The Hormonal Storm: How Estrogen and Progesterone Shape Sleep

Each month, as if by some unyielding rhythm, mere days before my period arrives, sleep becomes a distant dream. It’s as though a circuit in my mind has blown, leaving the off switch jammed. No matter how heavy my limbs feel with exhaustion, my thoughts remain sharp-edged and unrelenting, my brain humming like a restless machine. And when sleep does finally find me, it is fragile and fleeting. Each time I wake — which is often — my mind resumes its endless loop, revisiting the same restless musings that kept me from slumber in the first place. And this, from someone who can normally sleep through storms and chaos, undisturbed once the world fades away.

This is a reality many women know all too well, a recurring dread that can stretch into an unrelenting nightmare once peri-menopause begins, no longer bound to just a few days each month. The reason lies in the drop of our hormones — progesterone and estrogen — both of which weave their influence through nearly every stage of our sleep, shaping the quality of our rest in ways we often don’t realize until it’s gone.

First, estrogen plays a subtle yet vital role in the onset of sleep, indirectly fostering the production of melatonin — the hormone that orchestrates our sleep-wake cycle — by increasing the availability of serotonin, melatonin’s precursor. But as estrogen wanes during the late luteal phase, serotonin production falters, and melatonin’s flow diminishes.

This mighty hormone also dampens our stress response, enhancing the sensitivity of glucocorticoid receptors in the brain. These receptors act as sentinels, detecting cortisol levels and signaling the HPA axis to ease its output when stress hormones have reached their limit. Through this regulatory touch, estrogen helps to keep cortisol in check, ensuring the body stays within a healthy rhythm. But as estrogen levels fall, this feedback loop weakens, leaving the HPA axis more vulnerable to overactivation. Cortisol, unchecked, may rise or linger, particularly in moments of stress, and high cortisol further disrupts the production of melatonin. And thus the usual evening surge of this sleep-inducing hormone becomes muted or delayed.

Then there is progesterone, which I affectionately call my zen hormone. It fosters relaxation and soothes anxiety through its metabolite, allopregnanolone, which amplifies the calming influence of GABA-A receptors in the brain. GABA, our brain’s master peacemaker, silences overactive neurons. Yet, in the days before menstruation, progesterone levels also plummet, and with them, the tranquil effects of allopregnanolone fade. What remains is a storm of heightened brain activity, a restless body, and racing thoughts that refuse to settle.

But it is not just the mind that gets in the way of sleep in the absence of those hormones. Their shifts significantly disrupt the body’s ability to regulate temperature — a crucial process for initiating and maintaining sleep. During the luteal phase of the menstrual cycle, progesterone raises core body temperature by 0.3–0.5°C as the body prepares for potential pregnancy. This elevated temperature persists until progesterone levels sharply drop just before menstruation. Without sufficient progesterone, the body struggles to cool itself efficiently. Normally, blood vessels near the skin dilate to release heat, allowing core temperature to fall, but these hormonal changes interfere, leaving many women feeling overly warm, experiencing night sweats, or tossing and turning in discomfort.

Estrogen also plays a vital role in temperature regulation by stabilizing the hypothalamus, the brain’s thermostat. When estrogen levels drop, the hypothalamus becomes more sensitive to small changes in temperature, leading to heightened perceptions of heat or cold. This instability further disrupts thermoregulation, compounding the challenges of falling asleep.

And that’s just the battle of falling asleep — drowning out the day is only the first hurdle. The next challenge lies in staying asleep, and here, too, our hormones hold the reins. The struggles with thermoregulation don’t vanish once sleep takes hold; they linger, often pulling us from the depths of rest, sometimes tangled in sheets damp with sweat. This discomfort is made all the harder to ignore because the brain’s own mechanisms for dulling sensory input during sleep — its way of quieting the world — are also deeply tied to our hormones. Let me introduce you to sleep spindles and K-complexes. Here is where the story of sleep truly begins to get interesting.

Sleep spindles are brief, rhythmic bursts of brain activity that oscillate through Stage 2 of non-REM sleep, each lasting no more than a fleeting 0.5 to 2 seconds. Formed by the interplay between the thalamus and the cortex, these bursts shield the mind from both internal and external sensory input. They soften the impact of disturbances, muffling the intrusions of noise, light, or even temperature and so preserve the stability of our sleep. Those neural pulses are also deeply entwined with memory, weaving the day’s newly learned information into the fabric of long-term recollection.

