Ketones may change sleep patterns, but not always for the better

By Pooja Toshniwal PahariaReviewed by Susha Cheriyedath, M.Sc.Oct 28 2026

From fasting to bedtime supplements, researchers examine how ketones interact with deep sleep, REM cycles, and the body's internal clock.

Working model for ketone–sleep interactions. The figure summarizes the proposed model in which ketone bodies influence sleep through partially overlapping effects on substrate availability, neuronal excitability, inflammatory tone, redox biology, epigenetic regulation, circadian timing, and respiratory/metabolic physiology. The figure was created with assistance from ChatGPT-5.6 (OpenAI). The authors reviewed and verified all scientific content and labels. Review: Ketones and Sleep: A Narrative Review of Mechanisms, Preclinical Models, and Human Evidence

A recent review published in the journal Nutrients suggests that ketones may influence sleep, but responses vary with diet, age, sex, metabolic health, and circadian timing. The authors examined ketones as both energy sources and signaling molecules. The findings may help clarify whether nutritional strategies or ketone-based interventions could help people with sleep difficulties.

Sleep and metabolism are closely linked, and ketones may play a role in that connection. Acetoacetate (AcAc), acetone, and β-hydroxybutyrate (BHB) levels increase during fasting, carbohydrate restriction, prolonged exercise, or a ketogenic diet. Insulin deficiency can also raise ketone levels and, when severe, cause ketoacidosis, a dangerous condition distinct from nutritional ketosis. How these changes affect sleep quality and the time spent in different sleep stages remains unclear.

About the review

In the present narrative review, the researchers examined animal, human, and mechanistic studies on ketones and sleep, using PubMed searches through September 2026. The evidence covered fasting, calorie restriction, ketogenic diets, and ketone supplements, prioritizing objective sleep and breathing measures. ClinicalTrials.gov and reference lists provided additional studies. The initial PubMed search identified approximately 329 records, while the final review cited 89 peer-reviewed publications and two clinical-trial registrations. The authors did not conduct a meta-analysis.

Preclinical and human evidence linking ketones and sleep

Animal studies show that sleep responses to ketones vary by type, diet, age, and sex. In mice, AcAc administered directly into the brain increased EEG slow-wave activity during non-rapid eye movement (NREM) sleep, an effect not seen with BHB. AcAc also reduced glutamate release. Ketogenic diets altered rapid eye movement (REM) and NREM sleep in rodents. In aged rats, ketogenic interventions increased REM sleep in females, while a ketone ester reduced REM sleep in males; a ketogenic diet improved memory-related performance in both sexes.

In some healthy adults, short periods of fasting or carbohydrate restriction have been linked to more deep sleep and less REM sleep. Changes in individual sleep stages do not necessarily indicate better overall sleep. For people with epilepsy, a ketogenic diet has been associated with shifts in sleep patterns, fewer seizure-related electrical discharges at night, and improved quality of life. Studies in multiple sclerosis, migraine, and metabolic disorders report improved subjective sleep, but broader clinical and metabolic changes may contribute. Among trained male cyclists, taking ketone esters after exercise and before bed was linked to higher sleep efficiency, preservation of REM sleep, and less time awake after sleep onset following an intense evening workout. Repeated D-BHB supplementation also improved selected subjective sleep measures, but benefits have varied across studies.

Sleep and ketone metabolism may influence each other, but responses to ketogenic interventions vary. Some people experience sleep disturbances during early dietary adaptation, while others report no change during sustained ketosis. The authors also propose that improved daytime function, seizure control, or recovery from exercise may indirectly improve subsequent sleep. Differences in study design, diet, and sleep assessment make comparisons difficult, and it remains unclear whether ketones themselves drive these effects or other metabolic changes. Larger controlled trials using objective sleep measures are needed to identify who might benefit.

The recently completed Johns Hopkins K-SLEEP trial examined pre-sleep ketone supplementation using objective sleep and metabolic measurements. The ongoing STAK-Sleep + Feed trial compares a ketogenic diet, a mixed diet with placebo, and a mixed diet with ketone ester supplementation during sleep restriction. In the related STAK-Sleep trial, a ketogenic precursor increased wearable-measured deep sleep and improved selected waking-performance measures under restricted sleep conditions, but EEG confirmation of sleep-stage changes is needed. These varied outcomes have drawn attention to potential pathways linking ketones with sleep regulation.

Mechanistic links between ketone bodies and sleep

Beyond supplying energy, ketones may affect nerve cell activity, inflammation, oxidative stress, and gene expression. For example, acetoacetate (AcAc) may reduce excitatory signaling by limiting glutamate release. Ketogenic metabolism may also affect ATP-sensitive potassium (KATP) channels and adenosine signaling, both of which can dampen nerve cell activity. The relevance of these processes to sleep may differ with age, metabolic health, sleep loss, and recovery after exercise.

BHB may also influence inflammatory and epigenetic pathways. Experimental studies suggest that it can suppress the NLRP3 inflammasome, a protein complex involved in inflammation. BHB can also affect histone deacetylases and a chemical modification called histone β-hydroxybutyrylation, both involved in regulating gene activity. Such changes could help cells manage oxidative stress, adapt to physiological demands, and alter gene expression through pathways potentially relevant to sleep and neural recovery. The significance of these pathways for human sleep remains uncertain.

Circadian rhythms add another layer to this relationship. Mouse studies suggest that circadian clocks help control when ketones are produced, partly through pathways involving peroxisome proliferator-activated receptor alpha (PPARα). Ketogenic diets may also alter daily gene activity in peripheral tissues. Fasting and time-restricted eating affect ketone levels, glucose, insulin, and appetite-related hormones, so the contribution of ketones alone is hard to determine.

Changes in sleep may also arise from weight loss, improved breathing, or better seizure control during ketogenic therapy. In a study of patients with obesity hypoventilation syndrome, a ketogenic diet improved nocturnal breathing, but effects on sleep stages were not established. The exercise findings point to a possible role for preceding physiological stress, while a separate study found that ketone esters did not reverse hypoxia-related disruption of sleep architecture. The effects appear to vary with the person’s metabolic state and the circumstances in which ketones are used.

Conclusion

The findings suggest that ketones may affect sleep stages and continuity, but responses may differ with a person’s metabolic health, age, sex, body clock, and level of physiological stress. Larger, well-controlled studies could help determine whether particular doses improve sleep and identify people who would benefit most. Researchers have yet to identify an optimal ketone concentration or dosing schedule for sleep, and current evidence does not support ketogenic interventions as established treatments for insomnia. Future studies should measure nocturnal AcAc and BHB alongside objective sleep, respiratory, and next-day cognitive outcomes to distinguish direct effects on sleep regulation from those linked to broader metabolic changes.