DMT:

Absorption: DMT can be absorbed through various routes, including inhalation, injection, and oral
ingestion with an MAO inhibitor (Strassman, 2001).

Metabolism: Primarily metabolized by monoamine oxidase (MAO), specifically MAO-A (Shen et al.,
2011).

Half-Life: The half-life of DMT in the blood is about 15 minutes (Strassman, 2001).

Blood-Brain Barrier: DMT crosses the blood-brain barrier rapidly (Strassman, 2001).

Distribution: Distributed in the brain, liver, and kidneys, with metabolites excreted in the urine (Callaway
et al., 1999).

Endogenous Presence: DMT is endogenously produced in the human body (Barker et al., 2012).

5-HT2A Receptor Activation: DMT acts as an agonist at the 5-HT2A receptor (Ray, 2010).

Sigma-1 Receptor Binding: Interaction with the sigma-1 receptor may contribute to its psychoactive
effects (Frecska et al., 2013).

Action on Other Serotonin Receptors: Besides 5-HT2A, DMT also binds to 5-HT1A and 5-HT2C receptors
(Ray, 2010).

Dose-Response: The intensity of effects is dose-dependent, with higher doses leading to more intense
experiences (Strassman, 2001).

Potential Immune Modulation: DMT may have immunomodulatory effects (Frecska et al., 2013).

Neural Connectivity Alterations: DMT may increase neural connectivity (Tagliazucchi et al., 2016).

Modulation of Visual Cortex: Influences visual processing in the brain (Riba et al., 2004).

Default Mode Network Interaction: Affects the default mode network, which may underlie the altered
sense of self (Carhart-Harris et al., 2014).

Altered Brain Oscillations: DMT modulates brain oscillations, affecting consciousness (Riba et al., 2002).

Induction of Near-Death Experiences: Some users report near-death experience-like phenomena

(Timmermann et al., 2018).

Potential Antidepressant Effects: Preliminary evidence of antidepressant properties (Osório et al., 2015).

Impact on Addiction: Investigated for treating substance abuse disorders (Luis Eduardo Luna, 2011).

Induction of Mystical Experiences: Known to induce intense mystical or spiritual experiences (Griffiths et
al., 2018).

Psychotherapeutic Use with Ayahuasca: DMT is the active ingredient in Ayahuasca, used in traditional
and modern psychotherapy (Labate & Jungaberle, 2011).
Shrooms:

Psilocybin Absorption: Psilocybin is rapidly dephosphorylated in the liver to psilocin (Passie et al., 2002).

Oral Bioavailability of Psilocybin: Approximately 50%, due to conversion to psilocin (Tylš et al., 2014).

Distribution: Psilocin is distributed widely, with highest concentrations in the kidney and lungs (Hasler et
al., 1997).

Metabolism: Psilocin is primarily metabolized by the enzyme monoamine oxidase A (MAO-A) (Tylš et al.,
2014).

Half-Life of Psilocin: The plasma half-life is approximately 3 hours (Passie et al., 2002).

Excretion: Psilocin is mainly excreted in urine (Nichols, 2004).

Receptor Binding: Psilocin acts as an agonist at the serotonin 5-HT2A receptor (Nichols, 2004).

Receptor Affinity: Psilocin has high affinity for several other serotonin receptors, including 5-HT1A and 5-
HT2C (Ray, 2010).

Dose-Response Relationship: The intensity of psychedelic effects is dose-dependent (Nichols, 2004).

Induced Synesthesia: Psilocybin may induce synesthesia, where sensory modalities blend (Studerus et
al., 2012).

Impact on Time Perception: Psilocybin can alter the perception of time (Wittmann et al., 2007).

Heart Rate and Blood Pressure: Psilocybin can transiently increase heart rate and blood pressure (Hasler
et al., 2004).

Activation of 5-HT2A Receptor: Psilocin's activation of the 5-HT2A receptor leads to increased cortical
glutamate levels (Vollenweider & Kometer, 2010).

