Benefits of the DSIP peptide: effects, applications, and scientific evidence

Delta sleep-inducing peptide (DSIP) has been studied for its potential effects on sleep physiology, stress-related signaling, pain perception, withdrawal symptoms, mood-related parameters, and neuroprotection. However, none of these proposed benefits of DSIP have been confirmed as approved or consistently effective treatments in humans.

The published evidence is very uneven. DSIP produced measurable biological effects in laboratory studies, animal models, and a few small human studies, but most human research dates back several decades, and the results are often contradictory. Early publications described potential improvements in sleep, pain reduction, or alleviation of withdrawal symptoms, whereas better-controlled studies on insomnia showed effects that were minor, inconsistent, or of limited clinical significance [1–6]. Evidence regarding post-exercise recovery, bodybuilding, testosterone, or combining DSIP with other peptides is much weaker, and there is no direct evidence from human studies supporting such uses.

This distinction is important when asking what DSIP does or what the DSIP peptide is used for. The observed biological effect does not automatically mean a significant health benefit, and an effect demonstrated in an animal model does not confirm the same result in humans. Therefore, the following sections separate evidence from human studies, animal studies, ex vivo studies, and mechanistic studies, and determine the level of scientific support for each proposed use. Information regarding the peptide's discovery, amino acid sequence, molecular identity, and the name emideltide can be found in the main guide explaining what the DSIP peptide is.

What are the proposed benefits of the DSIP peptide?

Proposed benefits of the DSIP peptide include supporting sleep continuity, modulating stress-related signaling, reducing pain perception, alleviating symptoms associated with alcohol or opioid withdrawal, potential changes in anxiety or depressive symptoms, and protection against certain neurological factors or oxidative stress. Currently, these remain research hypotheses rather than medically confirmed benefits.

Evidence from human studies focuses mainly on sleep and a few exploratory studies regarding endocrine response, chronic pain, and withdrawal symptoms. Even in these areas, the number of participants was small, and the results could not be consistently replicated. Animal and ex vivo studies broaden the scope of the proposed action to include changes in GABA and NMDA signaling, seizure severity, cerebral ischemia, oxidative processes, and physiological adaptation to stress [7–12]. These experiments help explain why DSIP remains a subject of scientific interest, but they cannot demonstrate that comparable benefits occur in humans.

The following table summarizes the main research areas before discussing them in more detail.

DSIP and its effect on sleep

DSIP received its name after early experiments in rabbits demonstrated an increase in delta wave activity and sleep spindles on the electroencephalogram following the direct administration of the peptide into the brain. This observation led to the peptide being named and initiated decades of sleep-related research, but it did not demonstrate that DSIP acts as a natural human sleep hormone or that it is an effective treatment for insomnia [13]. Subsequent experiments yielded variable results depending on the species, dose, route of administration, timing of administration, and the DSIP analog used. A major review ultimately concluded that the proposed relationship between native DSIP and sleep remains insufficiently characterized [14].

However, several human studies have investigated whether intravenous DSIP can affect sleep. In a 1981 double-blind crossover study involving six healthy volunteers, researchers reported an immediate increase in sleep pressure as well as delayed changes in parameters such as sleep onset and sleep efficiency [15]. Because the study included only six participants, the results should be interpreted as an exploratory physiological signal rather than proof of a reliable clinical benefit.

A 1986 study involving 18 individuals with chronic psychophysiological insomnia reported an improvement in sleep parameters after a week of intravenous DSIP administration, with some changes persisting during follow-up [1]. The researchers described stronger effects in participants with more severe baseline sleep disturbances. However, the small sample size, limited independent replication, and the age of the study significantly limit the certainty of these results.

Other controlled studies yielded less favorable results. Monti and coworkers used a double-blind crossover design in individuals with chronic insomnia and observed an increase in certain parameters, including total sleep time and NREM sleep. However, several apparent differences were statistically insignificant or difficult to interpret due to baseline parameter imbalances, leading the researchers to consider the overall clinical improvement minor [2]. In 1992, Bes and coworkers evaluated 16 individuals with chronic insomnia in a double-blind, matched-pair study. DSIP caused only limited objective changes, did not clearly improve subjective sleep quality, and was deemed an unlikely source of significant therapeutic benefit [3].

