Overview of 5 major cannabis studies
Cannabis Abuse and Schizophrenia
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Question: Can a causal relationship between adolescent cannabis use and the onset of schizophrenia be inferred from the currently available research?
Answer: It is very difficult to ascertain a relationship between cannabis and the onset of schizophrenia due to many confounding factors that exist in the populations studied as well as the ethical considerations concerning performing a pure study of this relationship.
There are several studies that have attempted to establish a link between cannabis use and schizophrenia. Three notable studies are the Age, beginning and course of schizophrenia study (2000) by Martin Hambrecht and Heinz Hafner in Germany, the Dunedin multidisciplinary health and development study (2002) by Louise Arseneault et al., and the Christchurch health and development study by Fergusson et al. These three studies attempt to indicate a causal relationship between cannabis use and the onset of early psychotic symptoms. Veen et al. (2004) have contributed an important distinction regarding the understanding of this relationship and how the role of gender may influence the relationship’s causality. Other studies have shown a relationship between substance abuse and psychiatric disorders. However, only a handful of researchers have attempted to link, specifically, cannabis use prior to the onset of schizophrenia. The most important evidence so far in this link is the
Christchurch health and development study.
At the outset of this investigation, the initial question was: Does cannabis use induce symptoms of bipolar disorder? This question does not appear to be well investigated in the literature. A thorough search of CINAHL was performed using multiple search strings that included cannabis, marijuana, THC, tetrahydracannabinnol, bipolar disorder, bi-polar disorder, manic depression, affective disorder, and schizo-affective disorder. This search revealed very little regarding the initial topic. A review of those studies did reveal a significant amount of data relating to schizophrenia and cannabis. A change of focus in the question has revealed valuable literature for an understanding of this phenomenon. A subsequent search of CINAHL replacing the prior disorder with schizophrenia, psychosis, psychotic, and schizophrenoform, has revealed many studies. I have thoroughly reviewed 5 of those studied and have utilized an additional 5 studies that have pertinent information regarding understanding of this subject.
There is definitive evidence that shows a relationship between the use of cannabis at a young age and the development of schizophrenic symptoms. Arsenualt et al. (2002) performed a longitudinal study with a birth cohort of 1037 individuals born in Dunedin, New Zealand during 1972 and 1973. This study had a 96% follow up rate to age 26. The study contained data on psychotic symptoms at age 11, self-reported drug use at age 15 and 18 and a standardized psychiatric interview to obtain a DSM-IV diagnosis at age 26 (p.1212). A representative sample of 759 (n=759) individuals was extracted for complete data that fit the study’s criteria of adult psychiatric outcomes, adolescent use of illicit substances, and childhood psychotic symptoms (p.1212).
The Control group was composed of 494 (65.1%) individuals who had reported using cannabis “never,” “once,” or “twice,” at either age 15 or 18. The study groups comprised 236 (31.1%) who had reported first using “three times or more” at age 18, and 29 (3.8%) who had reported first using “three times or more” at age 15 (p.1212).
The results showed that subjects who used cannabis by age 15 and 18 exhibited more schizophrenia symptoms than the controls. These results remained significant when psychotic symptoms at age 11 were controlled for. A logistic regression analysis indicted that cannabis users at age 15 had a fourfold greater incidence of a schizophreniform disorder at age 26. The results continued to remain higher than the controls when psychotic symptoms at age 11 were accounted for. However, the risk was no longer statistically significant. Approximately 10% of the cannabis users by age 15 who did not have symptoms at age 11 developed schizophreniform disorders by age 26. This compares to approximately 3% of the remaining cohort. This study suggests that cannabis use at an early age is associated with a greater incidence of schizophrenia symptoms even when psychotic symptoms that preceded the use of cannabis are controlled for (Arsenault et al., 2002).
Hambrecht and Hafner performed a study of psychiatric hospital admissions between 1987 and 1989. The focus of this study was to examine the “clinical characteristics and temporal sequence of schizophrenia and comorbid cannabis abuse at the very onset of psychosis in order to contribute to the understanding of a possible causality between the two disorders” (Hambrecht & Hafner, 2000,). These individuals were first-time admissions for schizophrenia or paranoid disorders. The initial population contained 392 persons’, however, due either to refusal or too short a hospital stay, the final number was 267. An additional 35 patients were excluded due to discovery of prior psychotic episodes, leaving a total of 232 persons. A control group was obtained from the general population that the hospital served. This group was obtained using a random selection of municipal registrations files. The first 57 respondents who had no history of schizophrenia or paranoid disorders were selected. In the control group, 7% had a history of cannabis abuse and 12% had a history of alcohol abuse (p.470).
In this study, both patients and relatives were interviewed to report on “milestones” during the early course of schizophrenia. Assessments of patients were done using the Interview for the Retrospective Assessment of the Onset of Schizophrenia (IRAOS), Present State Exam, Scale for the Assessment of Negative Symptoms, and the Disability Assessment Schedule. Both patients’ and relatives’ reports of first psychotic episodes correlated significantly (Pearson Correlations; first symptoms 0.77, First positive symptoms 0.93, first negative symptoms 0.73) (Hambrecht & Hafner, 2000, p.470).
In this study, 90% of illicit drug users had abused cannabis at some time. 37% of the study group reported cannabis as their only substance abuse. Multiple substance abuse especially concomitant alcohol abuse was prevalent. 80% of first reported abuse involved cannabis. Group-wise comparisons were done to extract the individuals whose substance abuse involved primarily cannabis and correlated to first onset of symptoms of psychosis. These statistics were compared to both the general populations as well as non-drug abusing patients in the study (p.470-471).
