Does DSIP work? Reviews, Reddit experiences, evidence, and onset time

Delta sleep-inducing peptide (DSIP), also known as emideltide, showed some sleep-related effects in small, historical human studies. However, the overall body of evidence is inconsistent and too limited to conclude that DSIP reliably or immediately improves insomnia. The answer also depends on what is meant by the word „works.” Feeling relaxed, the onset of drowsiness, falling asleep faster, sleeping longer, spending more time in a specific sleep phase, and feeling better the next day are different outcomes. Reviews of DSIP often combine these experiences into a single general impression, whereas clinical studies typically analyze them separately. Published research includes a few positive experiments, a series of weak or statistically insignificant results, and considerable uncertainty as to whether modern DSIP products are comparable to the material administered intravenously in older studies [1–6].

Online reviews of DSIP and Reddit user experiences form another layer of mixed information. Some users report rapid drowsiness, vivid dreams, deeper sleep, or better recovery the next day. Others report no noticeable effect, delayed action, agitation, interrupted sleep, or worsened insomnia. Such experiences may point to questions worth further investigation, but cannot confirm efficacy, onset time, response rate, or causal relationship. Product identity, dosage, route of administration, other substances used, sleep conditions, and reporting errors are rarely controlled.

Does DSIP work? A short, evidence-based answer

DSIP may affect sleep under certain experimental conditions, but it has not been shown to act consistently enough to be considered an established treatment for insomnia. The best-documented historical studies involving humans were small, short-term, and primarily concerned the intravenous administration of DSIP. Their results were mixed.

In a randomized, double-blind study of 16 individuals with chronic insomnia, participants spent five consecutive nights in a sleep laboratory. Following an adaptation night and a baseline night, eight participants received intravenous DSIP and eight received placebo in the afternoon prior to three experimental nights. Objective measurements suggested improved sleep efficiency and a shorter sleep onset latency following DSIP. However, the effects were weak, some may have resulted from an unexpected worsening in the placebo group, and participants reported no improvement in subjective sleep quality. The researchers concluded that short-term DSIP treatment likely offers no significant therapeutic benefits [1].

In another double-blind crossover study, intravenous DSIP was compared with placebo for four nights in individuals with chronic insomnia. Several parameters changed in a favorable direction, including the number of awakenings, sleep onset latency in the NREM phase, total wake time, and wake after sleep onset. However, most of the changes were not statistically significant compared to placebo or baseline values. Differences regarding NREM sleep and stage 2 were also confounded by pre-existing baseline differences. The researchers considered the overall improvement to be of little clinical significance [2].

Previous research by another research group yielded more positive results. In a double-blind, crossover study involving six individuals, an immediate feeling of sleep pressure and an increased amount of sleep were observed during a 130-minute observation period following a morning intravenous infusion. Participants also exhibited a shorter sleep onset latency and better sleep efficiency during the subsequent night [3]. Subsequent small studies from the same research program described improvements during repeated administration of DSIP. One study involving 14 individuals described improvement from the first night of treatment, followed by additional changes over seven nights [4–6]. These results are scientifically significant, but their interpretation is limited by small sample sizes, closely related research groups, older methodologies, short observation periods, and inconsistent independent replication.

Available evidence therefore supports neither the extreme claim that „DSIP definitely works” nor that „DSIP never affects sleep.” A more precise conclusion is that biological and sleep-related effects have been observed, but reliable clinical efficacy has not been confirmed.

How quickly did DSIP work in published studies?

Observations regarding the duration of action vary significantly. Some studies described subjective sleep pressure shortly after the infusion, while others indicated effects appearing after about an hour, changes during the same sleep period, or additional improvement upon repeated administration.

These results cannot be combined into a single universal onset time because the studies involved different populations, designs, routes of administration, observation periods, and sleep parameters.

In an acute study involving six subjects, DSIP was administered in the morning via slow intravenous infusion. Participants reported immediate sleep pressure, and the median total sleep time during the subsequent 130 minutes increased compared to placebo. During the following night, the researchers also observed shorter sleep onset latency, less stage 1 sleep, and better sleep efficiency [3]. This experiment demonstrates that under controlled intravenous conditions, both immediate subjective effects and subsequent objective changes were recorded. However, it does not allow for conclusions to be drawn about what happens after subcutaneous or intranasal administration.