Overall, human sleep literature suggests that DSIP may influence specific physiological sleep parameters under certain experimental conditions, but it has not demonstrated consistent therapeutic efficacy. Available studies do not show reliable improvement simultaneously in objective polysomnography, subjective sleep quality, daytime functioning, and clinically significant insomnia outcomes. They also do not establish long-term safety or a standardized clinical regimen. A more detailed discussion of the timing of action, sleep phases, and conflicting study results can be found in a separate guide on DSIP for sleep.

Stress response and cortisol testing

DSIP has also been studied in the context of the stress response, as sleep, hypothalamic signaling, autonomic activity, adrenocorticotropic hormone (ACTH), and cortisol are physiologically interrelated. The most relevant human study does not support the simplistic claim that DSIP directly „lowers cortisol.” In a randomized, double-blind crossover study, 11 healthy men received a single intravenous dose of synthetic DSIP or saline. Plasma ACTH-like immunoreactivity decreased for at least three hours following DSIP administration, while plasma cortisol concentrations showed the expected diurnal decline and did not differ significantly from the control group. Urinary cortisol and monoamine metabolites also remained unchanged [5].

This study therefore supports the possibility of influencing an ACTH-related laboratory parameter in healthy men, rather than providing evidence of a reduction in psychological stress or inhibition of the entire hypothalamic-pituitary-adrenal axis. ACTH-like immunoreactivity is a biomarker, whereas perceived stress, disease symptoms, and clinically relevant outcomes are distinct endpoints. This distinction is particularly important because the change in the ACTH-related parameter did not translate into a measurable difference in cortisol levels in the same experiment.

Animal studies have described broader antistress or adaptogenic effects, including changes in neuronal activity, oxidative markers, stress-related behaviors, and survival following experimental ischemia. Some of these works focused on Deltaran, which is a combination of DSIP and glycine, rather than DSIP alone [16]. The results concerning the combination product do not make it possible to determine what portion of the observed effect resulted from the action of DSIP, glycine, or the interaction between them. Furthermore, animal models of stress often use severe and artificially induced experimental conditions that do not reflect the complexity of chronic stress, burnout, anxiety disorders, or trauma in humans.

The most accurate conclusion, therefore, is that DSIP has preliminary evidence regarding biomarkers in humans and a larger body of preclinical research related to the physiology of stress. However, it has not been demonstrated to provide a clinically significant cortisol-lowering effect or to treat stress-related disorders.

DSIP Studies on Pain and Opiate and Opioid Withdrawal

DSIP has become the subject of pain research after early experiments suggested possible interactions with endogenous opioid pathways. In one study in rodents, centrally administered DSIP produced a dose-dependent antinociceptive effect in the tail-pinch and hot-plate tests. Naloxone blocked this response, and DSIP did not produce the same effect in morphine-tolerant mice. The researchers interpreted the results as evidence that opioid receptors may be involved in this mechanism directly or indirectly at the supraspinal level [8]. These remain preclinical findings and do not confirm that peripherally administered DSIP acts as an effective analgesic in humans.

The main publication on pain in humans was a 1984 pilot study involving just seven patients with conditions such as migraine or vasomotor headache, tinnitus accompanied by pain, and episodes of psychogenic pain. Participants received intravenous DSIP for five consecutive days, followed by five additional injections at longer intervals. The researchers reported a significant reduction in pain levels in six of the seven participants and described a reduction in depressive symptoms [6].

Although the result is interesting, the evidence remains highly uncertain. The study was uncontrolled, involved a very small and clinically heterogeneous group, and compared changes over time rather than DSIP with a parallel placebo group. Pain is particularly susceptible to the placebo effect, regression to the mean, natural fluctuations in symptoms, concomitant treatments, and reporting errors. The study therefore does not allow us to determine what portion of the observed improvement was directly caused by DSIP. No sufficiently large, modern randomized trial has confirmed DSIP as a treatment for migraine, neuropathic pain, tinnitus, or chronic pain.

In an early report on withdrawal, intravenous DSIP was used as the sole intervention in 67 individuals reporting alcohol or opioid withdrawal symptoms. Eighteen participants, or approximately 27% of all enrolled individuals, were lost to follow-up or deemed ineligible for assessment. Among the remaining 49, the researchers reported a beneficial response in terms of somatic symptoms in all 22 evaluated individuals with alcohol withdrawal and in 26 of the 27 evaluated individuals with opioid withdrawal, while anxiety was reported to subside more gradually [7]. A subsequent related review discussed these findings along with a proposed mechanism involving the opioid system [17].