Neural Connectivity: Psilocybin increases neural connectivity, which might underlie altered
consciousness (Carhart-Harris et al., 2012).

Default Mode Network (DMN): Psilocybin disrupts the DMN, possibly contributing to ego dissolution
(Carhart-Harris et al., 2014).

Prefrontal Cortex Activation: Psilocybin modulates prefrontal cortex activity, potentially affecting
cognition and mood (Geyer & Vollenweider, 2008).

Therapeutic Potential for Depression: Psilocybin shows promise as a treatment for depression (Carhart-
Harris et al., 2016).

Anti-Obsessional Effects: Some evidence supports psilocybin’s use in obsessive-compulsive disorder

(Moreno et al., 2006).
 Potential in Substance Abuse Treatment: Psilocybin has been explored in treating addiction
(Bogenschutz et al., 2015).

Enhancement of Creative Thinking: Psilocybin may foster creativity and divergent thinking (Kuypers et
al., 2016)

LSD:

1. Absorption: LSD is rapidly absorbed orally, with peak plasma concentrations in 1-2
hours (Dolder et al., 2015).
2. Distribution: LSD's distribution is characterized by a large volume, primarily in the liver
and kidneys (Passie et al., 2008).
3. Metabolism: LSD is mainly metabolized in the liver by cytochrome P450 enzymes (Poch
et al., 2018).
4. Half-Life: Its elimination half-life is around 3.6 hours, but the psychoactive effects can
last much longer (Dolder et al., 2015).
5. Excretion: Excreted primarily in urine, with small amounts in feces (Passie et al., 2008).
6. 5-HT2A Receptor Agonism: LSD primarily targets the 5-HT2A receptor, causing its
psychoactive effects (Nichols, 2016).
7. Other Serotonin Receptors: Also acts on 5-HT1A, 5-HT2C, and 5-HT5A receptors
(Nichols, 2016).
8. Dopamine Receptor Interaction: Shows agonism at dopamine D2 receptors (Rickli et
al., 2016).
9. Adrenergic Receptor Activation: LSD interacts with adrenergic receptors, notably
alpha2A (Nichols, 2016).
10. Dose-Response: The psychoactive effects are dose-dependent (Schmid et al., 2015).
11. Alteration of Brain Networks: LSD disrupts the integrity of functional brain networks,
leading to altered perception (Carhart-Harris et al., 2016).
12. Default Mode Network Changes: Modulation of the default mode network may relate
to the ego-dissolution effect (Carhart-Harris et al., 2014).
13. Visual Cortex Modulation: Influences visual processing by activating the 5-HT2A
receptor in the visual cortex (Kometer et al., 2013).
14. Induction of Synesthesia: Can induce synesthetic experiences by enhancing cross-talk
between sensory modalities (Luke et al., 2012).
15. Effects on Emotional Processing: LSD alters emotional processing and enhances
emotional empathy (Dolder et al., 2016).
16. Therapeutic Applications: LSD has been explored for treating anxiety, depression,
PTSD, and addiction (Gasser et al., 2014; Bogenschutz et al., 2015).
17. Enhancement of Creativity: Shown to increase creativity and problem-solving (Harman
et al., 1966).
18. Mystical Experiences: Can induce profound mystical experiences, which may be
therapeutically beneficial (Griffiths et al., 2011).
19. Potential Risks: Risks include the potential for "bad trips," flashbacks, and exacerbation
of underlying psychiatric conditions (Abraham et al., 1996).
20. Legal Status: Currently classified as a Schedule I substance in many countries, limiting
its clinical research and use (Nutt et al., 2013).

