MDEA
N-ethyl-3,4-methylenedioxyamphetamine
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MDEA (3,4-methylenedioxy-N-ethylamphetamine) — Eve — is a synthetic empathogen of the phenethylamine class. It is the N-ethyl homolog of MDMA, producing a shorter and more sedating experience. MDEA is a triple monoamine releasing agent,[1][2] producing its effects by flooding synapses with serotonin, dopamine, and norepinephrine.
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Alexander Shulgin first synthesized MDEA in 1976 and later described it in PiHKAL.[3] Following MDMA's emergency Schedule I placement in 1985, MDEA circulated briefly as a legal substitute until it was itself scheduled in October 1987.[4][5] It remains a Schedule I substance in the United States with no accepted medical use and no registered clinical trials.
Subjective effects include entactogenic warmth, mood elevation, psychomotor stimulation, and subtle perceptual alterations. The experience occupies a quieter register than MDMA — more sedating, more inwardly focused, with retained metacognitive clarity at equivalent subjective intensity.[6][7] Post-dose low mood from serotonin depletion, elevated heart rate, and residual fatigue are characteristic unsought effects.[8]
No physical dependence has been characterized, and acute toxicity centers on overheating and cardiovascular stress.[4][8] Hot, crowded environments dramatically amplify the danger — documented fatalities involve cardiac arrhythmias in individuals with pre-existing heart conditions, and overheating drives the primary lethal pathway shared across the MDxx class.[7] The evidence base is exceptionally thin: one controlled human study, a handful of pharmacokinetic investigations, and rat neurotoxicity data constitute nearly the entire published literature.[6]
History[edit]
Discovery
Alexander Shulgin first synthesized MDEA in 1976 and documented the compound in PiHKAL.[3] His self-experiments noted MDEA's similarity to MDMA in character and potency but with faster onset and shorter duration. In 1986, David Nichols coined the term "entactogen" — meaning "to produce a touching within" — to describe the pharmacological class encompassing MDEA, MDMA, and MDA, distinguishing these compounds from both classical stimulants and hallucinogens.[1]
Scheduling and Prohibition
Following MDMA's emergency Schedule I placement on 31 May 1985, MDEA circulated briefly in the United States as a legal substitute.[4] The 1986 Federal Analog Act curtailed distribution by treating structural analogs of Schedule I substances as equivalently controlled when intended for human consumption. MDEA was formally placed in Schedule I in October 1987,[4][5] a process accelerated by a landmark 1987 JAMA report documenting five deaths associated with MDEA and MDMA use.[4]
Modern Status
No registered clinical trials for MDEA have been conducted, and the compound sees limited recreational circulation compared to MDMA. Street tablets sold as "Ecstasy" through the late 1980s and 1990s often contained MDEA alongside other MDxx compounds, though dedicated MDEA use has remained a niche within the broader entactogen market.[6]
MDEA's street name Eve was marketed as a companion to MDMA's colloquial name Adam — a pairing rooted in branding rather than pharmacology. The generic term "Ecstasy" came to encompass the entire MDxx class — MDA, MDMA, MDEA, and MBDB — and street tablets frequently contained mixtures of multiple ring-substituted amphetamines.[6]
Chemistry[edit]
Structure
MDEA belongs to the substituted methylenedioxyphenethylamine family, a subclass of phenethylamines defined by a methylenedioxy ring fused to the 3,4 positions of the phenyl ring. It is the N-ethyl homolog of MDMA (N-methyl) and the N-ethyl derivative of MDA (primary amine). The structural progression MDA → MDMA → MDEA represents successive N-alkylation of the amine nitrogen, with each step modifying transporter selectivity and subjective effect profile.[9]
| Molecular formula | C₁₂H₁₇NO₂ |
| Molecular weight | 207.27 g/mol |
The molecule comprises three defining features: the 1,3-benzodioxole ring system (the methylenedioxy pharmacophore), an ethylamine side chain with an alpha-methyl substituent, and an N-ethyl group on the terminal amine. The alpha-methyl group confers amphetamine-class oral bioavailability and resistance to monoamine oxidase metabolism. The methylenedioxy bridge is the key structural element shared across the MDxx series, contributing to SERT substrate recognition.
