ADVANCED PSYCHOPHARMACOLOGY
Psychology 572 Spring, 2005
Dr. John M. Morgan Tuesday & Thursday, 8am to 9:20
Natural Resources 201
Joanna Rocco
Erin C. Villa
Eric West
LSD
Erin C. Villa
Chemistry & synaptic transmitters involved
The most common psychoactive substances can be divided into
depressants (i.e., alcohol, sedatives, hypnotics), stimulants (i.e.,
cocaine, amphetamines, ecstasy), opioids (i.e., morphine and heroine),
and hallucinogens (i.e., PCP, LSD, cannabis). The brain has different
effects to different psychoactive substances. They bind to different
receptor types, and can increase or decrease the activity of neurons
through several different mechanisms. Consequently, these
psychoactive substances have different behavioral effects, different
rates of development of tolerance, different withdrawal symptoms, and
different short-term and long-term effects (Vaccarino & Rotzinger,
2004).
In this team project we will take a closer look at the
hallucinogen, LSD by explaining the chemistry and route of access of
LSD, synaptic transmitters and the parts of neurons affected,
inhibitory/excitatory potential changes, physiological changes, primary
behavior changes, side effects of behavior changes, and effects
reported by users.
LSD is considered to be one of, if not the, most potent
hallucinogenic drug known (Leicht, 1996). To understand LSD first we
will give a brief history of how LSD came into existence.
In 1938, Albert Hoffman was an employee in the pharmacological
department of Sandoz, in Basel, Switzerland. Hoffman was studying
derivatives of lysergic acid, including systematically reacting the acid
group with various reagents, to produce the corresponding amides,
anhydrides, esters, etc. One of these derivatives was the
diethylamide, made by addition of the –NC2H5)2 group, and it was
named LSD-25. But the new substance didn’t appear to have any
particularly useful medical properties, although the research report
noted, in passing, that “the experimental animals became restless
during the narcosis”. (May, 1998). LSD was not looked at for the next
five years until Hoffman couldn’t get this new substance out of his
mind and decided to reexamine LSD. Hoffman stated: “A peculiar
presentiment- the feeling that this substance could possess properties
other than those established in the first investigations- induced me,
five years after the first synthesis, to produce LSD-25 once again so
that a sample could be given to the pharmacological department for
further tests.” So, in the spring of 1943, he repeated the synthesis of
LSD-25. Hoffman is quoted in his laboratory journal on April 19, 1943.
17:00: Beginning dizziness, feelings of anxiety, visual distortions,
symptoms of paralysis, desire to laugh.
CHEMISTY OF LSD:
D-Lysergic acid diethylamide or LSD is a structure comprised of four
cyclic structures and three notable functional groups- two ethyl groups
and a methyl group. The structure of LSD bears a striking similarity to
that of serotonin, which is the molecule principally responsible for
determination of mood. A useful explanation for the brain’s receptivity
to LSD is its structural similarity to serotonin. (Fichman, 2004). 5-HT is
implicated in the regulation of many systems known to be effected by
LSD. This evidence indicates that many of the effects of LSD are
through serotonin mediated pathways. Subsequent research revealed
that LSD not only has affinities for 5-HT receptors but also for
receptors of histamine, Ach, dopamine, and the catecholines:
epinephrine and norepinephrine (Leicht, 1997).
Two areas of the brainstem that are thought to be involved in
LSD’s pathway are the Locus Coeruleus (LC) and the Raphe Nuclei.
The LC is a small cluster of norepinephrine containing neurons in the
pons beneath the 4th ventricle. The LC is responsible for the majority
of norepinephrine neuronal input in most brain regions (Snyder, 1986).
It has axons which extend to a number of sites including the
cerebellum, thalamus, hypothalamus, cerebral cortex, and
hippocampus. (Leicht, 1997).