Another review of five human studies described a time to onset of sleep-inducing effects of approximately one hour, with the action reportedly persisting beyond the initial period [7]. However, this observation came from several small, historical experiments rather than a modern pharmacokinetic concentration-response study. Therefore, the value of „one hour” should be treated as an observation from a specific research program rather than a clinically confirmed rule.

Repeated-dose studies also suggest that some measured effects may change over several nights. In 14 middle-aged individuals with severe chronic insomnia, seven nights of intravenous DSIP administration were analyzed in a placebo-controlled, double-blind setting. The researchers described significant improvement starting as early as the first administration and further changes during subsequent administrations. Some effects also persisted during the first night after treatment cessation [4]. Another study involving 18 individuals showed that by the end of six administrations, some sleep parameters approached normal values and remained improved during a one-week follow-up. The timing of these changes varied between middle-aged and elderly individuals [5].

In turn, in a randomized study involving 16 people, only weak, short-term effects were observed after three afternoon administrations, and a crossover study considered the observed changes to be of little clinical significance [1,2]. Published evidence therefore does not support precise claims such as „DSIP works after 20 minutes,” „DSIP always takes an hour,” or „DSIP only starts working after a few days.”.

Does DSIP work immediately?

DSIP has not been shown to produce a predictable immediate effect comparable to a conventional fast-acting sedative.

Some participants in early intravenous DSIP studies reported an immediate sleep pressure, but the physiological response was not consistently similar to typical sedation [3,7]. In one small experiment involving individuals with insomnia, researchers observed slight arousal in the first hour, after which sleep-promoting effects appeared mainly in the second hour [7].

This difference may partly explain seemingly contradictory experiences. Someone may not feel a calming effect even if certain sleep parameters change later. Another person may feel tired without falling asleep faster. In turn, sleep efficiency may improve without a clear conscious feeling directly after administration. Therefore, subjective sleepiness is not a reliable substitute for objective measurements of sleep onset latency, continuity, or architecture.

The pharmacokinetics of DSIP are also poorly characterized. The frequently repeated claim that DSIP has a „15-minute half-life” originates from in vitro studies measuring the proteolytic removal of the N-terminal tryptophan in brain tissue preparations. This is not a confirmed elimination half-life in humans [8]. This value does not allow for a reliable prediction of when a modern DSIP product should begin to work.

The peptide may also disappear from the circulation fairly quickly, but initiate biological signaling that persists longer. On the other hand, degradation or poor absorption can prevent significant exposure from being achieved.

Lack of an immediate noticeable effect should not be interpreted as proof that a larger amount of DSIP is needed. Published studies do not provide a validated schedule for self-administration or dose escalation, and modern products sold online may vary in chemical identity, purity, salt form, concentration, sterility, and route of administration.

Why do claims regarding the duration of action of DSIP differ?

Claims about how quickly DSIP works vary partly because „onset of action” is defined in different ways. One study might measure the first subjective feeling, another the moment of falling asleep, EEG changes, total sleep time accumulated over a few hours, next-morning alertness, or improvement after consecutive nights. These results are not equivalent.

The route of administration is another important factor. Most human sleep studies have utilized supervised, slow intravenous infusion. Modern online discussions frequently involve nasal sprays or subcutaneous products, but adequate human bioavailability and onset-of-action studies for these routes are lacking. Intravenous administration introduces the peptide directly into the circulation, whereas nasal and subcutaneous administration introduce additional variables related to absorption, local degradation, formulation, and administration technique.

Baseline sleep state may also influence the response. A person with severe chronic insomnia, irregular sleep patterns, acute sleep deprivation, sleep apnea, restless legs syndrome, circadian rhythm disorder, withdrawal syndrome, or medication-induced insomnia may respond differently. Some older DSIP studies suggested stronger effects in individuals with more severe baseline sleep disturbances [5]. However, this observation primarily serves to generate hypotheses and does not prove that more severe insomnia predicts a better response.

Other factors that may influence reported effects include:

• peptide identity, purity, aggregation, degradation, and actual concentration;
• route of administration, infusion rate, time, and experimental schedule;
• age, general health status, stress level, and baseline sleep architecture;
• caffeine, alcohol, nicotine, cannabis, sedatives, stimulants and prescription drugs;
• expectations created by product descriptions and online reviews;
• bedroom conditions, screen exposure, food intake, physical activity, and circadian rhythm;
• whether sleep is assessed subjectively, using a sleep diary, a wearable device, actigraphy, EEG, or polysomnography.

