Key Takeaways:
- Polysomnography data show that only approximately one third of nighttime wakefulness during the menopausal transition is associated with a hot flash, meaning the majority of sleep disruption occurs independently of VMS and will not respond to VMS-targeted treatment.
- Hormone therapy improves sleep primarily in women with concurrent hot flashes; neurokinin-targeted therapies appear to benefit both symptoms, with elinzanetant (Lynkuet) potentially offering more direct sleep benefit—but neither addresses sleep disruption that is independent of VMS.
- Cognitive behavioral therapy for insomnia is the gold standard recommended by sleep societies for sleep disruption in this population and is accessible through free, evidence-based digital platforms including a publicly available Veterans Administration program.
Only about one third of nocturnal wakefulness during the menopausal transition is directly attributable to hot flashes—and that single finding has significant implications for how clinicians should approach sleep as a treatment target in its own right, according to Pauline M. Maki, PhD, whose SWAN-based quality-of-life analysis was previously reported.1
The clarification matters because the temporal link between hot flashes and nighttime awakening is real but often overstated. Studies using wearable devices to track hot flashes and polysomnography to measure sleep confirm that women wake up following a hot flash between 60 and 75% of the time.
"That might give us the impression that sleep disturbance in the menopause transition is really due to the hot flashes," Maki said. "But if you look at the total amount of time that women are awake when they want to be sleeping, it's only about a third of that time that's associated with a hot flash." The other two thirds reflect disruptions to sleep circuitry that are independent of vasomotor events—and that will not respond to VMS-targeted treatment alone.
This distinction has direct clinical consequences. Hormone therapy, Maki noted, improves sleep primarily in women who also have hot flashes; its benefit independent of VMS is less clear. The neurokinin-targeted therapies—fezolinetant (Veozah) and elinzanetant (Lynkuet)—appear to benefit both symptoms, with elinzanetant's NK1 receptor antagonism potentially offering a more direct sleep mechanism.
"They work within a week, which is just marvelous," Maki said. But when sleep disruption is occurring largely independent of VMS, neither class of VMS treatment may be sufficient.
The intervention with the strongest evidence base for sleep disruption independent of VMS is cognitive behavioral therapy for insomnia—a recommendation from sleep medicine societies that Maki noted many ob-gyn clinicians may not be aware of or may not feel equipped to offer.
"If you ask a provider of midlife women how can I sleep better, they kind of draw a blank," she said. CBT-I does not require a referral to a specialist; evidence-based digital platforms are publicly accessible, including a Veterans Administration program that patients can access independently.
"Women can get this by googling Veterans Administration CBT—there's an evidence-based platform right there for women to guide their own sleep," Maki said.
The broader message is that sleep in the menopausal transition is not a single phenomenon. Some women have primarily VMS-driven sleep disruption; others have disruption that is largely independent of hot flashes; many have both.
"My experience of menopause isn't her experience of menopause," Maki said. Effective treatment depends on identifying which is driving the symptom burden in the individual patient—and being willing to reach beyond prescription therapies when the evidence points elsewhere.
REFERENCE
1. Maki P, Dinkel-Keuthage C, Nadimi M, et al. Associations between sleep disturbances, vasomotor symptoms and health-related quality of life in the menopausal transition and early postmenopause. Sleep. 2026;49(Suppl 1):A371
