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Could tackling insomnia with CBT-I help slow the body’s aging clock? Filmstax / Getty Images
  • A new study suggests that older adults who received cognitive behavioral therapy for insomnia (CBT-I) were nearly three times as likely to experience insomnia remission as those who received sleep education.
  • CBT-I was also associated with a slower pace of biological aging, measured using three epigenetic clocks analyzing blood samples.
  • However, as the study was small, further research is necessary to determine whether CBT-I actually extends life span or prevents age-related disease.

Insomnia is a common sleep disorder in the United States, with approximately one-third of adults reporting insomnia symptoms and up to 20% having symptoms that meet the criteria for insomnia disorder. The prevalence of insomnia increases to up to 40% for people older than 65 years of age.

Insomnia can negatively affect daytime functioning, mood, cognition, and overall quality of life. First-line care often involves cognitive behavioral therapy for Insomnia (CBT-I). This describes a structured form of therapy designed specifically for insomnia. Rather than simply providing information about sleep, it addresses thoughts and behaviors that can contribute to persistent difficulty falling or staying asleep, without the side effects linked to sleeping pills.

Now, a new study suggests that CBT-I may do more than improve sleep. In older adults with insomnia, the treatment was associated with a slower pace of biological aging.

The study from UCLA Health, published in The Lancet Healthy Longevity, found that treating insomnia with CBT-I was associated with both improved sleep outcomes and a slower pace of biological aging, as estimated by epigenetic clocks.

The randomized controlled trial involved nearly 100 adults ages 60 years or older meeting DSM-IV criteria for insomnia disorder and were recruited from Los Angeles, CA, USA.

Participants were assigned to one of two treatments: either CBT-I, or the control group, which received sleep education, providing general information about sleep and healthy sleep habits.

According to the researchers, people who received CBT-I were nearly 3 times as likely to experience remission of their insomnia compared with those who received sleep education.

The study also examined whether treating insomnia was associated with changes in biological aging.

Chronological age measures the number of years a person has been alive, whereas biological aging refers to changes occurring in cells and tissues over time. Researchers can estimate aspects of this process using epigenetic clocks.

For this study, researchers analyzed blood samples collected before the 8-week treatment began and at follow-up visits during the next 2 years. They used three measures of biological aging: DunedinPACE, GrimAge, and PC-PhenoAge.

The researchers found that CBT-I was associated with a significant slowing in the pace of biological aging, as measured by the DunedinPACE.

However, the findings do not suggest that CBT-I can reverse aging or make someone biologically younger. Rather, the researchers observed a difference in a biomarker-based measure of the rate of biological aging.

“I think the most important message is that there are treatment options for those who suffer from insomnia, and it is important to treat the insomnia, not just to help you sleep better but also to help protect your health,” lead author Judith Carroll, PhD, an associate professor of psychiatry at UCLA Health, explained to Medical News Today.

“The observed difference between the two treatment arms in the pace of aging was on average -0.02, which indicates that with each year of aging, those in the CBT-I were aging 2% slower. This is difficult to put into practical terms for an individual, but over time, this could become meaningful in terms of their health.”
— Judith Carroll, PhD

Previous research has linked insomnia with markers of accelerated biological aging.

Poor or insufficient sleep may affect several processes involved in health, including stress regulation, metabolism, inflammation, and cardiovascular function. Over time, disruptions in these systems could potentially contribute to age-related disease.

Therefore, the researchers suggest that improving sleep could be one way of influencing some of the biological processes associated with aging. However, the biological mechanisms behind the association remain uncertain.

“We understand that sleep is an important time to allow the biological processes in the body to recover from daytime activity and stressors. Sleep is a time when the body’s parasympathetic nervous system is active, which puts the brake on the sympathetic nervous system,” Carroll highlighted to MNT.

“When there is a rise in the stress response system, we see increased cellular activity such as inflammation and metabolism, which are sources of damage and can drive tissue damage and aging at the cellular level, increasing risk for declines in function and disease. By shutting down this during sleep and giving the body and cells time to repair damage, shut off the inflammatory signal, and heal, we think this then impacts biological aging pathways.”
— Judith Carroll, PhD

“CBT-I helps improve overall regulation of the nervous system through stress management techniques, identifying stress/anxiety triggers, learning to restructure how one responds internally to these triggers, and reconditions the body to begin again to associate bedtime and getting into bed with sleeping through sleep hygiene techniques.”

“CBT-I is a well-designed approach to treat insomnia and is highly effective for many — it is the gold standard treatment currently in medical practice,” she concluded.

The findings are promising, but they do not establish that CBT-I directly slows aging or that treating insomnia will prevent age-related diseases.

Although encouraging, the study involved fewer than 100 participants recruited from a single site in Los Angeles. Larger studies involving participants from multiple locations and more diverse populations will be necessary to determine whether the findings can be replicated.

The study also measured biological aging using epigenetic clocks. Although these measures are useful research tools, changes in an aging biomarker do not necessarily indicate longer life or a lower risk of a particular disease.

“The DunedinPACE is a measure of how fast someone is aging at that window of time, while the other measures give us an estimate of one’s biological age as compared to their chronological age. It is often compared to looking at the speedometer — how fast you are driving — vs. looking at the odometer, how far you have driven,” Carroll clarified.

“We think that this pace of aging might be more sensitive to lifestyle changes and give us a window into what seems to be helping, while the biological age may be less sensitive in a shorter window of time (2 years) but may capture aging over longer windows, for example if someone is able to sleep better and this sleep improvement is sustained for many years, we might see more significant changes in the biological clock.”
— Judith Carroll, PhD

“We’d like to study this more lasting long-term effect of treating insomnia to see if, after 5-10 years, someone looks younger in their biological system,” Carroll said.

“Funding for this type of research is important. Unfortunately, it has become much harder to obtain research funding from NIH with recent changes, but we remain hopeful that our representatives will continue to appropriate the funds to scientific discovery so we can continue our work,” she continued.

Further research will also be needed to determine whether responses differ between males and females and whether other insomnia treatments, including medications or other behavioral interventions, have similar effects on biological aging.

CBT-I is already a behavioral treatment specifically designed to address chronic insomnia. This study suggests that successfully treating persistent insomnia may confer broader health benefits, but it is too early to say that CBT-I slows aging or prevents age-related disease

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