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

Delta sleep-inducing peptide (DSIP), also known as emideltide, has shown some sleep-related effects in small, historical human studies. However, the overall body of evidence is inconsistent and too limited to state 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 stage, and feeling better the next day are all different outcomes. Reviews of DSIP often combine these experiences into a single general impression, whereas clinical trials usually analyse them separately. Published research includes a few positive experiments, a number 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 about DSIP and Reddit user experiences form another layer of mixed information. Some users report rapid drowsiness, vivid dreams, deeper sleep or better recovery the following day. Others report no noticeable effect, delayed action, stimulation, broken sleep or worsened insomnia. Such experiences may point to questions worth investigating further, but cannot confirm efficacy, onset time, response rate or causality. Product identity, dose, route of administration, other substances used, sleep conditions and reporting biases are rarely controlled.

Does DSIP work? A short, evidence-based answer

DSIP may affect sleep under specific 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 mainly concerned the intravenous administration of DSIP. Their results were mixed.

In a randomised, double-blind study involving 16 people 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 a placebo in the afternoons before three experimental nights. Objective measurements suggested an improvement in sleep efficiency and a shorter sleep latency following DSIP. However, the effects were weak, some of them may have been due to an unexpected deterioration in the placebo group, and participants did not report any improvement in subjective sleep quality. The researchers concluded that short-term treatment with DSIP is unlikely to provide significant therapeutic benefits [1].

In another double-blind crossover study, intravenous DSIP was compared with placebo over four nights in individuals with chronic insomnia. Several parameters changed in a favourable direction, including the number of awakenings, sleep onset latency in the NREM phase, total waking time and wake time after sleep onset. However, most changes were not statistically significant compared with placebo or baseline values. Differences concerning 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].

Earlier research by another research group yielded more positive results. In a double-blind, cross-over study involving six individuals, an immediate feeling of sleep pressure and an increased amount of sleep were recorded 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-scale studies from the same research programme described improvements during repeated administration of DSIP. One study involving 14 individuals described an improvement from the first night of treatment, followed by further changes over the course of seven nights [4–6]. These findings 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 considerably. Some studies described subjective sleep pressure shortly after the infusion, whereas others indicated effects appearing after approximately an hour, changes during the same sleep period, or additional improvement following repeated administration.

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

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

Another review of five human studies described a period of about one hour for the onset of the sleep-inducing effect, with the action reportedly persisting even after the initial period [7]. However, this observation came from several small, historical experiments rather than a modern concentration–response pharmacokinetic study. The „one-hour” value should therefore be treated as an observation from a specific research programme rather than as a clinically confirmed rule.

Repeat-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 analysed in a placebo-controlled, double-blind setting. The researchers described significant improvement starting from the very first administration and further changes during subsequent administrations. Some effects also persisted during the first night after treatment ended [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 differed between middle-aged and elderly individuals [5].

Meanwhile, in a randomised 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 cause a predictable immediate effect comparable to a conventional fast-acting sedative.

Some participants in early trials with intravenous DSIP reported 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 the seemingly contradictory experiences. Someone may not feel sedated, even if specific sleep parameters change later on. Another person may feel tired without falling asleep any quicker. Conversely, sleep efficiency may improve without any clear conscious feeling of this immediately after administration. Subjective sleepiness is therefore not a reliable proxy for objective measurements of sleep onset latency, continuity or sleep architecture.

The pharmacokinetics of DSIP is also poorly characterised. 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 reliably predict when a contemporary DSIP product should take effect.

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

A lack of an immediate noticeable effect should not be interpreted as proof that a larger amount of DSIP is needed. Published research does not provide a validated regimen for independent use 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 differ partly because „onset of action” is defined in various ways. One study might measure the first subjective feeling, another the moment of falling asleep, changes in the EEG, total sleep time accumulated over a few hours, alertness the following morning, or improvement after consecutive nights. These outcomes are not equivalent to one another.

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

Baseline sleep state can also affect the response. A person with severe chronic insomnia, an irregular sleep schedule, acute sleep deprivation, sleep apnoea, restless legs syndrome, a 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 disorders [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 the reported effects include:

• peptide identity, purity, aggregation, degradation and actual concentration;
• route of administration, infusion rate, time and experimental schedule;
• age, general state of health, stress levels and baseline sleep architecture;
• caffeine, alcohol, nicotine, cannabis, sedatives, stimulants and prescription medicines;
• 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 a review such as „it worked after 30 minutes” cannot be generalised to everyone. Similarly, someone claiming „after a week nothing happened” cannot conclude on that basis that DSIP is completely ineffective.

What do DSIP reviews and Reddit experiences 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 drowsiness, falling asleep faster, waking up less often, 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 arousal, difficulty falling asleep, broken sleep, unusual dreams, morning fatigue, a headache, or a subjective deterioration in sleep quality.

Such contradictory experiences are not surprising. Sleep naturally varies between nights, and products sold online are not standardised clinical interventions. Reviews rarely contain an independent analysis of the product, the full history of its storage, information about other substances used, a confirmed diagnosis of sleep disorders, pre-determined 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. Yet 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 imply 100% effectiveness, just as ten negative posts do not imply 100% ineffectiveness. It is not known how many people in total have come into contact with the product but have never posted anything.