Stereochemistry
MDEA has one chirality center at the alpha-carbon, yielding R- and S-enantiomers. The racemic mixture is the form encountered recreationally and studied in controlled trials. After oral administration, the R-enantiomer predominates in plasma with an AUC ratio of R:S = 3.1 and a longer half-life (R: 7.9 h vs S: 4.0 h),[10] reflecting preferential metabolism of the S-enantiomer.[11]
Identification
MDEA is typically encountered as the hydrochloride salt. A structural regioisomer exists with an identical molecular weight and similar mass spectral fragmentation, requiring chromatographic methods for definitive identification.[12] Standard immunoassay drug screens may detect MDEA as part of an amphetamine or MDMA panel but cannot distinguish it from MDMA or other MDxx compounds; forensic confirmation requires GC/MS or HPLC.[12]
Pharmacology[edit]
Mechanism of Action
MDEA enters presynaptic nerve terminals via the serotonin, dopamine, and norepinephrine transporters and triggers carrier-mediated release of stored monoamines into the synapse.[1][2] The primary driver of MDEA's entactogenic effects is serotonin release, where it is approximately equipotent with MDMA.[13]
The critical pharmacological distinction from MDMA is MDEA's reduced dopamine-releasing capacity. Where MDMA produces full dopamine release, MDEA functions as a partial releaser — achieving roughly 60% of MDMA's maximum dopaminergic output.[14] The potency order for dopamine release is MDA > MDMA > MDEA,[13] consistent with the general finding that extending the N-alkyl chain reduces dopaminergic activity.[9]
MDEA is also the least potent MDxx compound at the norepinephrine transporter.[15] This combination — full serotonergic potency with attenuated dopaminergic and noradrenergic activity — accounts for the more sedating, less stimulating character of the MDEA experience relative to MDMA.
No data on direct receptor binding at 5-HT₂A, alpha-adrenergic, or other off-target sites have been published for MDEA. MDMA interacts with organic cation transporters and the plasma membrane monoamine transporter as additional low-affinity targets;[16] MDEA may share these interactions by structural analogy, but this remains untested. inferred
Metabolism
MDEA undergoes two primary metabolic pathways: N-deethylation to MDA (an active metabolite) and O-demethylenation to a catechol intermediate.[11] Both pathways preferentially process the S-enantiomer, explaining why the R-enantiomer persists longer in plasma (R-MDE half-life: 7.9 h vs S-MDE: 4.0 h).[10]
The catechol metabolites undergo further processing through glucuronidation and sulfation,[17] and are O-methylated by COMT with pronounced stereoselectivity.[18] These catechol metabolites inhibit COMT-catalyzed dopamine methylation,[18] which may affect downstream dopamine tone.
No data on oral bioavailability, volume of distribution, protein binding, or renal clearance have been published for MDEA.
Neuroscience[edit]
Where It Acts
MDEA's serotonin release, equipotent with MDMA,[13] predicts comparable modulation of amygdala-mediated fear responses — the mechanism central to MDMA's therapeutic potential in PTSD. Its partial dopamine releasing activity[14] predicts attenuated activation of the mesolimbic mesolimbic pathway, providing a mechanistic basis for the reduced stimulation and euphoria reported with MDEA.[6][7] inferred
The only direct human neurobiological data come from a single challenge study documenting prolonged cortisol and prolactin elevation following 140 mg oral MDEA.[8] Prolactin release confirms central serotonin activity at pharmacologically active doses; cortisol elevation reflects stress-axis activation secondary to monoamine stimulation.
Why It Matters
MDEA occupies a boundary position within the entactogen class that Nichols defined as distinct from both stimulants and hallucinogens.[1][2] It sits at the minimum end of the dopaminergic spectrum — enough dopamine release to sustain a warm, emotionally engaged state, but too little for full stimulant-type reinforcement. This makes MDEA a natural reference point for understanding how much dopamine activity is required for entactogenic phenomenology.
The partial dopamine ceiling also carries practical implications: the "wanting" component of reward (driven by mesolimbic dopamine) is predicted to be attenuated, while the "liking" component (tied to serotonergic circuits) is relatively preserved — consistent with reports of retained emotional warmth alongside reduced compulsive redosing.
