Sleep

Sleep quality is a core vital sign in mainstream medicine. Ray Peat read poor sleep as a marker of low Thyroid, night hypoglycemia, high Cortisol or Estrogen, and excess darkness-hormone drive.

Some of the early sleep studies where they monitored brainwaves and could define the different levels of sleep found that hypothyroid people never got below the second level of sleep. They never reached deep restorative sleep, and so hypothyroidism very often involves difficulty getting to sleep but almost by definition it involves inadequate quality of sleep — waking up feeling unrested, often with pains that are worse in the morning before any activity than they were bedtime.

— Ray Peat

People who are low in thyroid usually have defective sleep, often insomnia.

— Ray Peat

Hypothyroidism decreased sleep stages 3 and 4 in a human polysomnography study.

Even mildly reduced thyroid function shows the same pattern. In a Chinese population study of 2,224 people with subclinical hypothyroidism against 12,622 euthyroid controls, the subclinical group had higher Pittsburgh Sleep Quality Index scores (6.83 vs 6.64), more poor sleepers (67.1% vs 64.8%), longer sleep latency, and shorter sleep duration after adjusting for confounders. A 2024 systematic review of eight studies (2,916 subclinical hypothyroidism patients, 18,574 controls) found seven of the eight studies agreed on a positive correlation between subclinical hypothyroidism and reduced sleep quality or duration.

In Ray Peat's framework, this same loss of deep sleep appears in schizophrenia and depression, variants of a torpor-like, serotonin-driven brain-stress state.

The characteristic sleep pattern of hypothyroidism and old age is similar to the pattern seen in schizophrenia and depression, a decrease of deep slow wave sleep. Serotonin, like torpor, produces a similar effect. In other words, a torpor-like state can be seen in all of these brain-stress states. Several studies have found that anti-serotonin drugs improve sleep, and also reduce symptoms of schizophrenia and depression. It is common for the "neuroleptic" drugs to raise body temperature, even pathologically as in the "neuroleptic malignant syndrome."

— Ray Peat

Darkness as a stressor

Peat's framing runs opposite the "sleep as pure rest" default: nocturnal sleep's main job is limiting the metabolic damage darkness itself causes, not just conserving energy.

I suspect that nocturnal sleep has the special function of minimizing the stress of darkness itself, and that it has subsidiary functions, including its now well confirmed role in the consolidation and organization of memory.

— Ray Peat

Prolactin and cortisone both rise in stress and in darkness, and both mobilize calcium; the same cortisol-driven mitochondrial disruption implicated in bone loss makes winter/darkness load an aging driver in its own right, distinct from simple sleep deprivation.

Both prolactin and cortisone are secreted during stress (and in darkness), and both mobilize calcium... Structural disruption of the mitochondria, as well as uncoupling phosphorylation from respiration, can be caused by cortisone. So it is interesting to see seasonal changes in the structure of the mitochondria, which are consistent with the ideas I have been talking about, that winter (and light deficiency in general) is what ages and kills us.

— Ray Peat

This is the mechanistic basis for pairing sleep recovery with daytime bright-light exposure rather than darkness/blackout strategies alone; see Estrogen dominance#Reducing xenoestrogen exposure for the related sunlight-exposure sourcing, and Basal temperature for tracking whether sleep is actually restorative.

Mitochondrial electron leak and sleep pressure

In Drosophila, mitochondrial electron leakage from the respiratory chain drives sleep need; reducing leak shortens sleep while increasing leak prolongs it, linking fat oxidation–linked ROS to conserved sleep pressure.

Lipid peroxidation memory and sleep pressure

In Drosophila, Hyperkinetic, the Kvβ subunit of the Shaker potassium channel, stores a lipid-peroxidation memory in the oxidation state of its bound NADPH cofactor: lipid-derived carbonyls from PUFA oxidation flip NADPH to NADP+, and NADP+ stays locked in the channel until membrane depolarization releases it. Sleep-inducing neurons read the collective NADP+/NADPH state of their Kvβ subunits as accumulated oxidative history, and spiking during sleep erases it by re-reducing the cofactor. After enforced wakefulness, brain phospholipids lose PUFA content, and slowing clearance of the resulting breakdown products increases sleep demand.

Chronotherapy for delayed sleep timing

In young adults with delayed sleep timing, adding a personalized wake-time advance and evening blue-light blocking to morning light therapy shifted circadian phase and reduced depression symptoms, while light therapy alone did not. See Circadian rhythm for the full comparison.