A single LC neuron can effect a large target area. Stimulation of
LC neurons results in a number of different effects depending on the
post-synaptic cell. The LC is part of the ascending reticular activating
system which is known to be involved in the regulation of attention,
arousal, and the sleep-wake cycle. Electrical stimulation of the LC in
rats results in hyper-responsive reactions to stimuli (visual, auditory,
tactile, etc) (Nichols, Martin, Wallace, 1992). LSD has been found to
enhance the reactivity of the LC sensory stimulations. While many
effects of LSD can be described by its effects on the LC, it is apparent
that LSD’s effects on the LC are indirect (Leicht, 1997).
While norepinephrine activity throughout the brain is mainly
mediated by the LC, the majority of serotoneric neurons are located in
the Raphe Nuclei (RN). The RN is located in the middle of the
brainstem from the midbrain to the medulla. It innervates the spinal
cord where it is involved in the regulation of pain. Like the LC, the RN
innervated wide areas of the brain. Along with the LC, the RN is part
of the ascending reticular activating system. 5-HT inhibits ascending
traffic in the reticular system; perhaps protecting the brain from
sensory overload. Post-synaptic 5-HT receptors in the visual areas are
also believed to be inhibitory. Thus, it is apparent that an interruption
of 5-HT activity would result in disinhibition, and therefore e
excitation, of various sensory modalities (Leicht, 1997).
Current thought is that the mechanism of LSD is related to the
regulation of 5-HT activity in the RN. The RN is also influenced by
GABAergic, catecholamergic, and histamergic neurons. LSD has been
shown to also have affinities for many of these receptors. Thus it is
possible that some of its effects may be mediated through other
pathways. Current research however had focused on the effects of
LSD on 5-HT activity. (Leicht, 1997).
NEUROTRANSMITTER INVOLVED:
In the body, the brain and spinal cord make up what is known as the
central nervous system (CNS). Neurons in the human body “connect”
to other neurons and communicates with one another through
electrical signals. These electrical signals must pass between the
small gap between neurons before it can be transmitted. These gaps
known as synapses are between neurons. Messages are constantly
passed through the synapses between our neurons, and these
messages allow us to sense, to think, and to act upon these feelings
and thoughts (Bacon, Cagle, Mikowski, Rosol, 1996).
There are two types of synapses between neurons: chemical and
electrical. Chemical synapses are more common and are the type
discussed in this paper. When an action potential (AP) travels down a
pre-synaptic cell, vesicles containing neurotransmitter are released
into the synapse where they effect receptors on the post synaptic cell.
Synaptic activity can be terminated through reuptake of the
neurotransmitter to the pre-synaptic cell, the presence of enzymes
which inactivate the transmitter, or simple diffusion (Leicht, 1996).
A pre-synaptic neuron can act on the postsynaptic neuron
through direct or indirect pathways. In a direct pathway, the post-
synaptic receptor is also an ion channel. The binding of a
neurotransmitter to its receptor on the post-synaptic cell directly
modifies the activity of the channel. Neurotransmitters can have
excitatory or inhibitory effects (Leicht, 1996). Excitatory
neurotransmitters make it easier for the cell to allow positive ions in,
and therefore decrease the threshold, or the smallest stimulation that
will cause the cell to generate an impulse. Inhibitory
neurotransmitters, on the other hand, make the neuron’s membrane
more permeable to negative ions, and increase the threshold (Bacon et
al., 1996). Many neurotransmitters that have system-wide effects such
as epinephrine, norepinephrine, and 5-HT work by an indirect pathway.
In an indirect pathway, the post-synaptic receptor acts on an ion
channel through indirect means such as a secondary messenger
system. Many indirect receptors such as muscarinic, Ach, and 5-HT
involve the use of G proteins. Indirect mechanisms often will alter the
behavior of a neuron without effecting its resting potential (Leicht,
1996).
Although the precise biochemical action of hallucinogens is
unknown, it is believed that it probably stems from a complex reaction
with serotonin (5-HT) from the cortex to the spinal cord. LSD seems to
closely resemble serotonin in structure. Serotonin exists mainly in the
Locus Coeruleus and RN. The chemical then is said to play a large
role in moderating behaviors and moods. The actions of serotonin and
the effects of LSD on the body are inextricably linked. The
numerological pathways that allow serotonin to regulate so many of
the body’s activities are the same ones that allow the LSD molecule to
profoundly affect the body. The serotonergic neurons and the bodies’
response to the disruption of the normal pathways are where the basis
of the chemistry lie (Bacon et al., 1996). Even to this day, there is still
much to study about how LSD affect the neurons, especially at the
synaptic level.