Despite the impressive response rates reported, this evidence is insufficient to justify clinical use. The publication lacked a randomized placebo or active-control group, a significant proportion of participants were excluded from the analysis, and the study predates current standards for the assessment of withdrawal symptoms, trial registration, adverse event reporting, and intention-to-treat analysis. Alcohol withdrawal can lead to seizures, delirium, autonomic instability, and death, while opioid withdrawal also requires appropriate medical evaluation and evidence-based treatment. DSIP should not be presented as an alternative to established methods of treating withdrawal symptoms.

It is also worth clarifying the terminology. „Opiate” traditionally refers to naturally occurring substances, such as morphine, while „opioid” is a broader, modern term encompassing natural, semisynthetic, and synthetic compounds that act on opioid receptors. Both terms have been used in historical publications, but these terminological differences do not diminish the methodological limitations of these studies.

DSIP and Mood, Anxiety, and Stress

There is no adequate clinical evidence to show that DSIP treats depression, generalized anxiety disorder, panic disorder, post-traumatic stress disorder, or other psychiatric disorders. Most observations related to mood and anxiety come from secondary findings in uncontrolled clinical reports or from measurements of animal behavior.

In a pilot study of pain involving seven participants, a reduction in depression scores was reported in parallel with a reduction in pain [6]. This cannot confirm a direct antidepressant effect, as pain relief alone may influence mood, no placebo comparison was conducted, and participants were not recruited as a representative group with a clearly defined depressive disorder. In a report on withdrawal, the researchers found that somatic symptoms improved rapidly, while anxiety subsided within a few hours [7]. However, withdrawal symptoms naturally vary over time; the study was uncontrolled; and anxiety was not analyzed independently as a psychiatric diagnosis.

Animal studies included an open-field test, an elevated plus maze test, experiments on stress resistance, and measurements of neuronal activity. In one long-term study in mice using Deltaran, a longer time spent in the open arms of the elevated plus maze was observed, which the researchers interpreted as an effect similar to an anxiolytic action [18]. However, the experiment involved female SHR mice and the DSIP–glycine compound, rather than native DSIP in humans with anxiety disorders. Behavior in the elevated plus maze is an experimental screening tool and should not be considered equivalent to a human diagnosis or subjective emotional experience.

Mechanistic studies have also described changes in GABA-activated currents and NMDA-related signaling in rat neurons [9]. Because GABA and glutamate pathways are involved in anxiety, mood, sleep, seizures, and many other neurological functions, these results provide a possible hypothesis regarding the neuromodulatory action of DSIP. However, they do not confirm the efficacy, selectivity, brain exposure, or safety required for an approved psychiatric treatment.

DSIP in Bodybuilding and Post-Workout Recovery

There is no direct, controlled evidence from human studies that DSIP increases muscle mass, strength, endurance, testosterone levels, fat loss, exercise adaptation, or post-workout recovery. Claims regarding the DSIP peptide in bodybuilding or sports recovery are therefore based on extrapolation rather than proven clinical results.

One argument that is often put forward is that DSIP could improve recovery if the peptide were to improve sleep, since adequate sleep supports proper physical recovery. The problem is that both parts of this reasoning require evidence. Sleep is undoubtedly important for health and athletic recovery, but human studies on DSIP have not shown consistent, clinically significant improvements in sleep [1–3]. No study has been identified in the available literature that measures resistance training performance, muscle protein synthesis, hypertrophy, delayed-onset muscle soreness, recovery time, body composition, or injury rate following DSIP administration.

Another extrapolation concerns cortisol. The main cross-over study in humans showed a reduction in ACTH-like immunoreactivity but did not reveal a significant change in plasma or urinary cortisol [5]. This does not support the characterization of DSIP as a bodybuilding peptide that lowers cortisol. Cortisol also performs essential physiological functions related to metabolism, blood pressure regulation, immune function, and adaptation to physical stress; therefore, its nonselective reduction would not automatically confer benefits.

DSIP should also not be mechanistically compared to anabolic steroids, growth hormone, selective androgen receptor modulators, or recognized ergogenic agents. There is no evidence that it directly activates androgen receptors, growth hormone receptors, or skeletal muscle hypertrophy pathways. Claims that DSIP accelerates recovery, increases lean body mass, or improves athletic performance remain unconfirmed until direct training studies in humans are conducted.

