Erowid
 
 
Plants - Drugs Mind - Spirit Freedom - Law Arts - Culture Library  
Path :   chemicalslsd
Donate Your Used Drug Books to Erowid
If you have old books about psychoactive drugs, contribute them to Erowid!
Your used books will find a good home either in our library or with a supporter. [details]
Excerpt from Dr. Rick Strassman's
"Adverse Reactions to Psychedelic Drugs: a Review of the Literature"
by Matt
v1.0 - Mar 25 1993
Originally published on alt.drugs
In article  Lawrence Curcio  writes:

>I'm sorry. I must take issue with the "Purely psychological" explanation
>for untoward, protracted reactions to LSD. This is just a manifestation
>of the EXISTENTIAL PSYCHOSIS MYTH. If you take a chemical, PHYSIOLOGICAL
>things can go wrong. These reactions also respond to the administration
>of other chemicals. 

>It is true that if the individual in question is manic depressive, then
>LSD may have had nothing to do with his reaction. It is POSSIBLE that
>LSD precipitated a latent tendency; HOWEVER there is no convincing
>research to show this drug cannot precipitate psychotic reactions in
>normal individuals - Psychiatric speculation maquerading as "Theory" to
>the contrary.

>I'm not a doctor, I'm just a lay person with little respect for psychiatry. 


The best review of this question is Rick Strassman's "Adverse Reactions 
to Psychedelic Drugs: a Review of the Literature" in _J. Nerv and Mental
Disease_ 172(10):577-595. 1984.  He writes:

The most common adverse reaction is a temporary (less than 24 hours)
episode of panic --the "bad trip".  Symptoms include frightening illusions/
hallucinations (usually visual and/or auditory); overwhelming anxiety
to the point of panic; aggression with possible violent acting-out behavior;
depression with suicidcal ideations, gestures, or attempts; confusion; and
fearfulness to the point of paranoid delusions.

Reactions that are prolonged (days to months) and/or require hospitalization
are often referred to as "LSD psychosis," and include a heterogenous
population and group of symptoms.  Although there are no hard and
fast rules, some trends have been noted in these patients.  There is a
tendency for people with poorer premorbid adjusment, a history of
psychiatric illness and/or treatment, a greater number of exposure to
psychedelic drugs (and correlatively, a great average total
cumulative dosage taken over time), drug-taking in an unsupervised
setting, a history of polydrug abuse, and self-therapeutic and/or
peer-pressure-submission motive for drug use, to suffer these consequences.

In spite of the impressive degree of prior problems noted in many of these
patients, there are occasional reports of severe and prolonged reactions
occuring in basically well adjusted individuals.  In the same vein,
there are many instance of faily poorly adapted individuals who suffer
_no_ ill effects from repeated psychedelic drug use.  In fact, it has been
hypothesized that some schizophrenics do not suffer adverse reactions
because of their familiarity with such acute altered states.  Another
possibility is that there individuals may be "protected" by possible "down-
regulation" of the receptors for LSD, bu the (over-)production of some
endogenous compound.  _Individual_ prediction of adverse reactions,
therefore, is quite difficult...
...

Major "functional" psychosis vs. "LSD psychosis"
-----------------------------------------------

A diagnostic issue dealth with explicitly in only a few papers is that of
LSD-precipitated major functional illnesses, e.g. affective disorders
or schizophrenia.  In other words, many of these so called LSD psychoses
could be other illnesses that were triggered by the stress of a traumatic
psychedelic drug experience.  Some of the same methodological issues
described earlier affect these studies, but they are, on the averagem
better controlled, with more family and past psychiatric history available
for comparison.

Hensala et al. compared LSD-using and non-LSD-using psychiatric inpatients.
They found that this group of patients was generally of a younger age and
contained more characteristically disordered individuals than the non-
LSD-using group.  Patients with specific diagnoses with or without LSD
histories were not compared.  Based on their observations, they concluded
that LSD was basically just another drug of abuse in a population of
frequently hospitalized individuals in the San Francisco area, and that
it was unlikely that psychedelic use could be deemed etiological in the
development of their psychiatric disorders.