ADHD and delayed sleep timing

Insomnia and sleep disturbances affect up to about 80% of adults with ADHD and up to about 82% of children; delayed sleep-wake timing occurs in up to about 78%; dim-light melatonin onset (DLMO) is delayed by about 45 minutes in children and about 90 minutes in adults. Melatonin and bright light therapy advanced DLMO in children and adults with ADHD; emerging data correlate phase advancement with ADHD symptom improvement. Behavioral sleep programs improve ADHD symptoms, sleep quality, and functioning in children. See ADHD, Melatonin, Circadian rhythm.

Vitamin E and insomnia

In a double-blind randomized trial of 160 postmenopausal women with chronic insomnia, 400 IU/day of mixed-tocopherol vitamin E for one month cut Pittsburgh Sleep Quality Index scores from a median of 13 to 6 (lower is better), significantly more than placebo (11 to 9); 15% of the vitamin E group also stopped using sedative drugs, versus a non-significant 7.5% in the placebo group.

Vitamin C and sleep

Higher dietary vitamin C intake went with fewer new sleep disorders and less sleep apnea in a large UK cohort. In hemodialysis patients with restless legs syndrome, 200 mg/day oral vitamin C for eight weeks lowered International Restless Legs Scale scores versus placebo, matching vitamin E and the combination arm. See Vitamin C.

Sleep deprivation and cognition

Acute total sleep deprivation impairs attention and working memory most consistently, and also long-term memory and decision-making; chronic partial sleep restriction mainly degrades attention, especially vigilance, and its effect on higher cognitive functions is less studied (review of studies published since 1990). One recovery sleep of at least eight hours reversed the cognitive effects of acute total deprivation on mostly simple attention tasks, while recovery after chronic restriction took longer; after seven nights of restriction, one 10-hour night did not restore vigilance performance.

In a 14-day laboratory trial, 48 healthy adults aged 21-38 were randomized to 4, 6, or 8 hours in bed per night or to 3 nights without sleep. Restriction to 4 or 6 hours produced cumulative, dose-dependent deficits on every cognitive task, and 6 hours or less per night matched up to 2 nights of total sleep deprivation; sleepiness ratings rose only slightly after the first days, leaving participants largely unaware of the decline.

I think deep sleep is important as a restorative part of your brain function.

— Ray Peat

See Brain.

Sleep deprivation and muscle protein synthesis

One night of total sleep deprivation cut postprandial skeletal muscle protein synthesis about 18% the next afternoon in 13 healthy young adults (randomized crossover), raised plasma cortisol about 21%, and lowered plasma testosterone about 24%, without a change in measured markers of protein degradation. See Roadmap/08 - Bodybuilding & Weight loss, Testosterone, Cortisol.

Sleep deprivation and amyloid

A single night of total sleep deprivation raised beta-amyloid in brain regions implicated in Alzheimer's disease by roughly 5% relative to a night of normal sleep in PET scans of healthy adults, with the increase concentrated in the right hippocampus and thalamus; the effect tracked worse self-reported mood the next day.

In mice, natural sleep and ketamine-xylazine anesthesia enlarged the cortical interstitial space, the fluid-filled gap between brain cells, by more than 60%: its share of tissue volume rose from about 14% awake to about 23% asleep, so the space taken by cells fell by roughly a tenth. Injected beta-amyloid was cleared twice as fast in sleeping mice as in awake mice (mouse study). A 2024 mouse study using fluorescent tracers found the opposite. Dye movement through the brain was the same in sleep, waking and anesthesia, and clearance from the brain fell markedly during sleep and anesthesia (mouse study).

Sleep deprivation and emotion

About 35 hours of total sleep deprivation raised amygdala reactivity to increasingly aversive pictures by about 60% relative to a night of sleep in healthy young adults, with a three-fold larger activated amygdala volume, and weaker functional connectivity between the amygdala and medial prefrontal cortex. See Emotion, Stress, Brain. Interventions that improve sleep also improve mental health: across 65 randomized trials, better sleep reduced depression, anxiety, rumination and stress, with a smaller gain for psychotic symptoms, and larger sleep gains brought larger mental-health gains.

In a trial of 54 inpatients with major depression who kept taking their usual medication, staying awake for 36 hours raised the day-3 response rate over a normal night of sleep. Hamilton depression scores did not differ between groups, and the benefit was gone by day 7.