These variables mean that an opinion like „it worked after 30 minutes” cannot be generalized to everyone. Similarly, someone who claims „nothing happened after a week” cannot conclude on that basis that DSIP is completely ineffective.

What do reviews about DSIP and experiences from Reddit most frequently describe?

Discussions about DSIP on Reddit, peptide reviews, German-language posts such as DSIP Erfahrung, and Polish opinions on DSIP usually contain several recurring types of experiences. These should be treated as anecdotal categories rather than reliable data regarding efficacy or the frequency of side effects.

Positive relationships may include a feeling of greater calm, the onset of sleepiness, falling asleep faster, waking up less frequently, vivid dreams, a higher „deep sleep” score on a wearable device, or feeling better the next morning. Neutral relationships often describe no clear effect or significant differences between individual nights. Negative or paradoxical experiences may include agitation, difficulty falling asleep, interrupted sleep, unusual dreams, morning fatigue, headache, or a subjective deterioration in sleep quality.

Such conflicting experiences are not surprising. Sleep naturally varies from night to night, and products sold online are not standardized clinical interventions. Reviews rarely contain independent product analysis, a full storage history, information on other substances used, a confirmed diagnosis of sleep disorders, predefined parameters, or complete observation.

Different users may also mean something else when they say that DSIP „worked.” One person might mean greater relaxation by that. Another – sedation. Still another might simply mean a higher sleep score shown by a wearable device.

It is not possible to calculate a reliable response rate based on online posts. Ten positive reviews do not mean the product is 100% effective, just as ten negative reviews do not mean the product is 100% ineffective. It is unknown how many people have used the product but never posted anything about it.

Positive, negative, and paradoxical sleep relationships

Positive experiences with DSIP are biologically plausible at least in a limited sense, as controlled experiments have described sleep pressure, shorter sleep onset latency, better sleep efficiency, and changes in total sleep time or NREM parameters [1–6].

However, biological plausibility does not confirm that a specific internet review describes an actual pharmacological effect. Someone could have simultaneously changed their sleep schedule, caffeine intake, screen exposure, physical activity, or other substances.

Negative relationships are also consistent with the uncertainty evident in published research. In a double-blind, crossover study, many favorable numerical changes did not differ significantly from placebo, and the researchers considered the clinical effect to be minor [2]. A randomized study involving 16 people showed weak objective changes without an improvement in subjective sleep quality [1]. The lack of noticeable benefits is therefore consistent with the available clinical evidence.

Paradoxical stimulation or sleep worsening should not be automatically dismissed just because DSIP is called the „sleep-inducing peptide.” One small human study noted an initial period of stimulation prior to subsequent sleep-promoting effects [7]. Some animal experiments have also shown increased wakefulness or circadian activity under specific conditions. These results do not prove that insomnia is a common side effect of DSIP, but they show why the peptide's name should not be interpreted as a guarantee of immediate sedation.

Available evidence thus allows for the possibility of positive, null, and paradoxical responses in a poorly characterized area of research. Persistent insomnia or significant sleep deterioration should be clinically evaluated, as conditions such as sleep apnea, mood disorders, pain, thyroid disease, restless legs syndrome, medication side effects, substance use, and circadian rhythm disorders require different diagnostic and treatment methods.

Why cannot anecdotes confirm effectiveness?

An anecdote describes what happened after using the product, but does not show what would have happened without that product. The lack of this comparison is one of the main reasons why placebo-controlled randomized trials are needed.

Selection bias strongly influences online reviews. Individuals experiencing exceptionally positive or negative effects may post more frequently than those who notice nothing special. Peptide-focused communities may also attract people who already expect a noticeable effect from these substances. Review sites controlled by sellers can further introduce commercial bias, moderation bias, or bias related to how reviews are verified.

Confirmation bias can further influence interpretation. If someone expects deeper sleep or faster sleep onset, they may attribute normal improvement to DSIP, while nights that do not meet expectations may be less remembered. Retrospective accounts also depend on imperfect memory, especially since people cannot directly observe their own sleep while sleeping.

Regression to the mean is another important phenomenon. People often start a new intervention after a few exceptionally bad nights. Even without effective treatment, sleep can naturally return toward a person's typical level. When improvement appears after starting a new product, this sequence of events can create a very convincing, but potentially false, impression of causality.

Product variability creates additional difficulties in the case of unapproved peptides. Two people using products labeled as „DSIP” may not actually be receiving chemically equivalent material. Online reviews rarely include authenticated, batch-specific analysis confirming identity, content, impurities, aggregates, sterility, or degradation. Therefore, a review may describe an experience associated with the product label rather than confirmed exposure to emideltide.