Then there are the K-complexes. Those grand, deliberate waves of brain activity also emerge during Stage 2 of non-REM sleep. Their distinctive patterns begin with a sharp downward dip, followed by a gentle upward rise, reflecting the brain’s way of acknowledging sensory input without fully waking. It’s a relic from our ancient feral past when sleep left us vulnerable to predators and the brain needed a way to monitor for danger without depriving us of sleep unnecessarily. Like sleep spindles, K-complexes arise from the collaboration between the thalamus and cortex, and guide us toward deeper stages of sleep.

By influencing neurotransmitters like acetylcholine, estrogen strengthens the thalamocortical networks responsible for producing these brainwaves. It enhances sleep stability, increasing the density and frequency of spindles. Yet, as estrogen declines in the late luteal phase, spindles grow weaker and less frequent, leaving the brain more exposed to disturbances from sensory input like noise or light, making deep sleep harder to achieve.

Progesterone also plays a critical role in sustaining these protective brain rhythms through its metabolite, allopregnanolone, which enhances the calming activity of GABA-A receptors. This interaction helps stabilize the brain’s electrical activity during sleep and indirectly strengthens the production of spindles and K-complexes. However, when progesterone levels drop before menstruation, this stabilizing effect diminishes. The resulting decline in GABAergic activity weakens the brain’s ability to generate these protective waves, leading to lighter, more fragmented sleep. Together, these hormonal shifts leave the brain vulnerable to disruption.

As if these challenges weren’t enough, the late luteal phase brings a surge in pro-inflammatory prostaglandins, hormone-like compounds that prepare the uterus for menstruation by triggering contractions to allow for the shedding of the uterine lining. But, their effects reach far beyond the uterus, increasing inflammation throughout the body where it often manifests as cramping, body aches, and headaches — common premenstrual symptoms that can make it difficult to find comfort. Adding to the challenge, prostaglandins may indirectly stimulate the brain’s stress pathways, amplifying irritability, restlessness, and an inability to unwind at night.

Alongside prostaglandins, the late luteal phase prompts a surge in pro-inflammatory cytokines, such as interleukin-6 (IL-6). These signaling molecules, while crucial for coordinating immune responses, can interfere with sleep architecture when elevated. They diminish the amount of slow-wave sleep — the deep, restorative phase — and increase episodes of wakefulness throughout the night. Without sufficient deep sleep, the body’s ability to heal, regulate immunity, and fully recover is compromised, leaving many women feeling drained and unrested, no matter how long they remain in bed.

For women with pre-existing inflammatory conditions, such as endometriosis or autoimmune disorders, the impact of prostaglandins and cytokines can be even more severe. Heightened inflammation intensifies pain and magnifies the struggle to fall and stay asleep. This inflammation-induced sleep disruption creates a vicious cycle: poor sleep exacerbates systemic inflammation, worsening symptoms and further impairing rest.

The last stage of our sleep cycle is REM (rapid eye movement) sleep. During this stage the brain hums with activity, its rhythms echoing those of wakefulness, marked by the dominance of beta waves. It is here, in this vivid dreamscape, that the body becomes motionless — paralyzed by a protective atonia that ensures dreams remain confined to the mind. REM sleep is fundamental to emotional processing and memory consolidation, particularly for memories tied to feelings and learned tasks. During this phase, the brain sifts through the day’s experiences, integrating fragments of information into creativity, problem-solving, and resilience. It is a time when the mind regenerates itself, balancing the weight of emotions and sharpening its cognitive edge.

The neurochemical environment of REM sleep is finely tuned. Acetylcholine surges, enhancing communication between neurons and fueling the vividness of dreams and the processing of emotional memories. Serotonin, which guides other phases of sleep, recedes, allowing seamless transitions into and out of REM. Meanwhile, cortisol, the body’s stress hormone, begins its quiet ascent near the night’s end, gently preparing the body to wake.

Estrogen plays a pivotal role in enhancing the brain’s production and release of acetylcholine, particularly in regions like the basal forebrain and brainstem. Acetylcholine is essential for activating the pons, a part of the brainstem responsible for generating the hallmarks of REM sleep: the vivid beta-wave activity and the dream world it brings to life.

When estrogen levels are high, acetylcholine release is at its peak, promoting the stability and length of REM sleep cycles. But as estrogen wanes, this signaling weakens, leaving REM sleep compromised. With these disruptions, the brain’s ability to process emotions and solidify memories becomes impaired, creating the ripple effect of emotional and cognitive difficulties often experienced during the premenstrual phase.

While the challenges of hormonal fluctuations can feel insurmountable, this awareness provides a path forward. Our bodies are complex, but an informed approach — one that incorporates nutrition, movement, and stress management- can provide substantial relief. And just how to do that, will be the topic of the next chapter.