Many years ago, someone noticed that depressed people who missed a night's sleep, or who were wakened several hours earlier than normal, came out of their depression, until they caught up on their sleep. Sleep deprivation has become a recognized treatment for depression.

— Ray Peat

Nocturnal leg cramps

A randomized trial of vitamin K2 (MK-7, 180 μg/day) cut nocturnal leg-cramps frequency from ~2.6 to ~1.0 per week and reduced cramp severity and duration in older adults.

Night stress and supports

Adrenaline, cortisol, and prolactin tend to rise during night-time sleep while thyroid and progesterone function fall, which makes darkness a major stressor. Blood sugar falls during the night and inflammatory mediators and adrenaline rise; a wool cap and stockings, or plenty of sugar at bedtime or on waking, can help.

Sleep restriction raised nocturnal free fatty acids and impaired insulin signaling in human trials Peat cited on glycemia writing. Peat's practical sleep notes include Milk with sugar and Salt, Gelatin before bed, adequate Thyroid, and Progesterone when appropriate.

Glycine is recognized as an "inhibitory" neurotransmitter, and promotes natural sleep.

— Ray Peat

See Dreams, Melatonin, Basal temperature, Harm reduction.

Nighttime light, sleep length, and heart remodeling

In 11,071 UK Biobank participants with wrist light sensing then CMR ~3 years later, high nighttime light (>3 lux) versus none associated with left-ventricular concentric hypertrophy and lower contraction fraction (about +2.4% LV mass indexed to height^1.7, +1.5% wall thickness, -1.9% myocardial contraction fraction), plus lower absolute LV strain indices and adverse right-ventricle and left-atrium volume/function measures; dose-response was linear and shorter sleep mediated about 24-49% of most associations. About one-quarter to one-half of those CMR associations were statistically mediated by shorter sleep duration. In a larger Biobank sample (n=73,286) followed 8-10 years, high versus no nighttime light (>3 lux) associated with higher incident heart failure (+29%), atrial fibrillation (+15%), myocardial infarction (+24%), stroke (+33%), and CVD mortality (+26%). See Light, Heart.

Weekend catch-up sleep and aging

In a NHANES 2017-2018 sample of 4,713 adults, people who slept longer on weekends than weekdays ("catch-up sleep") had a lower risk of accelerated biological aging (biological age exceeding chronological age) than those without catch-up sleep; up to 2 hours of catch-up was linked to roughly a fifth lower risk, but the benefit held only in people who usually went to bed before midnight and caught up less than 2 hours. This suggests weekend catch-up sleep partly offsets chronic weekday sleep restriction rather than being purely disruptive to circadian rhythm, at least within a modest 0-2 hour range and an earlier bedtime.

Camping resets circadian timing

Modern electrical lighting delays the human circadian clock relative to the natural light-dark cycle. A weekend camping trip with only natural light exposure shifted melatonin onset about 1.4 hours earlier and prevented the weekend circadian and sleep delay that shows up under normal indoor-lit conditions. See Sunlight, Circadian rhythm.

Sleep restriction and dieting

In a crossover study of 10 overweight adults on 14 days of calorie restriction, 5.5 hours of sleep instead of 8.5 meant that less of the weight lost was fat and more was lean tissue, with more hunger.

Carbon dioxide and sleep

In a randomized crossover study in healthy adults, breathing 2.5% CO₂ through a low-resistance open mask all night gave the highest sleep efficiency and the most deep (N3) sleep, while a higher dose cut REM sleep and added arousals. At 3.5% CO₂, sleep efficiency was no better than room air.

In a sham-controlled crossover trial run with the device's maker, poor sleepers using a bedside sprayer of mixed air and CO₂ slept about half an hour longer per night.

During the night, normal people tolerate more CO2, and so breathe less, especially near morning, with increased active dreaming sleep.

— Ray Peat

Circadian rhythm

Circadian rhythm is the roughly 24-hour timing of hormones, temperature, and behavior. Light is the main external cue (zeitgeber).

Peat's view

Prolonged darkness increases cortisol, which makes cells more susceptible to excitotoxic death and inhibits stem cell proliferation. Cell renewal requires a rhythmic decrease in cortisol exposure, and both aging and depression involve a diminished ability to lower cortisol rhythmically. Morning light, daytime activity, and dark nights support thyroid and steroid rhythms. Night shift, blue-heavy screens late, and irregular meals push stress chemistry. Food timing still loses to total fuel adequacy if under-eating.