Haz 3 trabajos sobre cada una de las sustancias de manera extensa y detallada, con el formato de una
presentación PowerPoint dividiéndolo en los subtemas, cada subtema con un mínimo de 3 diapositivas;
farmacocinética, farmacodinámica, mecanismo de acción y psicofarmacología, Se creativo con el título
de cada diapositiva, mantén citas por nombre y año de cada dato, Toma en cuenta los siguientes
artículos y citas, usándolos no solo como referencias sino también como elementos para ampliar tu
búsqueda de información sobre el tema:

DMT:

Absorption: DMT can be absorbed through various routes, including inhalation, injection, and oral
ingestion with an MAO inhibitor (Strassman, 2001).

Metabolism: Primarily metabolized by monoamine oxidase (MAO), specifically MAO-A (Shen et al.,
2011).

Half-Life: The half-life of DMT in the blood is about 15 minutes (Strassman, 2001).

Blood-Brain Barrier: DMT crosses the blood-brain barrier rapidly (Strassman, 2001).

Distribution: Distributed in the brain, liver, and kidneys, with metabolites excreted in the urine (Callaway
et al., 1999).

Endogenous Presence: DMT is endogenously produced in the human body (Barker et al., 2012).

5-HT2A Receptor Activation: DMT acts as an agonist at the 5-HT2A receptor (Ray, 2010).

Sigma-1 Receptor Binding: Interaction with the sigma-1 receptor may contribute to its psychoactive
effects (Frecska et al., 2013).

Action on Other Serotonin Receptors: Besides 5-HT2A, DMT also binds to 5-HT1A and 5-HT2C receptors
(Ray, 2010).

Dose-Response: The intensity of effects is dose-dependent, with higher doses leading to more intense
experiences (Strassman, 2001).

Potential Immune Modulation: DMT may have immunomodulatory effects (Frecska et al., 2013).

Neural Connectivity Alterations: DMT may increase neural connectivity (Tagliazucchi et al., 2016).
Modulation of Visual Cortex: Influences visual processing in the brain (Riba et al., 2004).

Default Mode Network Interaction: Affects the default mode network, which may underlie the altered
sense of self (Carhart-Harris et al., 2014).

Altered Brain Oscillations: DMT modulates brain oscillations, affecting consciousness (Riba et al., 2002).

Induction of Near-Death Experiences: Some users report near-death experience-like phenomena

(Timmermann et al., 2018).

Potential Antidepressant Effects: Preliminary evidence of antidepressant properties (Osório et al., 2015).

Impact on Addiction: Investigated for treating substance abuse disorders (Luis Eduardo Luna, 2011).

Induction of Mystical Experiences: Known to induce intense mystical or spiritual experiences (Griffiths et
al., 2018).

Psychotherapeutic Use with Ayahuasca: DMT is the active ingredient in Ayahuasca, used in traditional
and modern psychotherapy (Labate & Jungaberle, 2011).

Shrooms:

Psilocybin Absorption: Psilocybin is rapidly dephosphorylated in the liver to psilocin (Passie et al., 2002).

Oral Bioavailability of Psilocybin: Approximately 50%, due to conversion to psilocin (Tylš et al., 2014).

Distribution: Psilocin is distributed widely, with highest concentrations in the kidney and lungs (Hasler et
al., 1997).

Metabolism: Psilocin is primarily metabolized by the enzyme monoamine oxidase A (MAO-A) (Tylš et al.,
2014).

Half-Life of Psilocin: The plasma half-life is approximately 3 hours (Passie et al., 2002).

Excretion: Psilocin is mainly excreted in urine (Nichols, 2004).

Receptor Binding: Psilocin acts as an agonist at the serotonin 5-HT2A receptor (Nichols, 2004).

Receptor Affinity: Psilocin has high affinity for several other serotonin receptors, including 5-HT1A and 5-
HT2C (Ray, 2010).

Dose-Response Relationship: The intensity of psychedelic effects is dose-dependent (Nichols, 2004).

Induced Synesthesia: Psilocybin may induce synesthesia, where sensory modalities blend (Studerus et
al., 2012).