Whether MDEA produces neuroplasticity comparable to MDMA — relevant to any therapeutic potential — is unknown. The human neurotoxic dose threshold has not been established; all neurotoxicity data derive from rats at doses far exceeding typical human exposure,[19] and translation remains uncertain.[6]
Subjective Effects[edit]
MDEA's experiential core is entactogenic warmth with retained clarity. The emotional signature — openness, gentle stimulation, anxiolysis — is consistent across the dose range and relatively resistant to set-and-setting disruption compared to serotonergic hallucinogens. At higher doses, subtle perceptual shifts emerge, trending toward the hallucinogenic end of the MDxx spectrum, though full hallucinogenesis does not occur. The experience is frequently described as "easily controllable," with users retaining metacognitive awareness throughout.[6]
Compared to MDMA, MDEA produces a qualitatively more sedating, less energizing experience — a "stoning" quality noted across multiple characterizations.[7] The pro-social and empathogenic drive is present but muted, while the inward emotional warmth is preserved. This positions MDEA between MDMA's outward sociability and the quiet interiority of purely serotonergic compounds.
Effect Grid
At common doses, the full entactogenic profile manifests: pronounced emotional warmth and openness, feelings of closeness and empathy, relaxation combined with mild psychomotor stimulation, and a pleasant, easily controllable mood state. Mild perceptual alterations — enhanced color saturation, increased tactile sensitivity — may be present without frank hallucination.
Cardiovascular effects become measurable: tachycardia, systolic blood pressure elevation, and pupil dilation are expected. Jaw tension (trismus), appetite suppression, and mild temperature dysregulation occur. Serum cortisol and prolactin elevate significantly.
The experience lasts 3-5 hours with a relatively gentle offset. Sleep may be difficult for several hours after effects subside.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Light sensitivity · Sound sensitivity · Color enhancement · Dreaming enhancement · Visual haze / noise · Tracers · Color alteration · Auditory distortion · Visual breathing · Visual drifting · Taste enhancement · Symmetrical texture repetition · Peripheral misidentification · Synesthesia
Visual haze / noise · Tracers · Color alteration · Auditory distortion · Visual breathing · Visual drifting · Taste enhancement · Symmetrical texture repetition · Peripheral misidentification · Synesthesia
Spontaneous body sensations · Tactile euphoria · Stimulation · Dehydration sensation · Excessive sweating · Bruxism · Wakefulness · Appetite suppression · Dry mouth · Tingling / electric sensations · Physical fatigue · Insomnia · Muscle tension · Laughter fits · Vibrations / buzzing · Bodily heaviness · Brain zaps · Sexual arousal enhancement · Nausea · Headache · Heart rate perception changes · Pain suppression · Dizziness · Restlessness · Nystagmus (eye wobbles) · Respiratory stimulation · Bodily lightness · Sexual arousal suppression · Abnormal heartbeat · Increased urination · Trembling · Motor control impairment · Muscle relaxation · Vomiting · Involuntary body movements
Dehydration sensation · Excessive sweating · Bruxism · Wakefulness · Appetite suppression · Dry mouth · Tingling / electric sensations · Physical fatigue · Insomnia · Muscle tension · Laughter fits · Vibrations / buzzing · Bodily heaviness · Brain zaps · Sexual arousal enhancement · Nausea · Headache · Heart rate perception changes · Pain suppression · Dizziness · Restlessness · Nystagmus (eye wobbles) · Respiratory stimulation · Bodily lightness · Sexual arousal suppression · Increased urination · Trembling · Motor control impairment · Muscle relaxation · Vomiting · Involuntary body movements
Cognitive fatigue · Introspection enhancement · Aesthetic enhancement · Thought connectivity · Humor enhancement · Memory suppression · Analysis suppression · Cognitive flexibility · Language enhancement · Novelty enhancement · Conceptual thinking · Cognitive impairment · Creativity enhancement · Motivation enhancement · Pattern recognition enhancement · Motivation suppression · Thought deceleration · Compulsive redosing urge · Thought acceleration · Increased nature relatedness · Memory replays · Memory fragmentation · Thought disorganization · Confusion · Focus enhancement · Information processing enhancement · Amnesia
Thought connectivity · Humor enhancement · Memory suppression · Analysis suppression · Cognitive flexibility · Language enhancement · Novelty enhancement · Conceptual thinking · Cognitive impairment · Creativity enhancement · Motivation enhancement · Pattern recognition enhancement · Motivation suppression · Thought deceleration · Thought acceleration · Increased nature relatedness · Memory replays · Memory fragmentation · Thought disorganization · Confusion · Focus enhancement · Information processing enhancement · Amnesia
Anxiety suppression · Simultaneous emotions · Irritability · Emotional lability · Dysphoria · Anhedonia · Catharsis · Empathy suppression · Anxiety · Mania
Emotional lability · Dysphoria · Anhedonia · Catharsis · Empathy suppression · Anxiety
Emotional susceptibility · Communication enhancement · Craving · Flow state · Compulsive behavior reduction · Sociability suppression · Social disconnection · Depersonalization · Derealization · Boundary dissolution · Identity alteration
Compulsive behavior reduction · Sociability suppression · Social disconnection · Depersonalization · Derealization · Boundary dissolution · Identity alteration
Timeline
First alerts emerge as a subtle shift in body awareness — mild warmth in the chest and a lightening of mood. Faster onset than MDMA was noted by Shulgin.