DSIP for Men: Are There Gender-Specific Benefits?

No male-specific benefits of DSIP have been demonstrated. A 1989 endocrinological study involving 11 healthy men showed a transient decrease in ACTH-like immunoreactivity without a corresponding effect on cortisol [5]. Since only men participated in the study, it cannot be concluded on this basis that the response is specific to males, and the study does not address questions regarding testosterone, fertility, sexual function, prostate health, or physical performance.

Changes in luteinizing hormone signaling have been described in preclinical reproductive studies. In one experiment with rats, administration into the third ventricle increased luteinizing hormone levels but not follicle-stimulating hormone levels in ovariectomized female rats, while related ex vivo findings suggested a site of action in the hypothalamus [12]. This experiment did not assess testosterone levels in men. The hormonal changes observed in the ovariectomized rat model cannot be extrapolated to claims of increased testosterone, improved fertility, libido, or muscle growth in men.

Some DSIP studies were conducted on male rats, others on female mice, or in other sex-specific models. Biological sex is an important research variable, but the mere use of male animals does not constitute evidence of a „DSIP for men.” Demonstrating a significant sex-specific benefit would require sufficiently large human studies designed to compare biological sex, hormonal status, clinical outcomes, and safety.

DSIP vs. Epitalon, Selank, Pinealon, and Semax

DSIP, Epitalon or Epithalon, Selank, Pinealon, Semax, and Sermorelin are distinct compounds with different amino acid sequences, proposed mechanisms of action, and research histories. There are no reliable direct human studies showing that one of them is superior to another in terms of sleep, stress, recovery, cognitive function, or longevity. Similarly, simply combining these compounds does not constitute an evidence-based approach just because they are all classified as peptides.

The popular query „Epitalon vs DSIP” therefore has no evidence-based winner. Epitalon research focuses more heavily on cellular aging, telomere-related mechanisms, and the biology of the pineal gland and circadian rhythm, while DSIP research has primarily focused on sleep physiology, stress-related signaling, pain, withdrawal, and neurological models. These are distinct research programs, and both still rely largely on preclinical evidence or early studies. An older study of Epithalamin in elderly individuals described changes in the circadian production of melatonin; however, Epithalamin is a complex pineal-derived peptide preparation and should not be equated with either DSIP or purified Epitalon [19].

The phrase „DSIP and Epitalon” is also often used in the context of peptide stacking. No controlled human study has confirmed the efficacy, pharmacokinetics, interaction profile, or safety of combining these compounds. The same limitation applies to the combination of DSIP with Selank, Semax, Pinealon, Sermorelin, or other experimental peptides. Various proposed mechanisms may justify studying potential combinations, but they do not prove synergy and instead increase uncertainty regarding interactions and the attribution of any observed effect to a specific compound.

Animal study results versus human evidence

Animal studies are valuable in generating hypotheses, identifying biological mechanisms, and determining whether further research is warranted. However, they are not equivalent to evidence of benefit in humans. DSIP illustrates this distinction particularly well, as several animal experiments used administration directly into the brain chambers, the cerebellomedullary cistern, or spinal spaces. Such routes of administration result in a biological exposure that cannot be assumed following intravenous, subcutaneous, intranasal, or other peripheral administration in humans.

In rodent pain studies, centrally administered DSIP reduced nociceptive responses, and the effect was blocked by naloxone [8]. In ex vivo studies of rat neurons, DSIP modulated GABA and NMDA responses [9]. In seizure models, it reduced certain behavioral seizure parameters, but did not eliminate signs of epileptiform EEG activity [10]. In a focal stroke experiment in rats, an improvement in motor functions was noted following exposure to DSIP [11]. Other studies in rodents described changes in oxidative stress, antioxidant enzymes, membrane properties, age-related biomarkers, the incidence of spontaneous tumors, and behavior [18,20].

Each of these observations depends on the species, experimental model, DSIP preparation, route of administration, dose, time, and measured endpoint. A reduced response in the hot plate test is not equivalent to a lasting reduction of pain in humans; a longer time in the open arms of the elevated plus maze does not indicate effective treatment of anxiety disorders; motor improvement after stroke in a rat does not confirm functional improvement after stroke in a human; and a change in antioxidant enzyme activity does not prove a longer or healthier human life. Results concerning Deltaran require additional caution because the preparation contains both DSIP and glycine.

