Lecture 11 - Hallucinogens
XTC (Ecstasy)
Definition: MDMA (methylene-dioxy-metamphetamine), a derivative of amphetamine.
Relationship to Amphetamine:
Amphetamine chemical structure includes a nitrogen (NH) group and a methyl (CH3) group.
Adding a methyl group to amphetamine creates Methamphetamine (MA).
MDMA is methamphetamine with methylene and dioxy groups added.
XTC and Neurotransmission
Mechanism:
XTC causes monoamine release and inhibits reuptake, similar to other amphetamines.
It primarily affects serotonin release but also influences acetylcholine.
XTC and Serotonin
Serotonin (5-HT):
Increases release of serotonin.
Blocks serotonin reuptake.
Leads to acute depletion of serotonin in the brain.
Serotonin Effect in the Brain
Serotonin Pathways:
Serotonin pathways are widely spread throughout the brain, originating from the Raphe nuclei.
These pathways project to the thalamus, hypothalamus, basal ganglia, cortex, hippocampus, cerebellum, and spinal cord.
Acute Effects of XTC
Common Effects:
Heightened mood and increased emotional sensitivity.
Increased sensory awareness.
Reduced appetite.
Increased psychomotor drive.
Altered sense of time and space.
Brain Activity Imaging
Monkeys and MDMA:
Studies on conscious monkeys show that several brain areas are activated as blood levels of MDMA increase.
Visual stimulation response is stronger when MDMA is administered.
Problems with XTC
Toxic Effects:
When combined with intense physical activity, it can lead to hyperthermia, tachycardia, arrhythmia, pupil dilation, convulsions, jaw-clenching, and kidney failure.
Psychological Disturbances:
Depersonalization, paranoia, confusion, anxiety, panic, and suicidal thoughts.
Effects on Mood and Memory
Parrott et al. 2002 Study:
Examined XTC effects in new, moderate, and heavy users.
Heavier use correlated with more symptoms.
Short-Term Mood Effects:
During ecstasy use, individuals experience elevated mood.
After ecstasy, depression-like feelings and irritability can occur due to serotonin depletion.
XTC Effect on Memory
Heffernan et al. 2001 Study:
Compared 30 regular XTC users with 31 XTC-free controls.
XTC users reported more mistakes in prospective memory.
Halpern et al. Study:
Compared 52 ecstasy users and 59 non-users.
Found few consistent differences in verbal and visuospatial memory, verbal fluency, attention, processing speed, manipulative dexterity, and executive cortical functions.
Ecstasy users had lower vocabulary scores, possibly indicating pre-morbid ability differences rather than neurotoxicity.
Note: Not all studies find an effect on memory
Explanation for XTC Effect on Memory
Possible Explanations:
XTC might destroy serotonergic nerve terminals.
Ecstasy can damage brain areas controlling memory, leading to memory impairment.
Serotonergic Neurotoxicity
Long-Term Effect:
Serotonin levels in cerebral cortex neurons are affected long-term.
Studies (Hatzidimitriou et al. 1999) showed reduced serotonin presence in the brain even seven years after ecstasy use.
Serotonergic and Dopaminergic Neurotoxicity
Ricaurte et al. Study (Later Retracted):
Initial concerns arose from a study suggesting that even single doses of MDMA caused extensive damage to dopaminergic neurons in monkeys, raising fears of increased risk of Parkinson's disease with age.
The study was retracted after it was discovered that the drug used was actually methamphetamine, mislabeled as MDMA.
Most Recent Review
SERT Binding:
Consistent evidence shows that MDMA decreases SERT (Serotonin Transporter) binding.
It remains inconclusive whether this decrease is permanent and due to neurotoxicity.
Need for Further Research:
Large translational studies are needed to determine definitively whether ecstasy use is neurotoxic in humans.
Does XTC Cause Addiction?
Cottler et al. 2001 Study:
Examined withdrawal symptoms in ecstasy users.
Significant withdrawal symptoms were reported, including feeling tired (53%), appetite changes (49%), anxiety/irritability (39%), depression (37%), trouble sleeping (35%), and difficulty concentrating (33%).
