Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study
BMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7374.1199 (Published 23 November 2002) Cite this as: BMJ 2002;325:1199
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let me get this straight:
You take 50 thousand (give or take a few) subjects that were
interviewed 30 plus years ago, factor in how many at some point in the
next 30 years come down with schixophrenia, then use a correlation to
"prove" someone's agenda.
Especially given what we know now about the often overlooked onset of
mental illnesses in teen or even preadolescent years, it is not valid to
say that the subjects in question were or were not in the prodromal stages
of schixophrenia. Were any of the subjects back then assessed for related
symptoms?
What about all the people who smoke marijuana and DON'T develop
schixophrenia? Or all the people who don't smoke marijuana and DO develop
schixophrenia? THe study shows no comparison between the occurance of
schixophrenia in non-using groups vs. those that use cannabis. It only
shows that some people who smoke marijuana will develop schixophrenia at
some point in their lives.
There is another article in this journal, and, while I admittedly
didn't read it, the title alone suggested the notion that marijuana use
leads to risky behavior in adolescents. What about the adolescents who
are by nature risk takers? Would they not be inclined to experiment with
marijuana out of curiousity?
I only got a B in my graduate level research class, and got a C in
statistics ( had the shingles the day of the final) but even I can tell
when numbers are crunched to support someone's political or personal
agenda.
I am getting weary of all the 'scientific' information out there
about marijuana, a substance that has been smoked for thousands of years
with little negative social effect. Youth are not going to take drugs
seriously if the message is not credible.
I'm not impressed with this article one bit.
Competing interests:
None declared
Competing interests: No competing interests
Zammit et al have shown a clear association between cannabis use and
schizophrenia 1. However the nature of the relationship between
schizophrenia and cannabis is still unclear. The conclusion that this is a
causal association is at odds with the work of Jablensky et al who showed
that the incidence of schizophrenia in different cultures is remarkably
similar despite a great variety in the cultural use of cannabis 2. Johns
reports that cannabis use leads to adverse mental health effects in many
regular users. He reports that these are dose related but also can be
aggravated by constitutional factors including vulnerability to serious
mental illness 3. The association Zammitt described may be due to cannabis
unmasking schizophrenia in people with an underlying predisposition to
schizophrenia. It seems possible that this could be a specific effect of
cannabis and not other psychotropic drugs.
The association between cannabis use and relapse in schizophrenia is
another well-established association in which causality is difficult to
establish 4, 5. Examining why patients with schizophrenia use cannabis may
help throw some light on the nature of the relationship between
schizophrenia and cannabis. I carried out a qualitative study exploring
some of the reasons why patients with schizophrenia may use cannabis. The
study took place in central Scotland, a mixed rural and urban area.
Nineteen patients were interviewed in their homes, using a semi-structured
questionnaire. These patients were initially approached by their CPN to
take part in the study, which had local ethics approval. A number of
topics were covered including the reasons for using cannabis and patients
perceptions of cannabis’ effect on their schizophrenia. Participants whose
experiences were similar were grouped together in the analysis. Four
distinct experiences were identified. In the first group, patients were
regular users. They enjoyed the effects of cannabis, found it helped them
relax, feel less depressed and it helped them sleep. They denied that
using cannabis made their illness worse. This group was more likely to be
using other drugs. The second group were also regular users of cannabis.
They also reported that they used it to help them sleep and that it helped
them feel more relaxed but despite that they felt that using cannabis made
their illness worse. In the third group, patients were either infrequent
users or had only used cannabis once. They agreed that it made their
illness worse and they found the long-term effects unpleasant. The fourth
group denied every having used cannabis, this group did not use any
illicit drugs and also were generally tee total.
In this small qualitative study, patients seemed to have different
perceptions of the effects of cannabis on their illness, although there
was no objective evidence to corroborate their perceptions, it is
interesting that some patients felt a psychotherapeutic benefit from using
cannabis and seemed to be self-medicating. Why patients perceive different
effects from using cannabis is unclear but by exploring patients'
perceptions clinicians may be able to manage patients with schizophrenia
more effectively.
The effects of using cannabis on mental health is an under researched
area. I welcome Zammitt and his colleagues’ research but more work needs
to be done to establish the nature of the relationship between cannabis
and schizophrenia.
1. Zammit S, Allebeck P, Andreasson S, Lundberg I, Lewis G. Self
reported cannabis use as a risk factor for schizophrenia in Swedish
conscripts of 1969: historical cohort study. BMJ 2002;325:1199.