Night shift work and cancer classification

IARC (WHO's cancer research agency) classifies night shift work involving circadian disruption as Group 2A, "probably carcinogenic to humans," citing sufficient evidence in animals and limited evidence in humans for breast, prostate, and colorectal cancer, a specific classification tier, not a causal cancer finding.

Chronotherapy for delayed sleep and depression in young adults

Two pilot trials in emerging adults (ages 18-25) with delayed sleep timing and no-to-moderate depression compared morning bright light therapy alone against a combined protocol. Two weeks of morning light alone did not significantly shift circadian phase or reduce depression symptoms (n=21). Adding a personalized sleep-wake timing advance plus evening blue-light blocking glasses (worn 2 hours before bed) to the same light protocol advanced circadian phase by about 35 minutes and reduced depression symptoms (n=15). Both are small pilot samples; the authors call for larger randomized controlled trials with rigorous adherence monitoring before drawing firm conclusions.

ADHD evening chronotype and phase delay

ADHD associates with evening chronotype and phase-delayed biological markers: delayed sleep-wake timing in up to about 78% of people with ADHD, DLMO delayed by about 45 minutes in children and about 90 minutes in adults, plus blunted and delayed cortisol rhythms and attenuated peripheral BMAL1/PER2 rhythms. Melatonin and bright light therapy advanced DLMO in children and adults with ADHD; winter trials suggest circadian preference shifts best predict ADHD symptom improvement. See ADHD, Sleep, Melatonin.

Dreams

Dreams and sleep quality shift directly with metabolic state. Mainstream sleep medicine links REM dreaming to arousal systems and circadian timing; the bioenergetic view ties both dreaming and poor sleep generally to the same hormonal markers as everything else on this wiki: low Thyroid, high Cortisol, Estrogen dominance, night hypoglycemia, or excess darkness hormones.

The Ascending Reticular Activating System

Dreams function as the brain's "acceptor of action" operating independently of the sensory information it normally interacts with. During dreams, a system called the Ascending Reticular Activating System (ARAS) disconnects the brain from its sensory systems, letting it run the nervous equivalent of concentric muscle activity, in control of its own actions rather than reacting to input.

Active, dreaming sleep occurs more in the later part of the night as morning approaches, exactly when cortisol and other stress hormones are climbing toward their dawn peak, so it makes sense for the brain's defensive processes to run hardest right then. The dreaming phase itself pairs with deep muscle relaxation, plausibly part of the same trophic, restorative nerve action. In restful sleep generally, oxygen tension runs low enough and CO2 tension high enough to trigger stem cell and mitochondrial multiplication.

The same reticular formation that runs REM sleep also runs the waking "orienting reflex," the brain's response to anything novel. Both states share a distinct electrical signature, the pontogeniculo-occipital (PGO) wave, and both promote flexible, fluid thinking with heightened sensitivity to motion. Progesterone activates this reticular activating system directly and, given during sleep, increases the amount of REM. Novelist and philosopher Colin Wilson called the (rare) state of being fully awake to one's surroundings "dreaming into the world": when the perceptual system is strong enough to be fully realistic about a situation while still grasping the possibilities within it.

Dreams, mood, and coherence

Sleep is a time of revision and reinterpretation, especially during the REM phase when the activating system is enlivening the cortex. Dreams sometimes construct the mood and the sense of possibilities for the day, and when they are very successful, we wake up with a sense of newness, and direction. I think it's accurate to say that dreams maintain the organism's coherence.

— Ray Peat

Serotonin works against this process: it suppresses both slow wave sleep and REM, and its rise in old age tracks with the general loss of restorative dreaming that comes with aging and stress. Thyroid, sugar, and progesterone all lower brain serotonin and by that route support proper dreaming.

The consciousness of possibility, and the mood of exhilaration, that can sometimes be created by dreaming, are our direct experience of a metabolic and physiological process in which we are not only restored, but are reconstructed into something that never quite existed before. The things that allow us to dream properly are things that also correct our biochemistry and, on the microscopic level, our anatomy.

— Ray Peat

Melatonin and darkness

Melatonin is said to intensify dreaming, which is part of the process of arousal from sleep.