XTC: DSM-IV Abuse & Dependence
Reports and Studies:
Trimbos Institute reported few cases of XTC as a primary drug problem but frequent as a secondary issue.
Other studies showed limited evidence of primary addiction.
Withdrawal symptoms and continued use despite problems are most common.
Additional Information
Ecstasy Dosage and Contamination:
Danger stems mainly from unknown dosage and/or contamination with other substances.
Reports indicate rising ecstasy deaths due to super-strength pills and child-friendly appearance.
Psychedelics
Terminology:
Similar terms include hallucinogens, illusionogenic, entheogenic, psychotomimetic, and psychodysleptic.
Definition:
Psychoactive substances that cause temporary changes in perception, mood, cognition, and sense of self by affecting brain mechanisms.
Psychedelic-like Properties:
Substances like MDMA and ketamine also exhibit psychedelic-like properties.
Categories of Hallucinogens:
Serotonin-like / classical: LSD, DMT (in ayahuasca), psilocybin, mescaline.
Glutaminergic NMDA receptor antagonists / dissociative anesthetics: PCP, ketamine, dextromethorphan.
Anticholinergic: scopolamine, atropine.
Empathogens/entactogens: DOM, DMA, MDA, MDMA.
Opioid kappa receptor agonist: Salvinorin A.
Ibogaine.
Effects of Psychedelic Substances
Sensory-Perceptual Distortions:
Altered perceptions of colors, sounds, and shapes.
Complex hallucinations and synesthesia.
Psychological Effects:
Dreamlike feelings, depersonalization, and altered affect.
Somatic Effects:
Therapeutic Potential:
Emotional processing, cognitive flexibility, and mystical experiences may lead to therapeutic breakthroughs.
Drug, Set, Setting (Zinberg 1984)
Importance of Context:
Whether a psychedelic trip is positive or challenging depends on expectations, the environment, and the individual’s psychological state.
Drug-Induced Psychosis:
NIDA defines it as a distortion or disorganization of a person’s capacity to recognize reality, think rationally, or communicate with others.
History: Psychedelics in the 20th Century
LSD Synthesis:
1938: LSD was synthesized by Albert Hoffmann from ergot, a fungus (Claviceps purpurea) that grows on grain.
First LSD Trip:
April 19, 1943: Albert Hoffmann experienced his first LSD trip.
Key Figures:
Timothy Leary.
War on Drugs:
History: Psychedelics in the 20th Century
Timothy Leary’s Research:
1961: Timothy Leary started doing LSD research.
Good Friday Experiment:
1962: The Good Friday Experiment was conducted.
Leary Fired:
1963: Leary was fired from Harvard.
Nixon’s War on Drugs:
1971: LSD was made illegal.
Psychedelic Renaissance
Renewed Research:
In recent decades, research has revisited the therapeutic use of psychedelics.
Therapeutic Effects:
In 2016, a study demonstrated the therapeutic effect of psychedelics, and more studies have followed.
Psychedelics and the Brain
LSD Pharmacodynamics:
Affinity for 5-HT2A, DA-D2, and alpha2 adrenergic receptors.
Typical dose ranges from 25 to 100 micrograms taken orally.
Effects begin 30 to 90 minutes after ingestion, peaking at 3 hours, and lasting up to 12 hours.
Low toxicity; lethal dose in animal studies is 14,000 micrograms. Overdose in humans is practically impossible, but behavioral effects during intoxication pose risks.
Psilocybin Pharmacodynamics:
Chemically similar to LSD but less potent.
Psilocin is the active metabolite, more fat-soluble, and acts quicker in the brain.
Dose (dried): 2-4 mg for pleasurable, relaxed effects; >5mg for hallucinations and time distortion.
Peak effect at 2 hours, with effects lasting 6 to 10 hours.
Psychedelics and the Brain: Main Theories
5-HT2A Receptor Agonism:
Neuroplasticity.
REBUS Model (Carhart-Harris & Friston, 2019):
RElaxed Beliefs Under pSychedelics.
Entropic Brain Hypothesis (Carhart-Harris, 2014).