With the serotonin neurons, there appear to be two types of
receptors to which LSD and 5-HT both can attach. These are known
as 5HT1 AND 5HT2 receptors. The first is part of pre-synaptic neurons
and the latter is part of the post-synaptic neurons. When a molecule
becomes chemically attached to 5HT1 receptors the neuron slows or
stops in production of serotonin, creating a negative feedback loop,
where excess serotonin will halt further production. When a molecule
binds to the 5HT2 receptors, the post-synaptic neuron is inhibited, and
it is more difficult for it to generate an action potential. Serotonin will
attach itself to either of these two receptors with equal frequency, but
it has been proposed that LSD prefers the 5HT1 receptor to the 5HT2
receptor (Bacon et al.,1996).
References
Bacon, A., Cagle, H., Mikowski, P., Rosol, M. (1996). The
effect of LSD on the human brain. Retrieved Jan. 25,
2005, from http://www.cem.msu.edu/˜cem181h.projects/96/
lsd/drug.html.
Leicht, I. (1997). LSD- Origins and neurobiological
implications. Retrieved Jan. 25, 2005, from
http://www.cs.hmc.edu/˜ivl/writing/non_fiction/lsd/.
May, P. (1998). Lysergic acid diethylamide- LSD. December
1998. Retrieved Jan. 25, 2005 from
http://www.chm.bris.ac.uk/motm/lsd/lsd1_text.htm.
Nicholls, J., Martin, R., Wallace, B. (1992). From neuron
to brain: Acellular and molecular approach to the
function of the nervous system. Retrieved Jan. 25,
2005.
Palfai, T., Jankiewicz, H. (2001). Drugs and human
behavior. New York, NY: McGraw-Hill.
Snyder (1986). Drugs and the brain. Sci-Am Books Inc.
Retrieved Jan. 25, 2005, from http://www.cs.hmc.edu/˜
ivl/writing/non_fiction/lsd/.
World Health Organization. (2004). Neuroscience of
psychoactive substance use and dependence summary.
Geneva, Switzerland: Franco Vaccarino and Susan
Rotzinger.
Eric West
LSD: Parts of the neuron affected and inhibitory or excitatory
potential changes
Lysergic Acid Diethyl amide (LSD) has been implicated in a
variety of studies to determine its potential for influence on certain
neural activities. To date, little that can be certified as concrete fact
has been found, though a number of theories with considerable
support exist. Although dopamine, epinephrine, and norepinephrine
may be implicated in some LSD studies, serotonin seems to be the
main focus of scientific inquiry with respect to LSD. Leicht (1996),
postulates four theories concerning serotonin (5-HT) pre- and post-
synaptic transmitter sites and the potential for LSD to affect these
sites, in particular. All of these theories point to the synaptic neuronal
dendrites and terminal buttons as the main suspects with regard to
LSD and its particular target area on the neurons themselves. After
considerable dialogue which analyses studies by Aghajanian and
colleagues, Leicht came to the conclusion that the evidence points
toward certain types of activities on particular pre- and post-synaptic
serotonergic neurons. The theories are as follows:
1: LSD Pre-synaptically inhibits 5-HT neurons.
2: LSD Post-synaptically antagonizes 5-HT2 receptors.
3: LSD Post-synaptically partially agonizes 5-HT receptors.
4: LSD Post-synaptically agonizes 5-HT receptors.
Neural clusters in the Raphe Nuclei, which spread out from there,
mainly into the frontal and prefrontal cortices have been identified as
serotonergic. They are also auto-reactive, and LSD appears to inhibit
the spontaneous firing of the neurons at that site, when the drug is
systemically administrated. 5-HT2 receptors have been identified as
pH dependent, while LSD molecules have been identified as pH
independent. 5-HT2 receptors are connected to a second messenger
system (phosphatidyloniitol, or PI). PI turnover has been found to be
affected by 5-HT2 in an antagonistic fashion, but is stimulated by 5-HT.