2. Jablensky A, Sartorius N, Ernberg G, Anker M, Korten A, Cooper JE et
al. Schizophrenia: manifestations, incidence and course in different
cultures. A World Health Organization ten-country study.
Psychol.Med.Monogr Suppl 1992;20:1-97.
3. Johns A. Psychiatric effects of cannabis. The British Journal of
Psychiatry 2001;178:116-22.
4. Linszen. Drug and alcohol problems among individuals with severe
mental illness in south London. Archives General Psychiatry 1994;51:162-
74.
5. Martinez-Arevalo MJ, Calcedo-Ordonez A, Varo-Prieto JR. Cannabis
Consumption as a prognostic Factor in Schizophrenia. Actas Luso Esp Neurol
Psiquiatr Genc Afines 1995;23:189-92.
Competing interests:
None declared
Competing interests: No competing interests
I am curious why data regarding serum and dietary homocysteine,
folate, docosahexaenoic acid, eicosapentaenoic acid, pyridoxal 5
phosphate, methionine and others were not controlled for in this study.
The dearth of published data on the topic of cannabis and altered
cognitive function fails to provide any concept of MECHANISM for cognitive
decline let alone psychosis, schizophrenia or depression. However little
argument should be found suggesting that cannabinoids do in fact modify
the cellular metabolism of the CNS.
The compounds listed above are known to influence phospholipid
membranes, neurotransmitter production, monoaminergic neurotransmission
and neurogenesis and other areas which are known pathophysiological
factors in psychosis, schizophrenia and depression. If a subject is not
nutritionally replete how is it possible for the CNS to meet the cellular
changes that cannabinoids are known/anticipated to produce?
It has been my experience that most doctors and researchers have
almost no nutrition education and certainly no understanding of even basic
nutritional biochemistry(late 20th century nutrition). As such when one
begins to formulate a hypothetical framework it therefore is devoid of the
modifying effect of these areas of scientific knowledge.
As an example: Hyperhomocysteinemia has been associated with poor
memory recall[Am J Clin Nutr 2001;73:927-33] and blood homocysteine
concentrations are inversely correlated with some cognitive-function
tests.[Arch Neurol 1998;55:1449-55, Am J Clin Nutr 1996;63:306-14, Acta
Psychiatr Scand 1992;86:386-90,Int J Geriatr Psychiatr 1998;13:235-9.
Circulating homocysteine concentrations reflect B-vitamin status, and
B-vitamin deficiency might lead to hypomethylation of chemicals that are
crucial to brain function(B-6(pyridoxal 5 phosphate) as a co-enzyme is
instrumental in the production of the putative neurotransmitters,
dopamine, norepinephrine, serotonin, GABA and taurine as well as the
sphingolipids and polyamines. [Annals of New York Academy of Sciences Vol.
585 1990: Vitamin B-6 page 128]
The hypothesis that cannabis is a causative in CNS illness is
interesting in light of the fact that none of the studies seem to have
controlled for the rational confounders I have mentioned above.
Additionally there is data (including international numerous patents
held by various parties including the US Government: EP1071419A1)
suggesting that cannabinoids are actually antioxidants and
neuroprotectants. [J. Neurosci. 1999;19 (8): 2987, JPET 2000;293 (3): 807,
PNAS 1998; 95 (14): 8268.
Considering that the first evidence of the medicinal use of cannabis
is found in the book Pên-ts’ao Ching, attributed to the Emperor Shen-nung
of about 2000 B.C. I wonder if perhaps it's more recent changes in dietary
repleteness that might be triggering the pathophysiological changes in the
CNS of heavy pot smokers... or for that matter anyone that suffers from
psychiatric illnesses...
A bit of non-peer review please take is as such...
Be well,
Ken Jacobie, LMT
An unflinching determination to take the whole evidence into account
is the only method of preservation against the fluctuating extremes of
fashionable opinion.
Alfred North Whitehead
http://www.parl.gc.ca/37/1/parlbus/commbus/senate/com-e/ille-e/library-e...
Competing interests:
Ethnobotanical Enthusiast and Practicing Human Being
Competing interests: No competing interests
EDITOR-Dr Zammit and his colleagues have shown an association between
cannabis use and schizophrenia, but as they themselves state, attribution
of causality is problematic, not least because of evidence suggesting that
those with schizophrenia may have had abnormalities detectable in
childhood (1) and therefore predating any cannabis use. There is another
difficulty with the proposition that cannabis use causes some cases of
schizophrenia; as Rey and Tennant (2) point out, we lack the crucial
epidemiological evidence demonstrating the expected increase in incidence
of schizophrenia within populations exposed to high levels of cannabis. It
is therefore important to carefully consider alternative explanations for
the association.