— Ray Peat

Melatonin rises with darkness and stress; its chronic elevation tracks with lower body temperature, vasoconstriction, and inhibition of both Progesterone and thyroid hormones.

Thyroid and gelatin (or glycine, as in magnesium glycinate) are protective against the serotonin and melatonin toxicities.

— Ray Peat

Progesterone and Glycine both show up directly in sleep-support contexts for exactly this reason.

Dreams, precognition, and Persinger's research

The cited account describes an experience that looked like precognitive dreaming: a period of a few weeks in 1956, and again roughly 56 years later, in which an out-of-context image would appear in the last dream before waking, and something unexpected matching it would happen a few hours afterward. It connects the timing of experiences like this to the work of neuroscientist Michael Persinger, who correlated reports of clairvoyant and telepathic experience with the Earth's geomagnetic activity, finding such experiences more common during geomagnetic calm and more disturbed during high geomagnetic activity. Persinger had begun that line of research after observing that a subject's brainwaves would synchronize with another person's during accurate psychic readings, and went on to test whether an artificial field matching the Earth's own (around 7 Hz) could link two separated people's perceptions.

Peat placed this alongside similar claims by Andrija Puharich, who built on Wilhelm Reich's orgone accumulator design, and Rupert Sheldrake's idea of a "creative formative field," while treating all of it as an open, unresolved area of research rather than settled fact.

Insomnia

Insomnia in Ray Peat's framework is tied directly to overnight blood sugar and stress-hormone patterns, not treated as a purely psychological or sleep-hygiene problem.

The overnight cascade

Because hypothyroid people store little glycogen, blood sugar falls soon after the last meal, triggering adrenaline and cortisol release that can begin almost as soon as a person lies down (see Hypoglycemia for the full quote and citation). Waking with a racing heart in the middle of the night is, in this framework, often this adrenaline peak rather than a purely psychological disturbance.

A controlled human trial supports the mechanism directly: an induced fall in blood glucose during sleep woke most healthy subjects in early sleep and all of them in late sleep, far more than on a control night, along with surges in epinephrine, cortisol, and ACTH.

Salt and sugar before bed

Peat's direct practical recommendation was salty and sugary food at bedtime or during the night, specifically because both lower adrenaline:

Salty and sugary foods taken at bedtime, or during the night, help to improve the quality and duration of sleep. Both salt and sugar lower the adrenalin level, and both tend to raise the body temperature.

— Ray Peat

Histamine and serotonin

Histamine and serotonin both promote wakefulness, and endotoxin from intestinal bacteria raises both, which makes poor digestion a common cause of insomnia in Peat's framework. A 2026 single case report of a 74-year-old man with post-viral insomnia refractory to five sleep medications recorded wearable sleep scores rising from 30–40 to about 75 after cyproheptadine was started along with supplements and removal of scented products; with one patient, bundled interventions, and a consumer ring as the outcome, it shows association only.

Heart failure and hypnotics

In the Norwegian HUNT cohort of 54,279 adults free of heart failure at baseline, people reporting all three insomnia symptoms (trouble falling asleep, trouble staying asleep, and non-restorative sleep) had about 4.5 times the hazard of heart failure over roughly a decade, after adjustment for established cardiovascular risk factors. One or two symptoms carried no significant excess (prospective cohort).

In a retrospective Veterans Affairs cohort of patients newly diagnosed with insomnia, benzodiazepine users had about 47% higher all-cause mortality than matched nonusers. Z-drug users also had higher mortality. Users of serotonin antagonist and reuptake inhibitors, the class that includes trazodone, had lower mortality. No hypnotic class changed the risk of nonfatal major adverse cardiovascular events, so the differences rest on deaths from any cause.

At night adrenaline and cortisol normally rise, even in young people, because night is a fasting state; with low thyroid or in old age they are higher, and the night becomes more stressful. If not enough glycogen was stored during the day, stress hormones rise to break down fat and muscle, and their side effect is mental alertness; insomnia is a daytime disorder that shows up at night.

Very bright incandescent light from sundown until bedtime can lower the nightly rise of stress and inflammatory hormones a little more. Progesterone lowers the stress hormones, deepens sleep and keeps breathing regular, and sleep apnea has long been treated with thyroid and progesterone.

Sleep loss and mood

A single night of lost sleep can lift depression briefly. Depressed inpatients kept awake for 36 hours responded more often by day 3 than those who slept, though their Hamilton scores ended up no different and the lift faded within a week.