LSD, in micrometric doses, can inhibit 1000 times that amount of 5-HT,
which supports theory #2, as well as supporting, partially, theory #3;
when LSD is administered in a variety of doses, it apparently acts as a
partial agonist. Though LSD and 5-HT are highly compatible, 5-HT is
more effective at the serotonin receptor site, but LSD can compete
with it at the 5-HT2 site. The conclusion is, “…since 5-HT is a more
potent agonist than LSD, the effects of LSD would appear
antagonistic.“ Finally, for theory #4, Leicht cites Dr. Glennon’s
explanation of LSD’s relationship with post-synaptic 5-HT receptors.
He (Glennon) concluded that, since 5-HT2 and 5-HT1c receptor sites
were compatible, higher doses of LSD can increase antagonism of the
5-HT2 receptor, through agonism of 5-HT1 receptors.
Although Leicht clearly states that there is a “lack of
understanding about the mechanisms of LSD,” he comes to the
conclusion that LSD is a partial 5-HT agonist, and may be either
antagonistic or agonistic to 5-HT2 receptors, depending on the dose of
LSD and the presence or absence of other molecules in the synaptic
site. It may also be true that LSD plays a role in synaptic auto receptor
activity in serotonergic neurons. Low doses of LSD do not depress
firing of serotonergic neurons, and repeated dosage of LSD still effects
neuron firing, even though inhibitory activity is believed to play an
important role in the regulation of serotonergic synaptic activity,
especially with regard to neurological reactivity to hallucinogenic
drugs. LSD, and other hallucinogens, apparently have the properties
that enable them to affect synaptic transmission of serotonin, as well
as reuptake in the pre-synaptic neuron. Evidence for this lies largely in
the findings of studies of laboratory rats, but also in the close
resemblance of LSD molecules to serotonin.
Palfai & Jankiewicz (2001) relate it as “…imbalancing a natural
system--for example, by blocking 5-HT at the synapse, which is
followed by a rebound of serotonergic over-activity or receptor
hypersensitivity.“ This appears to be a bit short of the mark, as a
number of receptor types (5-HT1, 5-HT2, and subtypes, etc.) are also
implicated, but does put it in a basic, simplistic light.
LSD: Ion Channels Affected
As related above, LSD has, as its main targets, serotonergic
systems, from the Raphe Nuclei to cortices in the brain. These neurons
do not follow typical neuronic firing pattterns; they typically follow a
rhytmic, pulsing patttern (Jacobs, 178), much like that of an
attenuating current (AC) flow of electricity. There is a
hyperpolarization spike-decay-spike, which constitutes a constant
flow of impulse in the nerve clusters. This occurs due to Calcium (Ca+)
dependent Potassium (K+) currents inherent to the natural ionic
exchange cycles in the serotonergic system. LSD slows this activity,
theoretically creating overactivity at the receptor sites from rebound
effects, due to the tendency of the serotonergic system to rebalance
itself to normal functioning.
When LSD is introduced to the system, a significant decrease
occurs in the levels of K+ outside the cell, altering the positive and
negative potentials in and around the axon, which, in turn, alters the
action potential, or the all-or-none nerve impulse. LSD causes
hyperpolarization, cessation of spontaneous nerve firing, and
decreases membrane resistance (Jacobs, 177). The increased
hyperpolarization creates slower firing at longer intervals due to the
necessary time for the system to add more positively charged ions to
the area so that ion channels may reach the voltage potential of about
-80mV, thence opening the ion channels. LSD seems to sustain this
hyperpolarization by blocking the normal impulse decay in the spike-
decay-spike cycle. When resistance is lowered, K+ is allowed into the
hyperpolarized area, leaving less K+ outside the cell. Because LSD
somehow pushes its way into and increases K+ conductance of
serotonin, it may be that LSD can recruit K+ through other K+ channels
that are not directly attributable to serotonin (Jacobs, 177-178).