Roy, Breakey et al., and Vardy and Kay have attempted to relate LSD use to
the onset and revelopment of a schizophrenia-like syndrome.  A few comments
regarding this conceptual framework seem in order, before their findings
are discussed.  The major factor here is that of choosing schizophrenia,
or in the Vardy and Kay study, schizophreniform disorders, as the
comparison group.  There is an implication here that LSD psychoses are
comparable, phenomenologically, to schizophrenia-like disorders, and that
LSD can "cause" the development of such disorders.  The multiplicity of
symptoms and syndromes described in the "adverse reaction" literature
should make it clear that LSD can cause a number of reactions that can last
for any amount of time--from minutes to, possibly, years.  I believe what
is being studied here is the question of the potential role of LSD in
accelerating or precipitating the onset of an illness that was "programmed"
to develop ultimately in a particular individual--in a manner comparable
to the major physical or emotional stress that often precipitates a bona
fide myocardial infarction in an individual with advanced coronary
atheresclerosis.  The stress did not _cause_ the heart disease; it was
only the stimulus that accelerated the inexorable process to manifest
illness.

In looking at the relevant studies, Breakey et al. found that schizophrenics
who "used drugs" had an earlier onset of symptoms and hospitalization than
non-drug-using schizophrenics, and had possibly better premorbid personal-
ities than non-drug using patients (although Vardy and KAy have challenged
this analysis of Breakey's data).

Bowers compared 12 first-admission patients with psychosis related to LSD
use, requiring hospitalization and phenothiazines, to 26 patients hospital-
ized and treated with phenothiazines with no history of drug use.  Six
of these controls had been previously hospitalized.  Drug-induced psychotic
patients were found to have better premorbib histories and prognostic
indicators than the nondrug groups.  There was no difference in rates of
family history of psychiatric illness.  However, several issues flaw
this study.  One is the poly-drug abusing nature of the "LSD-induced"
psychotic patients, compared to the controls.  The role of LSD, therefore,
in causing or precipitating these symptomatic disorders, is open to dispute.
The other is the lack of an adequate comparison control group, i.e. the
controls were specified only as "psychotic," and did not necessarily
match the LSD group in either symptoms or diagnostic classification.
A follow-up study of the patients occured between 2 and 6 years later.
One half did well and one half did poorly, although the lack of a control
group for a follow-up in a similarly symptomatic control group makes 
interpretation of the data difficult.

Roy, in a somewhat different design, compared chronic schizophrenic
patients (diagnosed according to DSM-III criteria) who had used LSD
within the week preceding hospitalization, and found no difference
in age of symptom onset or hospitalization compared to patients without
a history of illicit drug use.

Vardy and Kay, in an elegant study with a 3- and 5- year follow-up period,
demonstrated that patients hospitalized for a schizophrenic picture
that developed within two weeks of LSD use (patients with other diagnoses
were explicitly excluded form comparisons with non-drug-using
schizophrenics) were "fundamentally similar to schizophrenics in
geneology, phenomenology, and course of illness (165, p. 877).  Pre-
morbid adjustment, age of onset of symptoms and hospitalization, family
history of psychosis or suicide, and most cognitive features were also
equal between groups.  Family histories of alcohol abuse were markedly
great in the LSD group.

I believe these data, taken as a whole, limited as they are in terms of
comparing subgroups (i.e. LSD-using vs. non-LSD-using) of "schizophrenia-
like" disorders, point towar, at most, a possible precipitory role in
the development of these disorders, in a non specific and not
etiologically related manner.

---

So there you have it, folks.  

It's a good article, so rush out to the library and get it so you can
appear knowledgable the next time someone at a cocktail party starts to
talk about LSD turning people to vegetables.  Nothing wins the
admiration of potential mates like knowling references to _J. Nerv. Ment_ 
and _Br. Med. J._!

      --Matt