Varma and Sharma (3) found an increased prevalence of cannabis use
disorder in the first-degree relatives of schizophrenic probands. Working
from the other direction, McGuire et al (4) found that within a sample of
patients admitted with acute psychosis, the morbid risk of schizophrenia
was increased for the relatives of probands who had tested positive for
cannabis on urinary screening. These findings are consistent with the
notion of a common genetic risk factor for cannabis abuse and
schizophrenia.
By adjusting for abuse of other substances, Zammit et al have
concluded that the association between cannabis use and schizophrenia
cannot be explained by a general factor predisposing to schizophrenia and
all substance misuse, but their findings do not rule out the possibility
of a similar risk factor more specific to cannabis use. This paper is a
valuable and timely caution to legislators and policy makers, but the case
for cannabis as a causative agent in schizophrenia is presently unproven.
1. Jones P, Rodgers B, Murray R, Marmot M. Child development risk
factors for adult schizophrenia in the British 1946 birth cohort. Lancet
1994;344(8934):1398-402.
2. Rey JM, Tennant CC. Cannabis and mental health. British Medical Journal
Clinical Research Ed. 2002;325:1183-4.
3. Varma SL, Sharma I. Psychiatric morbidity in the first-degree relatives
of schizophrenic patients. British Journal of Psychiatry 1993;162:672-8.
4. McGuire PK, Jones P, Harvey I, Williams M, McGuffin P, Murray RM.
Morbid risk of schizophrenia for relatives of patients with cannabis-
associated psychosis. Schizophrenia Research 1995;15(3):277-81.
Competing interests:
None declared
Competing interests: No competing interests
Study deeply flawed
Criticism of the Zammit paper “Self-reported cannabis use as a risk
factor for schizophrenia in Swedish conscripts of 1969: historical cohort
study”
This study has been widely reported, and it has been used to back-up
a claim that cannabis increases the risk of schizophrenia by seven times.
The seven-fold increase in mental ill-health has been seized on by several
tabloids and prejudice against cannabis thus increased. The last
paragraph of the paper includes the really relevant figure produced by the
report. Total elimination of cannabis from the population would according
to the study cause a reduction in schizophrenia cases of 13%.
The above statement is not as eye-catching as “danger increased by
seven times”, and thus the research gets misrepresented. However, there
are other questions about this research that need answering. The big one
is that self-reporting illegal drug use in a non-anonymised questionnaire
would as the authors acknowledge result in under-reporting of cannabis
use, especially as the results would be known to military authorities.
The bald statement that “under-reporting of cannabis would again tend to
underestimate the true effect size” is challengable.
The proportion of the cohort who were stupid enough to tell the
Swedish authorities that they used illegal drugs before being conscripted
was 10.8%, or 5391 young men. Of these, 73 developed schizophrenia, or
1.4% of self-repo0rted cannabis users. The figures for developing
schizophrenia are much more reliable, as they were derived from medical
records of hospitals. Thus the percentage of actual cannabis users who
then develop schizophrenia would be much lower. A more likely figure for
cannabis use in the cohort would be 25% in 1969. Therefore it can be
expected that 0.58% of cannabis users developed schizophrenia.
Even the report's percentage, based on under-reported use, 1.4 % of
cannabis users developed schizophrenia. The figures for comparison are
only derived from derivative analysis of the various data, utilising a
“logistic progression” technique. This analysis tool is designed to
“yield the biggest mean differences between the groups”. In other words
the statistical techniques used explicitly accentuate the difference
between the categories, or groups, that are being examined, in this case
cannabis users and non-cannabis users. Because schizophrenia is so
uncommon in society as a whole, such an analysis tool can be justified in
order to show proportional differences in very small percentages.
Unfortunately, the “soundbite” extracted from the paper obscures more
than it illuminates, and many tabloids now regularly refer to the
“Swedish” study to back a claim that cannabis use makes someone seven
times more likely to develop mental illness. The Zammit paper refers
only to a 30% risk, if there is a casual relationship with cannabis, of
developing schizophrenia in users. Adjustment for under-reporting
cannabis use at time of conscription would reduce that risk by at least
half.
James Derieg
Project Worker
GDAS Stroud
December 8, 2004
Competing interests:
Fron line Drugs Worker
Competing interests: No competing interests