Psychedelics & Neuroplasticity
5-HT2A Receptor Agonism:
Studies (de Vos et al., 2021) show that single and repeated administration of psychedelics increases neuroplasticity one month after administration and enhances learning behavior.
Clinical Studies:
Single administration leads to rapid neuroplastic changes (BDNF↑).
Window of Plasticity:
Critical period reopening is proportional to the duration of acute subjective effects (Nardou et al., 2023).
Parallel Effects:
These effects parallel the clinical effects of psychedelics, potentially underlying them.
Mystical Experience
Griffiths et al. 2008 Study:
Double-blind design with 36 hallucinogen-naive adults.
Participants had sessions with psilocybin vs. methylphenidate.
Definition:
Profound altered state of consciousness where a person feels deeply connected to something greater than themselves, often with a sense of unity, peace, and insight.
Follow-up Results
Meaning and Significance:
Mystical-type experiences mediated the attribution of personal meaning and spiritual significance 14 months later.
Among Top Experiences:
Ranked among the top 5 personally meaningful experiences of a lifetime.
Ranked among the top 5 spiritually significant experiences of a lifetime.
Increased Well-being:
Increased current personal well-being or life satisfaction
Positive Behaviour Change
Psychedelics-Assisted Therapy
Clinical Research:
Used in treating PTSD, depression, end-of-life anxiety, eating disorders, and addiction.
Integration:
Weeks following the session, the participant meets with a clinician to make sense of their experience and incorporate any insights into their life going forward.
Are Psychedelics Addictive?
Addiction Potential:
No direct effect on the dopaminergic system, less rapid tolerance, and no withdrawal symptoms result in low abuse potential for classical psychedelics. Abuse potential for substances like ketamine differs.
Historical Context:
Bill Wilson, founder of Alcoholics Anonymous, explored psychedelics for treating addiction.
Psychedelics to Treat Addiction
LSD for Alcoholism:
Studies have shown short-term effects (Krebs & Johansen, 2012).
Psilocybin:
May reduce alcohol and tobacco use in addicted samples (Johnson et al., 2017).
Ketamine:
Used to treat alcohol dependence (Grabski et al., 2022).
Ayahuasca:
Observational study showed reductions in alcohol, cocaine, and tobacco use, along with improved wellbeing (Thomas et al., 2013).
Ibogaine:
Shows promise for opioid addiction but carries risk of extreme physiological reactions.
Psilocybin to Treat Alcohol Use Disorder
Bogenschutz et al., 2022 Study:
Double-blind, active placebo-controlled clinical trial (n=95).
Participants received 2 doses of psilocybin (25-40mg/70kg) + psychotherapy (motivational enhancement therapy and CBT) over 12 weeks.
Results:
Number of heavy drinking days decreased at 32-week follow-up.
Number of standard drinks per day decreased at 32-week follow-up.
Psilocybin + psychotherapy produced robust decreases in % of heavy drinking days over and above those produced by active placebo and psychotherapy.
Roadblocks
Challenges:
Michael Pollan effect, placebo control group issues, therapist training requirements, politics, stigma, legalisation challenges, safety concerns (psychedelics not for everyone).
Access and Equity:
Need for equitable access for women, BIPOC, non-western, queer people.
Commercial Exploitation:
Concerns about “psychedelic capitalism”/psychedelic bourgeoise”.
Indigenous Traditions:
Conclusion:
Between hype and hope.
Take Home Messages
Unique Alterations:
Psychedelics uniquely alter perception, emotion, and self-awareness, enabling insights and therapeutic breakthroughs.
Mechanism of Action:
They mainly act on serotonin 5-HT2A receptors, boosting brain plasticity and reducing default mode network activity.
Theoretical Models:
REBUS and Entropic Brain models explain how psychedelics loosen rigid thoughts and increase brain flexibility.
Clinical Effectiveness:
Clinical research indicates psychedelics can treat depression, PTSD, addiction, and anxiety by enhancing emotional and cognitive change.
Risks and Ethics:
Use involves risks and ethical challenges, including safety, unequal access, and respect for Indigenous knowledge.d use.