How to compare user reports with clinical evidence?

The reliability of clinical evidence increases with the quality of control and measurement methods. A spontaneous Reddit comment sits near the bottom of the evidence hierarchy because neither the exposure nor the outcome is properly controlled.

A prospectively maintained sleep diary is more useful for observing an individual's sleep pattern, but it still cannot confirm a causal relationship. Blinded randomized comparisons using validated parameters provide much stronger evidence. Independent replication in adequately powered studies has even greater value.

Research on DSIP has reached the level of controlled trials, but available studies were small and led to contradictory conclusions.

The evidence has not reached the level of a replicated modern clinical development program encompassing standardized product chemistry, pharmacokinetics with dose-finding studies, route-dependent analyses, clinically relevant endpoints, and long-term safety monitoring.

Placebo effect, expectations, and sleep monitoring

Insomnia is particularly susceptible to the influence of expectations and the method of measurement. A meta-analysis of participants with insomnia receiving placebo showed a significant improvement in subjective sleep onset latency and subjective total sleep time. In contrast, the corresponding reduction in sleep onset latency measured by polysomnography was much smaller and did not reach statistical significance [10]. Another analysis showed a small to moderate, but significant, placebo response across various insomnia parameters [11].

This does not mean that sleep-related symptoms are imagined. Expectations, participation in the study, changes in evening habits, monitoring, and natural fluctuations in sleep can affect subjectively and sometimes objectively measured parameters.

Subjective and objective sleep measurements may also differ. People with insomnia may underestimate their sleep time or overestimate their wake time. Other people may have physiological sleep disorders that they do not consciously notice. A sleep diary records a person's actual experience, which is of clinical importance, but is not equivalent to an EEG measurement.

This distinction matters when someone claims that DSIP „worked” even though data from their wearable device did not change, or concludes that DSIP did not work despite feeling more rested the next day.

Consumer wearable devices can provide useful long-term information, but are not equivalent to polysomnography. A 2025 meta-analysis showed significant differences between wrist-worn devices and polysomnography in terms of total sleep time, sleep efficiency, sleep onset latency, and wake after sleep onset [12]. Consumer devices generally detect sleep better than quiet wakefulness, and sleep stage estimates depend on proprietary algorithms. A single increase in the „deep sleep” index on a device does not, therefore, prove that DSIP increased slow-wave sleep as defined by EEG.

A more structured observational approach would involve consistently recording variables such as bedtime, estimated sleep onset time, awakenings, final wake-up time, perceived sleep quality, daytime functioning, caffeine, alcohol, exercise, and other medications before introducing any changes. Even then, self-monitoring can only identify associations and cannot transform an unapproved substance into a proven treatment method. Excessive focus on the results of sleep-tracking devices can also increase sleep-related anxiety, sometimes referred to as orthosomnia.

How to evaluate claims about DSIP on the internet?

The quality of a claim regarding DSIP can be evaluated based on what was measured, how, and with what comparison. A general statement such as „DSIP improves sleep” conveys significantly less information than a claim specifying the population, route of administration, schedule, comparison group, sleep endpoint, effect size, and level of uncertainty.

A credible scientific claim should clearly indicate whether the supporting evidence comes from human clinical trials, human observational studies, animal experiments, ex vivo studies, or mechanistic studies. An animal experiment with intracerebroventricular administration should not be used to promise an immediate effect from a nasal spray in humans.

Statistical significance and clinical significance should also be considered separately. A numerical improvement can achieve statistical significance while at the same time being too small to provide a noticeable benefit.

Warning signals in a commercial message include guaranteed onset times, claims that everyone responds, presenting opinions as clinical evidence, suggesting that a „research use” label confirms product quality, and usage recommendations based solely on vial size. The „5 mg” or „10 mg” designation describes the nominal content of the vial. It does not constitute evidence of a clinically justified dose nor does it confirm how much intact peptide is actually in the product.

It is also worth checking whether the review accounts for negative results. A balanced assessment of DSIP should consider both early positive experiments and controlled studies describing weak, statistically insignificant, or clinically minor effects [1–6]. Ignoring either side leads to a skewed picture of the evidence.

Finally, CAS numbers, PubChem entries, regulatory database records, and the very existence of published research on DSIP do not mean that DSIP is an approved drug. Proof of the existence of a specific chemical compound is not the same as proof of its clinical efficacy.