Muschamp, et al (2004), also did a study implicating LSD, other
hallucinogens, and 5-HT2A receptors, the activation of which caused a
calcium-dependent increase of excitatory postsynaptic potentials
(EPSP's). Out of the findings, they proposed a hypothesis that
"...glutamate release represents a common pathway for the actions of
serotonergic hallucinogens."
References
Leicht, I. (1996). Postulated mechanisms of LSD. Retrieved from:
http://www.cs.hmc.edu/~ivl/writing/non_fiction/lsd/
Jacobs, B. L. (1985). Hallucinogens: Neural, behavioral, and clinical
perspectives. New York Raven Press.
Palfai, T. & Jankiewicz, H. (2001). Drugs and Human Behavior, 2nd ed.,
McGraw-Hill.
Muschamp, J. W., Regina, M. J., Hull, E. M., Winter, J. C., & Rabin, R. A.
(2004). Lysergic acid diethylamide and [--]-2,5-dimethoxy-4-
methylamphetamine increase extracellular glutamate in rat
prefrontal cortex. Brain Research 1023, 134-140. Retrieved from:
www.elsevier.com/locate/brainres
Joanna Rocco
Primary behavior changes and side effects of LSD
LSD (D lysergic acid diethylamide) is a very potent synthetic
hallucinogen. It is manufactured from lysergic acid, found in ergot,
which is a fungus that grows on grains. In its original form, LSD is a
white or clear, odorless, water soluble crystal that can be crushed into
a powder and dissolved. LSD goes by the street name “acid” or
“blotter” and is sold in tablets, capsules and sometimes liquid form.
Oftentimes LSD is added to absorbent paper and sold in individual
squares or “doses” which are then dissolved on the tongue.
LSD is an extremely potent mood changing chemical. A person’s
subjective world changes drastically once LSD is taken (Blacker,
Jones, Stone, & Pfefferbaum, 1968). Users refer to their experience
with LSD as a “trip.” These experiences generally begin about 30 to 90
minutes after taking the drug, and last from 6 to 12 hours. LSD is
sometimes described as a drug that breaks down barriers, but the
results of taking LSD are complex and variable. Every trip is different
and users show a wide range of reactions (Terrill, 1964). The first
signs of LSD are usually physical, and can include dilated pupils,
salivation, sweating and nausea, loss of appetite, sleeplessness,
tremors, dry mouth, chills, raised body temperature, rapid heartbeat
and elevated blood pressure. As the trip progresses, one’s mood,
perceptions and sensations become affected (Palfai & Jankiewicz,
2001).
In the first phase of the trip there may be abnormal body
sensations, changes in mood, space and time distortions and visual
hallucinations (Palfai & Jankiewicz, 2001). Time may seem to stand
still, or race forward or backward (Terrill, 1964). Emotions can
become very intense, and reactions my range from euphoria to
depression. Users at this stage may also feel an increased sensitivity
to interactions with other people and can become hurt or paranoid. As
stated by Palfai and Jankiewicz (2001), the second phase of the trip
can contain a release of personal material and memory, complex
imagery and ego disruptions.
At the peak of the trip there is a flurry of strange and intense
effects. There is a flood of information from the sensory system, and
the user experiences increased sensitivity to sounds and sights. One
may lose critical perception, even becoming part of the hallucinated
imagery. Distortions of body image can occur, and one may feel they
have become separate from their body. There is often a combination
or “crossing” of sensations. For example, one may feel colors, or see
music. Objects may seem to come alive, and things once seen as
ordinary may become achingly beautiful (Terrill, 1964). At this point
the user may feel that they are losing themselves or losing control.
Thinking can become difficult and there may be a flight of ideas and
problems organizing information. One may sense that he is visiting
other worlds or unlocking deep secrets (Palfai & Jankiewicz, 2001).
Tripping on acid can produce very deep and profound
experiences in many of its users. Some may even consider the results
to be mystical. People often report a feeling of understanding and
“connectedness” when using the drug. The person may become aware
of being part of something larger, a part of everything in existence.