Emotional warmth builds progressively. Heart rate and blood pressure begin to rise. Mild anxiety or restlessness may accompany the transition as effects intensify.
Full entactogenic state: emotional openness, feelings of closeness, relaxation with mild stimulation. Cardiovascular effects (tachycardia, systolic hypertension) and neuroendocrine changes (cortisol, prolactin elevation) are maximal.
Effects remain present but gradually diminish in intensity. The emotional warmth persists with decreasing stimulation. A sedating, "stoning" quality may predominate during the plateau.
Progressive return to baseline. Mild fatigue and emotional flatness emerge as serotonin stores deplete. Appetite may begin to return.
Residual mood changes — either gentle positivity or mild dysphoria — may persist for 6–12 hours. Some users report a low-mood period over the following 1–2 days consistent with serotonin depletion.
⚠ Do not drive or operate heavy machinery until after a full night of sleep, as residual cognitive and psychomotor impairment may persist beyond subjective awareness of effects.
Safety[edit]
- Acute toxicity
- Moderate
- Chronic toxicity
- Moderate
- Withdrawal
- Mild
- Tolerance buildup
- rapid
- Tolerance reset
- 14 days
- Physical
- Low
- Psychological
- Moderate
- Compulsive redosing
- Low
- Dose escalation
- Moderate
- Cross-tol.
- MDMA · MDA · serotonin releasing agents
Toxicity
Acute Toxicity
No lethal dose has been determined for MDEA in any species. safety citation needed
Overheating is the primary acute lethal mechanism for the MDxx class. MDEA produces dose-dependent temperature elevation, requiring approximately twice the dose of MDMA for equivalent hyperthermic effect in animal models.[19][13] Dangerous overheating and potentially fatal high fevers are documented in human MDEA users.[7]
Heart and Circulation
A controlled study of 140 mg oral MDEA in healthy volunteers produced significant increases in heart rate and blood pressure.[8] Fatal heart rhythm disturbances have been documented in individuals with underlying heart conditions who used MDEA or MDMA.[4]
Muscle Breakdown and Clotting Failure
Muscle breakdown and widespread clotting failure are documented as fatal complications of MDxx poisoning, particularly when combined with overheating.[7]
Fatal Cases
A 1987 JAMA report documented five deaths associated with MDMA and MDEA use, three involving individuals with pre-existing heart disease.[4] A Belgian forensic review of 34 amphetamine-related deaths (1976–2004) included MDEA cases, with acute cardiopulmonary failure as the most frequent cause.[20] A UK analysis of 605 ecstasy-related deaths (1997–2007) found victims were younger (mean age 28.3 years) and less likely to be known drug users than amphetamine or methamphetamine fatalities.[21]
Liver Damage
Liver damage is listed among MDxx class adverse effects,[22] but no MDEA-specific cases have been reported. This risk is inferred from structural analogy to MDMA. inferred
Low Sodium
Dangerously low sodium levels from inappropriate water retention and excess water intake are documented for MDMA but not specifically for MDEA. The risk is inferred from shared pharmacology. inferred
Psychological Risks
No controlled studies of MDEA's psychological adverse effects exist. The experience is described as "easily controllable",[6] suggesting lower incidence of acute psychological distress compared to serotonergic hallucinogens. The absence of systematic data does not establish safety — adverse reactions may be underreported.