What do current evidence confirm, and what do they not confirm?

Available evidence shows that intravenously administered DSIP altered certain subjective and objective sleep parameters in small, historical human experiments.

They also show that the results were inconsistent. Some apparent improvements did not clearly separate from placebo, and at least two controlled trials considered the clinical benefit to be weak or limited [1–8].

Evidence does not support a reliable response rate to DSIP, an immediate onset of action, an optimal time of administration, an effective intranasal or subcutaneous protocol, a long-term benefit, or a predictable effect from the contemporary product sold online.

They also do not confirm that an increase in the „deep sleep” metric on a consumer device means a real increase in slow-wave sleep measured polisomnographically. Reddit experiences and other online reviews also do not allow for predicting whether a specific person will respond.

Limitations of evidence on efficacy

Most DSIP sleep studies date from the 1980s and early 1990s. The study groups were usually very small, often comprising from six to fewer than twenty participants.

Treatment periods were short, most human studies used intravenous administration, and a few favorable publications came from overlapping research groups. Differences in methodology, baseline insomnia severity, timing of administration, and analyzed endpoints make it difficult to pool the totality of the evidence.

Modern clinical trials would require a chemically standardized formulation, validated pharmacokinetics, adequate randomization and blinding, pre-specified clinically relevant endpoints, adequate statistical power, independent replication, route-dependent evaluation, and longer safety follow-up. Such data are not currently available for DSIP.

Internet reviews have even greater limitations. Usually, the product identity, actual exposure, other concurrent interventions, diagnosis of sleep disorders, and method of outcome assessment are unknown. Anecdotal experiences should therefore be treated as examples of questions requiring investigation rather than as proof of efficacy or response rate.

FAQ regarding DSIP efficacy

Does DSIP work for sleep?

DSIP altered sleep parameters in some small, historical studies, but the results were inconsistent and often had little clinical significance.

Current evidence does not support DSIP as a reliable treatment for insomnia [1–6].

Does the DSIP peptide cause drowsiness?

Some study participants reported sleep pressure, while in another small experiment a brief initial arousal was observed, followed by subsequent sleep-promoting effects [3,7].

It has not been shown that DSIP causes drowsiness in everyone, and the feeling of drowsiness does not necessarily mean an improvement in sleep architecture or overall sleep quality.

How long does DSIP take to start working?

There is no validated, universal onset of action time.

Historical intravenous studies described immediate sleep pressure in some participants, a latency of about one hour in one study summary, changes during the same night, and additional effects during subsequent nights [3–7]. These observations do not allow for determining the duration of action of intranasal or subcutaneous products.

Does DSIP work immediately?

Not in a predictable way.

One very small intravenous study showed immediate subjective effects, while other studies described delayed, weak, absent, or initially stimulatory reactions [1–3,8].

Does DSIP help you fall asleep faster?

Some experiments have shown a reduction in objective sleep latency, but the results were weak or did not consistently differ from placebo [1,2].

Current evidence therefore does not confirm a reliable benefit regarding falling asleep.

Why doesn't DSIP work for me?

Possible explanations include actual lack of efficacy, differences between expected and measured effect, natural sleep variability, underlying sleep disorder, differences in administration route or absorption, interactions with other substances, or issues with product identity or degradation.

Available evidence does not justify increasing exposure to an unapproved peptide simply because no immediate effect was observed.

Why do some reviews of DSIP describe stimulation or worse sleep?

In one small human study, a brief initial phase of stimulation was described. The sleep response may also depend on the time of administration, baseline sleep state, route of administration, other substances, and product quality [8].

Anecdotal accounts do not make it possible to determine how often paradoxical effects occur.

Are reviews about DSIP on Reddit reliable?

Reddit experiences show what individual users report, but cannot confirm product identity, causality, response rate, or replace controlled clinical trials.

Both positive and negative relationships can be influenced by selection bias, expectations, confirmation bias, and imperfect memory.

Can a sleep monitoring device show whether DSIP is working?

A wearable device can help track personal sleep patterns over time, but consumer devices differ from polysomnography in several important sleep parameters and may misclassify sleep stages [12].

Just changing the sleep score on the device does not prove that DSIP caused a biological change.

Is a positive subjective experience meaningless?

No. Feeling more rested or functioning better the next day may be significant for a specific individual.

However, one person's experience cannot confirm that DSIP caused the improvement, that the effect will repeat, or that the product is safe and effective for others.