Thoughts may become very lucid, and the mind may seem to be able to
see relationships between things on many different levels, often all at
the same time (Pahnke, 1967). As stated by Palfai and Jankiewicz
(2001), some users get a new perception of their personality and even
a sense of unity with God or the Universe. Accompanying this may be
feelings of awe and reverence. These feelings and new
understandings may persist long after the actual trip is over, leading to
new attitudes and behaviors regarding both self, others and life itself.
Exploration into LSD’s possible clinical applications (e.g. Pahnke,
1967), such as helping terminal cancer patients become more
comfortable with the idea of dying, have had mixed results.
Side Effects
Side effects or adverse effects of LSD can be unpleasant and
even scary, but are usually not life threatening. There is no known
human lethal dose for LSD. Death can occur as a result of the
psychological actions of the drug on users (i.e., suicide). There is also
no clear evidence that LSD alone causes brain damage, but long time
users sometimes complain of memory loss and may feel as if they have
been permanently altered (Blacker et al., 1968). It should also be
noted that when LSD is acquired on the street, it may contain other
substances that could be harmful or fatal if ingested. The results of
the drug become even more unpredictable when mixed or combined
with other drugs such as MDMA.
Anytime one finds the aspects of an LSD experience to be
frightening or objectionable, especially if it constitutes the majority of
time under the influence, it can be considered a bad trip. A bad trip
can include hallucinations, intense anxiety, depression, rapid mood
swings and extreme confusion (Ungerlieder, Fisher, Fuller, & Caldwell,
1968). A person experiencing a bad trip may feel like he has no
control over the situation, or have the sense that he is losing his
identity. One may also feel trapped, or as if the experience will never
end, which in turn leads to panic. One may also feel paranoid or
persecuted. A bad trip can be a very traumatic experience. These
psychotic reactions can be severe and prolonged enough as to require
hospitalization (Palfai & Jankiewicz, 2001).
The effects of LSD are unpredictable, and it is not entirely clear
what exactly makes for a bad LSD experience. Some people believe
that one is more likely to have a bad trip if one is inexperienced with
the drug, but there are also reports of people have had numerous
positive trips on LSD and then have a bad trip for no apparent reason.
Factors that seem to have some importance in the occurrence of a
good trip versus a bad trip are the amount taken, attitude of the user
toward the experience, the setting in which one takes the drug and
goes through the trip, and the presence of any preexisting mental
illness (Palfai & Jankiewicz, 2001; Ungerlieder et al., 1968).
It is important to note at this point that some effects are
pleasant or expected when one is on the drug, but can be unwanted
when the drug has worn off and the effect is still present or sometimes
present. As defined by Palfai and Jankiewicz (2001), a flashback
occurs when the elements of a trip come back after a period of time
off the drug. A flashback can include any and all elements of an LSD
trip such as hallucinations, delusions, and emotional changes. A
flashback occurs suddenly, often without warning, though some
believe that flashbacks are more likely to occur under emotional
distress, when overly tired, or when under the influence of alcohol and
marijuana. Length and frequency of flashbacks are extremely
variable. If these flashbacks cause a significant amount of distress or
impairment in one’s life or affect one’s ability to work or socialize with
others, they can constitute a disorder called Hallucinogen Persisting
Perception Disorder (American Psychological Association, DSM IV TR,
2000).
Lastly, there is the occurrence of long term perceptual
distortions. One such side effect of LSD is known as “trailing.” This is
when one sees a moving thing in individual movements, almost as if in
slow motion. There may also be color trails associated with this
phenomenon. Some users report that they experience trailing for up to
a year after taking the drug. LSD does affect the optic pathways of the
brain, and the drug may decrease the brain’s ability to “screen out”
certain sensory input (Asher, 1971). One study showed chronic users
of LSD to be very sensitive to low intensity visual stimulation, also
backing up the theory that long time users may organize sensory input
differently than non users (Blacker et al., 1968).
Most users of LSD decrease use or stop its use over time. This
may be due in part to the inconsistent effects and potential adverse
reactions of LSD as well as one’s need to recover and reorient after an
LSD experience. LSD does produce tolerance, but it doesn’t produce
compulsive drug-seeking behavior typical of addictive drugs such as
heroin (LSD JustFacts).