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].

Biological plausibility does not, however, confirm that a specific internet review describes a real 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 seen in published research. In a double-blind, crossover study, many favourable numerical changes did not differ significantly from placebo, and the researchers considered the clinical effect to be small [2]. A randomised study involving 16 people showed weak objective changes with no improvement in subjective sleep quality [1]. The lack of noticeable benefits is therefore consistent with the available clinical evidence.

Paradoxical stimulation or worsening of sleep should not be automatically dismissed just because DSIP is called the „sleep-inducing peptide”. In one small human study, an initial period of stimulation was noted before subsequent sleep-promoting effects [7]. Some animal experiments have also shown increased wakefulness or circadian activity under certain 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 therefore allows for the possibility of positive, zero, and paradoxical responses in a poorly characterised research area. Persistent insomnia or significant sleep deterioration should be clinically evaluated, as conditions such as sleep apnoea, 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 efficacy?

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

Selection bias strongly influences online reviews. Individuals experiencing exceptionally positive or negative effects may be more likely to post than those who notice nothing out of the ordinary. Peptide-focused communities may also attract individuals who already expect noticeable effects from these substances. Review sites controlled by vendors can additionally introduce commercial, moderation-related, or review-verification biases.

Confirmation bias can additionally influence interpretation. If someone expects deeper sleep or faster sleep onset, they may attribute ordinary improvement to DSIP, whilst nights that fail to meet expectations may be less remembered. Retrospective accounts also depend on imperfect memory, particularly as people are unable to directly observe their own sleep whilst sleeping.

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

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

How to compare user accounts with clinical evidence?

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

A prospectively kept sleep diary is more useful for observing an individual's sleep pattern, but it still cannot confirm a causal relationship. Blinded randomised 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 have been small and led to contradictory conclusions.

The evidence has not reached the standard of a repeated contemporary clinical development programme incorporating standardised product chemistry, pharmacokinetics with dosing 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 a placebo showed significant improvements in subjective sleep onset latency and subjective total sleep time. In contrast, the corresponding reduction in sleep onset latency measured polysomnographically 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, taking part in a study, changes to evening habits, monitoring, and natural fluctuations in sleep can influence 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 clinically significant, but is not equivalent to an EEG measurement.

This distinction matters when someone claims that DSIP „worked” even though the 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 they 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” metric on a device therefore does not 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 latency, awakenings, final wake-up time, perceived sleep quality, daytime functioning, caffeine, alcohol, exercise, and other medications prior to making any changes. Even then, self-monitoring can only identify associations and cannot transform an unapproved substance into a proven treatment. Excessive focus on the results of sleep-tracking devices can also increase sleep-related anxiety, a condition sometimes referred to as orthosomnia.

How to evaluate claims about DSIP on the internet?

The quality of a claim regarding DSIP can be assessed based on what was measured, how, and with what comparison. A generic 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 state whether the supporting evidence comes from human clinical trials, human observational studies, animal experiments, ex vivo studies or mechanistic research. An animal experiment involving intracerebroventricular administration should not be used to promise an immediate effect from a nasal spray in humans.

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

Warning signs 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 dosage recommendations based solely on vial size. The „5 mg” or „10 mg” designation describes the nominal content of the vial. It does not constitute proof 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 distorted 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 medicine. 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 does it 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, immediate onset of action, optimal timing of administration, effective intranasal or subcutaneous protocol, long-term benefit, or predictable effect from the modern product sold online.

They also do not confirm that an increase in the „deep sleep” metric on a consumer device translates to a genuine increase in slow-wave sleep measured polisomnographically. Reddit experiences and other online reviews also fail to predict whether a specific individual will react.

Limitations of evidence regarding effectiveness

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

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

Contemporary clinical trials would require a chemically standardised formulation, validated pharmacokinetics, appropriate randomisation 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. The identity of the product, actual exposure, other concurrent interventions, diagnosis of sleep disorders, and the method of effect evaluation are usually unknown. Anecdotal experiences should therefore be treated as examples of questions requiring investigation, rather than as proof of efficacy or response frequency.

FAQ on the effectiveness of DSIP

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, whilst in another small experiment a brief initial arousal was observed, followed by subsequent sleep-promoting effects [3,7].

DSIP has not been shown to cause 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 time.

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

Does DSIP work immediately?

Not in a predictable way.

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

Does DSIP help you fall asleep faster?

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

Therefore, current evidence does not confirm a reliable benefit regarding falling asleep.

Why isn't DSIP working for me?

Possible explanations include actual lack of efficacy, differences between expected and measured effect, natural sleep variability, underlying sleep disorder, differences in route of administration 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 has been noticed.

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

In one small human study, a brief initial phase of arousal was described. The sleep response may also depend on the timing 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 tracking device show if 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].

Simply altering 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 important for the individual.

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

What would be proof that DSIP actually works?

Stronger evidence would require suitably powered and independently replicated randomised trials using a verified DSIP formulation and clinically relevant endpoints.

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

Disclaimer

The content is for educational and scientific-information purposes only. It does not constitute medical advice, diagnosis, therapeutic recommendations, dosage information, 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 behaviour. 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 normalise 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). Characterisation, 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