Human evidence is generally more informative for questions regarding human benefits, but study design remains crucial. A sufficiently large, randomized, and blinded study using clinically relevant endpoints provides more reliable evidence than an uncontrolled case series. In the case of DSIP, controlled human studies are small and inconsistent, whereas some of the most spectacular claims come from early uncontrolled reports. Therefore, the proper scientific conclusion is not that every proposed effect of DSIP is false, but that current research does not allow us to determine which effects are reproducible, clinically relevant, and sufficiently safe to justify therapeutic use.

What is DSIP used for in research?

In formal research, DSIP is utilized as an experimental compound to study sleep regulation, EEG activity, neuroendocrine signaling, stress physiology, pain pathways, interactions with the opioid system, neurotransmission, oxidative biology, seizure susceptibility, and ischemic injury. DSIP analogs have also been studied to determine how sequence modifications, phosphorylation, resistance to degradation, or formulation changes affect biological activity.

Sleep studies evaluated endpoints such as sleep latency, total sleep time, sleep efficiency, wakefulness after sleep onset, NREM sleep stages, REM sleep, and EEG spectral activity. Endocrinological studies analyzed ACTH, cortisol, luteinizing hormone, and related hypothalamic or pituitary signaling. Neurophysiological studies evaluated GABA-activated currents, NMDA receptor-mediated responses, calcium uptake, neuronal activity, seizure-like behavior, and motor function following experimental ischemia [5,9–12].

In experiments on stress and aging, oxidative products, antioxidant enzyme activity, membrane stability, organ function, spontaneous tumor incidence, behavior, and lifespan of rodents were evaluated. These results belong to preclinical studies and should not be translated into therapeutic claims for humans. Studies utilizing phospho-DSIP, KND, truncated analogs, Deltaran, or DSIP-like immunoreactivity material should also clearly specify the exact material studied instead of indiscriminately grouping all results under the heading of „DSIP benefits”.

Aside from formal research, DSIP is marketed online in the context of sleep, regeneration, stress management, and bodybuilding. Commercial availability does not make these uses evidence-based. Vendor descriptions, vial strengths, user reviews, and online community accounts cannot replace controlled clinical trials or pharmaceutical-grade verification.

Most frequently asked questions about DSIP benefits

What does the DSIP peptide do?

Experimental conditions have demonstrated that DSIP alters selected parameters of sleep, endocrine functions, neuronal and autonomic activity, and behavior; however, both the direction and clinical significance of these changes vary across studies. Available human studies do not confirm a single consistent therapeutic effect [1–7,15].

What is the DSIP peptide used for?

DSIP is used primarily as a research compound to analyze sleep physiology, stress signaling, ACTH response, pain pathways, withdrawal symptoms, neurotransmission, seizure models, and ischemic injury. It is not an approved treatment for any of these uses.

What are the main proposed benefits of DSIP?

The main proposed benefits of DSIP include improved sleep, modulation of stress-related signaling, reduced pain perception, alleviation of withdrawal symptoms, and possible neuroprotection. Sleep outcomes remain inconsistent, reports on pain and withdrawal in humans are uncontrolled, and most neuroprotective evidence comes from preclinical experiments.

Does DSIP improve sleep quality?

Some small human studies have shown improvements in selected sleep parameters, while other double-blind studies have shown little clinical significance or no clear subjective improvement [1–3,15]. Current evidence does not support DSIP as an effective treatment for insomnia.

Does DSIP lower cortisol?

Not according to a major randomized human endocrine study. DSIP decreased ACTH-like immunoreactivity, but plasma cortisol, urinary cortisol, and measured monoamine metabolite concentrations did not differ significantly from the control [5].

Does DSIP help with anxiety?

There is no adequate clinical evidence demonstrating that DSIP treats anxiety disorders. Changes in anxiety were described in an uncontrolled withdrawal report, whereas anxiolytic-like behavioral results have been observed in animals, including in experiments using Deltaran instead of DSIP alone [7,18].

Does DSIP help with depression or improve mood?

In an uncontrolled pilot pain study involving seven participants, lower depression scores were noted in parallel with a reduction in pain [6]. Because the study lacked a control group, it is impossible to separate the direct effect on mood from changes related to pain reduction, expectations, natural symptom fluctuations, or other factors, and the study does not support DSIP as an antidepressant treatment.