Class-level risks inferred from the MDxx series include post-dose low mood secondary to serotonin depletion, anxiety during onset, and potential worsening of depression in vulnerable individuals. No MDEA-specific data on persisting perceptual changes, psychosis, or long-term psychiatric outcomes exist. inferred
Tolerance and Dependence
No MDEA-specific tolerance or dependence studies have been published.[6][23] The primary tolerance mechanism, inferred from MDMA, is serotonin depletion: MDEA-induced release acutely empties serotonin stores, producing diminished response on subsequent dosing until reserves rebuild over several days. Cross-tolerance extends to other serotonin-releasing agents (MDMA, MDA). inferred
MDEA's partial dopamine releasing activity predicts lower reinforcement potential than MDMA, but this has not been empirically tested. No self-administration or abuse liability studies have been conducted.
Drug Interactions
Serotonin Overload
The most dangerous interactions involve compounds that increase synaptic serotonin through complementary mechanisms. MAO inhibitors (phenelzine, tranylcypromine, selegiline, moclobemide) prevent serotonin breakdown; combined with MDEA's massive serotonin release, this can produce fatal serotonin syndrome — a medical emergency involving dangerous overheating, muscle rigidity, and cardiovascular collapse. safety citation needed
Tramadol combines serotonin reuptake inhibitor with opioid activity and carries lethal risk via serotonin syndrome and seizure threshold lowering.[24]
Concurrent use of MDMA produces dangerous additive serotonin load with compounded overheating risk.[6][19]
Cardiovascular Compounding
Cocaine combined with MDEA carries lethal risk through combined cardiovascular strain — both substances independently increase heart rate, blood pressure, and oxygen demand on the heart.[4]
Metabolism-Based Interactions
Drugs that inhibit CYP2D6 — including SSRIs (fluoxetine, paroxetine), bupropion, and protease inhibitors (ritonavir) — may significantly increase MDEA blood levels by blocking its primary breakdown pathways, potentially intensifying and prolonging effects.[11] inferred
Contraindications
Pre-existing heart conditions — including arrhythmia history, structural heart disease, and long QT syndrome — are absolute contraindications based on documented fatality risk.[4]
Concurrent MAO inhibitor therapy is an absolute contraindication for all serotonin-releasing agents due to fatal serotonin syndrome risk. safety citation needed
Concurrent tramadol use carries lethal interaction risk.[24]
Concurrent cocaine use carries lethal interaction risk through combined cardiovascular strain.[4]
Hot, crowded environments dramatically increase overheating risk and represent the primary contextual risk factor for MDxx class fatalities.[7]
CYP2D6 poor metabolizer status may constitute a relative contraindication, as impaired metabolism could substantially increase MDEA blood levels and prolong effects. No pharmacogenomic dosing data exist. inferred
Harm Reduction[edit]
Forms & Identification
MDEA typically appears as the hydrochloride salt in pressed tablets or crystalline powder. Because it shares an identical molecular weight with a structural regioisomer and produces similar results on standard immunoassays, laboratory confirmation (GC/MS or HPLC) is the only definitive identification method.[12] Street "Ecstasy" tablets have historically contained variable mixtures of MDxx compounds,[6] making reagent testing essential but insufficient for confirming MDEA specifically. Reagent results can rule out some dangerous substitutions but cannot distinguish MDEA from MDMA or MDA.
Guidelines
- Test all material with reagent kits before use — visual identification alone cannot confirm MDEA
- Start with the lower end of the common dose range and wait at least 90 minutes before considering whether to redose
- Avoid redosing; serotonin stores deplete rapidly, and additional doses increase cardiovascular and neurotoxic risk without proportional return of desired effects
- Stay cool — take regular breaks from physical activity, seek ventilated areas, and monitor body temperature
- Drink water at a moderate pace (approximately 250 mL per hour when active); do not overhydrate, as dangerously low sodium is a recognized MDxx risk
- Eat a light meal several hours before and prepare recovery nutrition for afterward
- Plan for a full day of rest following use to allow serotonin recovery
Set & Setting
MDEA's effects are described as "easily controllable",[6] with lower psychological volatility than serotonergic hallucinogens. Cool, well-ventilated environments with access to water are essential — hot, crowded settings dramatically amplify overheating risk, the primary contextual danger for the MDxx class.[7] A trusted companion and familiar surroundings reduce the likelihood of anxiety during onset.