Practice

A small protein/carbohydrate snack with some salt before bed, and again if waking in the night, addresses the mechanism directly rather than treating insomnia as unrelated to diet. Supporting thyroid function reduces the underlying glycogen-storage problem that sets the overnight pattern up in the first place. See Hypoglycemia, Thyroid, Salt.

In postmenopausal women with chronic insomnia, a month of daily vitamin E (400 IU of mixed tocopherols) improved self-rated sleep quality more than placebo, and fewer of them still needed sleeping pills.

For every 30 minutes of sun exposure before 10am, sleep onset moved 20 minutes earlier and sleep quality improved significantly.

Night sweats

Night sweats are drenching sweat during sleep, from infection, hormonal shifts (menopause), low blood sugar with adrenaline release, or medication. New or drenching sweats need medical workup to rule out infection and other serious causes.

The overnight blood sugar link

For the hormonal/metabolic cases, Ray Peat's overnight cascade (see Hypoglycemia for the full citation) applies directly: because hypothyroid people store little glycogen, blood sugar falls soon after the last meal, and adrenaline and cortisol rise as a result, sweating is a classic adrenaline symptom, alongside the racing heart covered on Insomnia.

Blood sugar falls at night, and...hypothyroid people store very little sugar. As a result, adrenalin and cortisol begin to rise almost as soon as a person goes to bed.

— Ray Peat

For menopausal night sweats specifically, the same morphine-withdrawal/opioid mechanism described for hot flashes applies, since night sweats and hot flashes are often the same underlying event happening during sleep. In the naloxone/morphine-withdrawal animal model of this mechanism, brain-targeted estradiol blunted the resulting temperature spike by 25% (see Hot flash for the full study).

Night-sweat practice

A protein/carbohydrate snack with salt before bed (see Insomnia) addresses the blood-sugar-driven cases directly. Persistent or drenching night sweats, especially with weight loss or fever, need medical evaluation to rule out infection or other causes before assuming a hormonal explanation.

Sleep apnea

Sleep apnea is repeated airway collapse (obstructive) or repeated pauses in breathing drive (central) during sleep. Each event drops blood oxygen and pulls the sleeper toward waking, which raises stress hormones, blood pressure and daytime fatigue. Body weight, low thyroid function, alcohol and nasal obstruction all contribute. It is a medical condition that needs a proper sleep study, not a self-diagnosis.

Weight and thyroid

Weight is the best-documented driver. In 690 adults followed for four years, a 10% weight gain predicted a 32% rise in the apnea-hypopnea index (events per hour of sleep) and a six-fold higher chance of developing moderate-to-severe disease, while a 10% loss predicted a 26% fall. A meta-analysis of 1,615 patients found clinical hypothyroidism in about 8% of people with obstructive apnea and subclinical hypothyroidism in about 11%, with worse apnea indices in the hypothyroid group, though obesity confounds the comparison.

What CPAP does and does not do

CPAP (continuous positive airway pressure) reliably removes the events: in the SAVE trial of 2,717 adults with moderate-to-severe apnea and existing heart or brain-vessel disease, the apnea-hypopnea index fell from 29.0 to 3.7 events per hour, and snoring, daytime sleepiness and mood improved. It did not reduce heart attacks, strokes or cardiovascular deaths over 3.7 years (17.0% versus 15.4% with usual care), though average use was only 3.3 hours a night. It is the standard treatment for symptoms and should not be dropped on the strength of a diet or supplement plan.

Breathing chemistry and progesterone

Acetazolamide (Diamox), caffeine, thyroid and progesterone are the treatments named as very effective in the Peat email archive, with acetazolamide stimulating respiration by changing CO2 and pH. A crossover trial in 13 men with hypertension and moderate-to-severe apnea found acetazolamide lowered the apnea-hypopnea index and mean arterial pressure by about 7 mmHg, which CPAP alone did not; the drop in blood bicarbonate tracked the fall in events. The progesterone evidence is thinner and mixed. Seven morbidly obese patients given medroxyprogesterone for two to four weeks had no change in apnea episodes, although waking blood oxygen improved, while in two case reports of a synthetic progestin one obstructive apnea became a milder hypopnea and one central apnea disappeared. Acetazolamide is a prescription drug with its own side effects.

See also

• Blue light
• Light therapy
• Obesity
• Alcohol
• Lipid peroxidation