Impact on Time Perception: Psilocybin can alter the perception of time (Wittmann et al., 2007).
Heart Rate and Blood Pressure: Psilocybin can transiently increase heart rate and blood pressure (Hasler
et al., 2004).

Activation of 5-HT2A Receptor: Psilocin's activation of the 5-HT2A receptor leads to increased cortical
glutamate levels (Vollenweider & Kometer, 2010).

Neural Connectivity: Psilocybin increases neural connectivity, which might underlie altered
consciousness (Carhart-Harris et al., 2012).

Default Mode Network (DMN): Psilocybin disrupts the DMN, possibly contributing to ego dissolution
(Carhart-Harris et al., 2014).

Prefrontal Cortex Activation: Psilocybin modulates prefrontal cortex activity, potentially affecting
cognition and mood (Geyer & Vollenweider, 2008).

Therapeutic Potential for Depression: Psilocybin shows promise as a treatment for depression (Carhart-
Harris et al., 2016).

Anti-Obsessional Effects: Some evidence supports psilocybin’s use in obsessive-compulsive disorder

(Moreno et al., 2006).

Potential in Substance Abuse Treatment: Psilocybin has been explored in treating addiction
(Bogenschutz et al., 2015).

Enhancement of Creative Thinking: Psilocybin may foster creativity and divergent thinking (Kuypers et
al., 2016)

LSD:

1. Absorption: LSD is rapidly absorbed orally, with peak plasma concentrations in 1-2 hours (Dolder
et al., 2015).

2. Distribution: LSD's distribution is characterized by a large volume, primarily in the liver and
kidneys (Passie et al., 2008).

3. Metabolism: LSD is mainly metabolized in the liver by cytochrome P450 enzymes (Poch et al.,
2018).

4. Half-Life: Its elimination half-life is around 3.6 hours, but the psychoactive effects can last much
longer (Dolder et al., 2015).

5. Excretion: Excreted primarily in urine, with small amounts in feces (Passie et al., 2008).

6. 5-HT2A Receptor Agonism: LSD primarily targets the 5-HT2A receptor, causing its psychoactive
effects (Nichols, 2016).

7. Other Serotonin Receptors: Also acts on 5-HT1A, 5-HT2C, and 5-HT5A receptors (Nichols, 2016).

8. Dopamine Receptor Interaction: Shows agonism at dopamine D2 receptors (Rickli et al., 2016).
9. Adrenergic Receptor Activation: LSD interacts with adrenergic receptors, notably alpha2A
(Nichols, 2016).

10. Dose-Response: The psychoactive effects are dose-dependent (Schmid et al., 2015).

11. Alteration of Brain Networks: LSD disrupts the integrity of functional brain networks, leading to
altered perception (Carhart-Harris et al., 2016).

12. Default Mode Network Changes: Modulation of the default mode network may relate to the
ego-dissolution effect (Carhart-Harris et al., 2014).

13. Visual Cortex Modulation: Influences visual processing by activating the 5-HT2A receptor in the
visual cortex (Kometer et al., 2013).

14. Induction of Synesthesia: Can induce synesthetic experiences by enhancing cross-talk between
sensory modalities (Luke et al., 2012).

15. Effects on Emotional Processing: LSD alters emotional processing and enhances emotional
empathy (Dolder et al., 2016).

16. Therapeutic Applications: LSD has been explored for treating anxiety, depression, PTSD, and
addiction (Gasser et al., 2014; Bogenschutz et al., 2015).

17. Enhancement of Creativity: Shown to increase creativity and problem-solving (Harman et al.,
1966).

18. Mystical Experiences: Can induce profound mystical experiences, which may be therapeutically
beneficial (Griffiths et al., 2011).

19. Potential Risks: Risks include the potential for "bad trips," flashbacks, and exacerbation of
underlying psychiatric conditions (Abraham et al., 1996).

20. Legal Status: Currently classified as a Schedule I substance in many countries, limiting its clinical
research and use (Nutt et al., 2013).