Aftercare & integration. The days following MDEA use involve serotonin recovery. Low mood, fatigue, and irritability in the 24–72 hours afterward reflect depleted serotonin stores rather than lasting harm. Prioritize sleep, nutritious food, gentle activity, and social connection during this window.
Avoid using MDEA or other serotonin-releasing substances for at least several weeks to allow full neurochemical recovery. Repeated use on consecutive days compounds neurotoxic risk without meaningful return of desired effects.
If low mood persists beyond a week or the experience surfaced difficult emotional material, professional support from a therapist familiar with substance-related concerns is appropriate.
Recovery & Support
MDEA's lower reinforcement potential relative to MDMA may reduce compulsive use patterns, but psychological habituation to the entactogenic state can develop with any substance that reliably produces emotional warmth and connection.
Patterns worth examining include using MDEA to access emotional states that feel unavailable sober, escalating frequency despite diminishing returns, or difficulty engaging socially without the substance. Peer support communities, harm reduction organizations, and addiction counselors experienced with club drugs can provide appropriate support.
Recovery resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency: Body temperature that can be felt through clothing, chest pain, seizures, loss of consciousness, or extreme confusion all require immediate medical help. An uncomfortable but manageable experience — mild anxiety, nausea, or elevated heart rate — can typically be managed with reassurance, a cool environment, and rest.
Immediate steps:
- 1. Call emergency services if the person is unconscious, seizing, experiencing chest pain, or dangerously overheated
- 2. Move the person to a cool, quiet area
- 3. If unconscious but breathing, place in the recovery position (on their side)
- 4. Remove excess clothing and apply cool water to the skin if overheating is suspected
- 5. Do not restrain the person unless they are in immediate danger of self-harm
- 6. Do not induce vomiting
What to tell the dispatcher: Name the substance (MDEA or "ecstasy-type drug"), estimated amount, time of ingestion, and current symptoms. Good Samaritan laws in many jurisdictions protect people who call for help during a drug emergency.
Legal Status[edit]
MDEA is a controlled substance in all major jurisdictions, uniformly classified at the highest restriction levels. Its scheduling followed MDMA's classification and was accelerated by early reports of MDEA-associated fatalities.[4] In the United States, the 1986 Federal Analog Act provided interim legal coverage prior to explicit scheduling by treating structural analogs of Schedule I substances as equivalently controlled when intended for human consumption.
| Jurisdiction | Classification | Key provisions |
|---|---|---|
| United States | Schedule I (CSA) | Effective October 1987. Covered by Federal Analog Act (1986) prior to explicit listing. No accepted medical use; high abuse potential.[4][5] |
| United Kingdom | Class A (Misuse of Drugs Act 1971) | Controlled under the generic substituted phenethylamine class provision.[5] |
| Germany | Anlage I (BtMG) | Non-tradable; permitted only for scientific purposes under specific government authorization.[5] |
| Canada | Schedule I (CDSA, 1996) | Controlled as explicit listing or structural analog under the Controlled Drugs and Substances Act.[5] |
| Australia | Controlled substance | Prohibited under the Poisons Standard and Therapeutic Goods Act framework.[5] |
| European Union | Varies by member state | All EU countries control the MDxx class under national legislation. No EU-wide specific scheduling instrument exists separate from national laws. |
Analog Act Considerations
In the United States, MDEA's structural analogy to MDMA made it effectively controlled from the passage of the Federal Analog Act (21 U.S.C. § 813) in 1986, prior to its explicit Schedule I placement in 1987. The Act treats any substance "substantially similar" in chemical structure or pharmacological effect to a Schedule I or II substance as equivalently controlled when intended for human consumption. This framework remains relevant for novel MDxx analogs not yet explicitly scheduled.
references
- [1] ^abcdNichols DE (1986) Differences between the mechanism of action of MDMA, MBDB, and the classic hallucinogens. Identification of a new therapeutic class: entactogens — Journal of Psychoactive Drugs PMID:2880944
- [2] ^abcNichols DE (2022) Entactogens: How the Name for a Novel Class of Psychoactive Agents Originated — Frontiers in Psychiatry doi:10.3389/fpsyt.2022.863088
- [3]
- [4]
- [5]
- [6]