What would be proof that DSIP really works?

Stronger evidence would require appropriately powered and independently replicated randomized trials using a validated DSIP formulation and clinically relevant endpoints.

These studies would also have to include route-dependent pharmacokinetics and appropriate safety monitoring. A modern clinical program of this type currently does not exist for DSIP.

Disclaimer

The content is for educational and scientific-informational purposes only. It does not constitute medical advice, a diagnosis, therapeutic recommendations, information regarding dosage, or a recommendation for the use of DSIP.

Delta sleep-inducing peptide (DSIP, emideltide) is not approved by the US Food and Drug Administration, the European Medicines Agency, or the UK Medicines and Healthcare products Regulatory Agency for the treatment of insomnia or any other uses discussed in this article.

Available evidence is limited and includes small historical human studies, animal studies, and mechanistic data. Internet reviews and Reddit user experiences are anecdotal and do not confirm efficacy or safety.

The article does not recommend purchasing, dosing, preparing, injecting, or otherwise administering DSIP.

References

[1] Bes, F., Hofman, W., Schuur, J., & Van Boxtel, C. (1992). Effects of delta sleep-inducing peptide on sleep of chronic insomniac patients: A double-blind study. Neuropsychobiology, 26(4), 193–197. https://doi.org/10.1159/000118919

[2] Monti, J. M., Debellis, J., Alterwain, P., Pellejero, T., & Monti, D. (1987). Study of delta sleep-inducing peptide efficacy in improving sleep on short-term administration to chronic insomniacs. International Journal of Clinical Pharmacology Research, 7(2), 105–110. https://pubmed.ncbi.nlm.nih.gov/3583493/

[3] Schneider-Helmert, D., Gnirss, F., Monnier, M., Schenker, J., & Schoenenberger, G. A. (1981). Acute and delayed effects of DSIP (delta sleep-inducing peptide) on human sleep behavior. International Journal of Clinical Pharmacology, Therapy, and Toxicology, 19(8), 341–345. https://pubmed.ncbi.nlm.nih.gov/6895513/

[4] Schneider-Helmert, D. (1987). Effects of delta-sleep-inducing peptide on 24-hour sleep-wake behaviour in severe chronic insomnia. European Neurology, 27(2), 120–129. https://doi.org/10.1159/000116143

[5] Schneider-Helmert, D. (1986). Efficacy of DSIP to normalize sleep in middle-aged and elderly chronic insomniacs. European Neurology, 25(6), 448–453. https://doi.org/10.1159/000116050

[6] Schneider-Helmert, D., & Schoenenberger, G. A. (1983). Effects of DSIP in man: Multifunctional psychophysiological properties besides induction of natural sleep. Neuropsychobiology, 9(4), 197–206. https://doi.org/10.1159/000117964

[7] Schneider-Helmert, D., & Schoenenberger, G. A. (1981). The influence of synthetic DSIP (delta-sleep-inducing-peptide) on disturbed human sleep. Experientia, 37(9), 913–917. https://doi.org/10.1007/BF01971753

[8] Schoenenberger, G. A. (1984). Characterization, properties and multivariate functions of delta-sleep-inducing peptide (DSIP). European Neurology, 23(5), 321–345. https://doi.org/10.1159/000115711

[9] Graf, M. V., Saegesser, B., & Schoenenberger, G. A. (1987). Degradation and aggregation of delta sleep-inducing peptide (DSIP) and two analogs in plasma and serum. Peptides, 8(4), 599–603. https://doi.org/10.1016/0196-9781(87)90031-3

[10] McCall, W. V., D’Agostino, R., Jr., & Dunn, A. (2003). A meta-analysis of sleep changes associated with placebo in hypnotic clinical trials. Sleep Medicine, 4(1), 57–62. https://doi.org/10.1016/S1389-9457(02)00232-6

[11] Winkler, A., Rief, W., & Colloca, L. (2015). Effects of placebo administration on polysomnographic and subjective sleep indices in insomnia disorder: A meta-analysis. Psychotherapy and Psychosomatics, 84(6), 367–374. https://doi.org/10.1159/000436683

[12] Lee, Y. J., Lee, J. Y., Cho, J. H., Kang, Y. J., & Choi, J. H. (2025). Performance of consumer wrist-worn sleep tracking devices compared to polysomnography: A meta-analysis. Journal of Clinical Sleep Medicine, 21(3), 573–582. https://doi.org/10.5664/jcsm.11460