial dataset focused on sleep apnea rather than excessive daytime sleepiness.
For another, there is no way to know from this research what differences in telomere length actually mean in terms of individual health. Though the findings link daytime sleepiness with shorter telomeres, and in turn, with a higher risk of cardiovascular problems, what kind of difference in length translates to effects on “real life” isn’t yet known.
“When we have something that is like, 100 base pairs difference in telomere length, what does that mean, for my likelihood of having a heart attack twenty years down the line? I have no idea,” Bock says. “I don't think anybody could honestly answer that question for you.”
Bock is also curious as to whether or not telomere length is consistent, or if it can fluctuate over time — only more time and research will tell.
Ultimately, drawing out the links between different bodily functions, like sleep and cardiovascular health, could open the door to better treatment, Bock says.
“My mindset is to try to find something that's a bit more holistic as a way to kind of promote telomere lengthening and individuals with sleepiness,” he says. To that end, his next series of projects investigate the gut microbiome as a source of inflammation and how that may relate to telomere length, too.
Abstract: Traditionally regarded as a consequence of sleep-disordered breathing, excessive daytime sleepiness (EDS) is now recognized as an independent risk factor for cardiovascular disease. Evidence also links the shortening of telomeres, responsible for protecting DNA, with increased cardiovascular disease risk. Interestingly, recent data illustrate telomere lengthening in patients with obstructive sleep apnea (OSA); however, whether EDS is associated with telomere length independently of OSA remains unknown. To examine this potential relationship, we studied 169 subjects with polysomnography assessment who answered “yes” or “no” to experiencing EDS; 70 subjects (41%) reported EDS (59M, 44±12yrs, 30.3±5.5kg/m2) whereas 99 did not (59%, 71M, 40±15yrs, 28.6±7.5kg/m2). Telomere length was quantified via qPCR of genomic DNA isolated from peripheral blood samples and did not differ between individuals reporting EDS compared to those who did not (4,856±280 vs. 4,880±340bp, respectively, P=0.31). However, 50% of subjects reporting EDS had moderate-to-severe OSA (apnea-hypopnea index ≥15events/hr) compared to 28% of the non-EDS group (P<0.01). To account for the confounding effects of OSA on telomere length, we conducted a series of subgroup analyses. Subjects without OSA who reported EDS (n=35, 27M, 39±11yrs, 27.4±5.0kg/m2) had shorter telomeres (4,805±165 vs. 4,875±231bp, P=0.05) than those not reporting EDS (n=71, 47M, 35±11yrs, 26.8±5.4kg/m2). Interestingly, within the OSA subgroup, there were no differences in telomere length (4,897±235 vs. 4,858±251bp, P=0.45) between those with (n=35, 32M, 48±11yrs, 33.2±4.5kg/m2) and without EDS (n=28, 24M, 53±16yrs, 33.1±9.7kg/m2). These effects do not appear to be influenced by subject demographics as no differences were found between compared groups (EDS-OSA vs. nEDS-OSA and OSA+EDS vs. OSA-EDS). Collectively, our data suggest individuals reporting EDS may be at greater risk of developing cardiovascular disease due to accelerated telomere shortening. It also appears OSA and EDS exert differential effects on telomere length.