Does DSIP relieve pain?

Animal studies support the possibility of an antinociceptive mechanism involving opioid pathways, and a very small uncontrolled human study showed improvement in six of seven participants [6,8]. Before DSIP could be considered an evidence-based analgesic, larger randomized human trials would be necessary.

Can DSIP treat opioid or alcohol withdrawal symptoms?

An early uncontrolled report described improvement in 49 evaluable participants, but approximately 27% of all enrolled patients were excluded or lost to follow-up, and the study did not include a placebo or active control group [7]. The evidence is insufficient to support DSIP as a treatment for withdrawal, and alcohol or opioid withdrawal should be managed under appropriate professional medical care.

Does DSIP increase testosterone?

No published human studies confirm that DSIP increases testosterone. In an experiment on rats, it affected hypothalamic luteinizing hormone signaling under specific conditions, which cannot be extrapolated to claims regarding testosterone, fertility, libido, or bodybuilding benefits in humans [12].

Is DSIP useful in bodybuilding?

There is no direct evidence in humans that DSIP improves muscle growth, strength, body composition, fat loss, physical performance, or recovery. Bodybuilding claims are based primarily on indirect assumptions derived from uncertain sleep or stress data.

Is DSIP better than Epitalon?

No direct clinical trials demonstrate the superiority of DSIP or Epitalon. DSIP has been studied primarily in the context of sleep and neuroendocrinology, whereas Epitalon has been more frequently analyzed in studies concerning aging, cell biology, and the pineal gland. The differing research profiles do not provide a basis for considering either of these compounds generally superior.

Can DSIP be combined with Epitalon, Selank, Semax, or Pinealon?

No controlled human studies confirm the benefits, pharmacokinetics, interactions, or safety of combining DSIP with Epitalon, Selank, Semax, Pinealon, or similar experimental peptides. Combining unapproved compounds increases uncertainty and should not be described as confirmed synergy.

Do the benefits of DSIP differ between men and women?

No sex-specific clinical benefits have been established. Available human studies are too small to allow reliable comparisons, while results obtained in men, male rats, female mice, or ovariectomized rats cannot independently confirm benefits characteristic of men or women.

How quickly do the effects of DSIP appear?

The reported onset time varies significantly depending on the measured outcome, route of administration, formulation, and experimental design. Some early intravenous studies described physiological changes within hours, but inconsistent results and a lack of formulation equivalence mean there is no reliable, evidence-based onset time that can be applied to modern commercial DSIP products.

Limitations of evidence

The evidence base regarding DSIP is limited by small sample sizes in human studies, conflicting sleep data, older research methodology, insufficient independent replication, heterogeneous populations, and the use of intravenous or direct central routes of administration, which may differ significantly from products currently available on the market. Some of the most spectacular results come from uncontrolled studies with a high risk of bias, while many other proposed benefits are based on animal studies, isolated tissues, surrogate biomarkers, combination preparations, or chemically distinct DSIP analogues.

The absence of signals regarding serious adverse events in small historical studies should not be interpreted as proof of safety. Rare adverse events, drug interactions, endocrine changes, cardiovascular reactions, contamination risks, inaccurate dosing, and long-term consequences cannot be adequately characterized based on the available evidence. Questions regarding product identity, purity, sterility, stability, and concentration are also distinct from the biological studies summarized in this article and cannot be answered solely on the basis that the product is labeled as DSIP. For a detailed discussion of safety, please refer to the separate guide on adverse effects of the DSIP peptide.

Disclaimer

This article is for educational and scientific-informational purposes only and does not constitute medical advice, diagnosis, therapeutic guidance, dosage instructions, advice on combining peptides, purchasing advice, reconstitution instructions, guidance on treating withdrawal symptoms, or a recommendation for the use of DSIP. Delta sleep-inducing peptide is not approved by the US Food and Drug Administration or the European Medicines Agency for sleep, stress, pain, withdrawal, mood disorders, bodybuilding, post-exercise recovery, or any other use discussed in this article. Available evidence consists of small and relatively old human studies, uncontrolled clinical reports, animal studies, ex vivo experiments, and mechanistic results, and these data do not support clinical efficacy, long-term safety, a standardized method of administration, or the safety of combining peptides.

References

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