In conclusion, it is worthy of noting that while LSD may seem
less dangerous than some other illicit substances, it is an illegal drug
that can lead to serious penalties. It is also a drug for which
appropriate doses are hard to calculate, and can contain other
substances that may be harmful. Anyone who has been diagnosed
with a mental disorder or has had psychological problems in the past
should be extremely cautious about taking this drug as it may
precipitate a psychotic break. (Palfai & Jankiewicz, 2001).
Following are some LSD experiences reported by anonymous
users, both positive and negative, that illustrate much of the
information given in this paper.
“It kicked in quickly and hard. The moving fractals took over my
entire vision. The TV screen poured out onto the carpet like a
waterfall. The walls cracked and defused. Everything disappeared,
even my body melted into the void that I was now in. All that was left
was my consciousness, and the very basic thought process.
Everything I could see was oozing, melting, swirling, decaying,
transforming. I watched as the music came out of the speakers like a
tidal wave. Things I touched were transformed into smells…an
endless play on my senses ensued, relentlessly bashing my fragile
consciousness.”
“She was wearing fingernail polish that was clear, but shiny.
Suddenly I started to notice that when she moved her arms about,
making gestures, I was able to see the trails following her fingertips.
This is when I realized that everything around me was different. It was
like being in a whole different universe. I remember sitting on the
front steps, enjoying all of these new sensations, and then looking at a
few long blades of grass that were blowing in the breeze. They were
stretching toward me, reaching out to me. I remember reaching out to
touch these blades of grass, then suddenly becoming aware that I was
in the midst of so much life. I began to feel like I was connected to all
of life and nature.”
“My gaze lifted to the sky and the sky’s gaze fell upon me. Each
cloud was now a giant type of amoeba type organism, covered in dots
which pulsed in color like the skin of a cuttlefish. Each giant amoeba
had a giant blue human looking eye observing me. I briefly saw
existence as a giant clock face of a billion dots between each second.
The dots were ticking forward in a relentless advance. Each dot was
the equivalent of someone’s lifetime. I could hear air raid sirens and
the sound of buzzing. In the sea of holes was a giant cross which had
a festering bloody pile of guts and organs spread across it staining the
wood crimson. It was an image of impossible pain.”
“Thought loop after thought loop, over and over, uncontrollable. I
could have bitten through nails I was clenching my jaw so hard.
Nothing stayed still, buildings oozed, the street and cars breathed and
waved as if they were on rough seas. The branches of the trees grew,
in any direction, I couldn’t tell. This universe was getting too big for it
all. I felt the universe collapse. I saw every particle come together in
a fantastic implosion of everything I knew and didn’t know or ever
knew or ever will know. Finally, everything this trip has been riding on
and every thought and visual and everything that had ever happened in
the universe came down to a single answer. Everything came down to
this one single moment. I was sure that this is where I would meet
God.”
References
American Psychiatric Association. (2000). Diagnostic and statistical
manual of mental disorders (4th ed TR.).
Washington, DC: Author.
Asher, H. (1971, March). “Trailing” phenomenon, a long lasting LSD
side effect [Letter to the editor]. American Journal of Psychiatry, pp.
1233-1234.
Blacker, K.H., Jones, R.T., Stone, G.C.,& Pfefferbaum, D. (1968).
Chronic users of LSD: the “acidheads.” American Journal of
Psychiatry, 125, 341-351.
LSD JustFacts. (n.d). Retrieved February 8, 2005, from
http://www.cesar.umd.edu/cesar/jf/drugs/lsd.asp
Pahnke, W. (1967, March). LSD and religious experience. Paper
presented to a public symposium at Wesleyan University, Middletown,
CT.
Palfai, T., & Jankiewicz, H. (2001). Drugs and human behavior (2nd ed.).
New York: McGraw Hill.
Terrill, J.(1964). LSD, the consciousness expanding drug. New York:
David Solomon.
Ungerleider, J.T., Fisher, D.D., Fuller, M., & Caldwell, A. (1968). The
“bad trip.” The etiology of the adverse LSD reaction. American Journal
of Psychiatry, 124, 1483-1490.
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