This study suggests three possible interpretations of the subgroups defined. Group 1 comprised patients whose onset of cannabis abuse occurred years prior to the onset of first symptoms. Group 2 comprised patients whose onset of both cannabis abuse and signs of first symptoms were within the same time period. Group 3 comprised individuals whose onset of cannabis abuse occurred after the initial onset of first symptoms. The researchers suggest specific psychosocial and biological theories for the interpretations of these behaviors (p. 473).
Group 1 has been named the “vulnerability group.” A chronic deterioration of mental health and coping skills has been caused by cannabis abuse leading to onset of first symptoms and a reduction of the vulnerability threshold (p.473).
Group 2 has been named the “stress group.” These individuals have may have been potentially vulnerable to schizophrenia due to genetic or pre/peri natal influences. Cannabis is theorized to precipitate the onset of psychosis due to the dopaminergic stress factor attributed to cannabis (p.473).
Group 3 is called the “coping group.” These individuals consume cannabis as a “self-medication regimen” to cope with the negative symptoms of schizophrenia. These patients discover how the cannabis may appear to mask the unpleasant hypodopaminergic prefrontal state due to the dopaminergic affect of cannabis (p.473).
Within group 1 it is difficult to fully ascertain the confounding variable that may exist. Neurodevelopmental and morphological brain anomalies were not ruled out as preceding factors to the onset of schizophrenia. Additionally, subtle cognitive, perceptual, affective or social deficiencies may have contributed to the initial substance abuse. These deficiencies may also contribute to the predisposition of development of schizophrenia.
This study’s limitations, particularly the control groups’ small size and the geographical bias, limit the generalizations that can be drawn for all populations. Additionally, many confounding factors that could not be controlled for are prevalent in this study. More prospective studies as well as in depth case studies need to be performed to better understand the causality issue in the etiology of schizophrenia (Hambrecht & Hafner 2000 p.473-474).
The Christchurch health and development study (CHDS) published in 2005 in the journal Society for the Study of Addiction by Fergusson et al., has attempted with tremendous rigor to control for both observable as well as non-observable confounding factors as they relate to a causal relationship between cannabis and schizophrenia. This 25 year longitudinal study contained a birth cohort of 1265 New Zealand children. A total of 1055 participants were identified who met the criteria for both cannabis use and psychotic symptoms during the study’s framework. One focus of this study that has added to the rigor is the addition of data regarding frequency of use and the incidence of psychotic symptoms at ages 18, 21 and 25 years (Ferguson et al., 2005, p.354-361).
The intense depth of modeling that has been employed in this study, coupled with the time-dynamic covariate factors and fixed covariate factors has threshed out most of the confounding factors that have plagued prior research to reveal a very solid model of causality in this relationship (p. 362-364).
The analysis shows, within all ages of the study, a clear and statistically significant trend toward increased use of cannabis with increasing rates of psychotic symptoms. A rate of 2.3 to 3.3 times higher was observed over non-cannabis users in the study. When covariate factors were adjusted for, all models showed consistent data in the range of 1.6 to 1.8 times higher incidence of psychotic symptoms compared to those who did not use cannabis (Fergusson et al., 2005, p. 362).
This study employed a reciprocal cause model that measured causality of cannabis abuse and psychotic symptoms in both directions. These models were calculated for both observed variables as well as non-observed fixed effects. In each case, the incidence of increasing cannabis use was associated with an increase in psychotic symptoms. These models also show that the effect of psychotic symptom on cannabis use was negative. This evidence implies that it is unlikely for psychotic symptoms to cause an increase in cannabis use. Rather schizophrenia may in fact have an inhibitory effect on cannabis use. This suggestion of a direction of causality has been further supported by data indicating a dose response relationship between frequency of cannabis use and rates of psychotic symptoms. Daily users of cannabis had a 1.6 to 1.8 times higher incidence of psychotic symptoms over non-cannabis users even when all confounding factors were taken into account (p. 363).
The authors of this study have suggested two causal pathways for the linkage of cannabis and psychosis. The first is that cannabis use causes biochemical changes in the brain that may lead to increased rates of psychotic symptoms amongst susceptible users. The second is that those individuals who are prone to psychotic symptoms may have a greater tendency to use cannabis as a consequence of their condition or for self-medication. This study indicates clear evidence that the latter is not likely to be supported by further study. However the data do suggest that increasing the frequency and/or the dose, of cannabis is associated with increase in onset of psychotic symptoms. Furthermore, the data suggest that, with the onset of psychotic symptoms, cannabis use is decreased. There may be a confounding factor that has not been accounted for regarding the institutional milieus these individuals have experienced. This
was not noted in the study (p.362).
One further focused retrospective study was done in the Netherlands, Cannabis use and age at onset of schizophrenia, (Veen et al., 2004) attempts to assess the independent influence of gender and cannabis on the early course of schizophrenia. Veen et al. investigated a population in which cannabis use is neither illegal nor highly stigmatized. The Comprehensive Assessment of Symptoms and History (CASH) and the IRAOS tools were used along with patient medical records to assess for early signs and symptoms of schizophrenia. A cohort of 126 patients was selected from hospital admission from April 1997 to April 1999. The gender composition of the study was male (N=97) and female (N=36). A control group of non-cannabis users was also gathered for this study from the hospitalized population. The breakdown of this cohort was cannabis users (N=70), non-users of cannabis (N=63). In both cohorts the basis for qualification as a cannabis user was based on self-reported use of cannabis “greater than four times” and that the cannabis use had preceded the onset of first symptoms. Some of these patient indicated additional use of amphetamines and or cocaine in the period preceding the first symptoms (p.502). The tools used in the study categorized milestones in the patients’ histories to compare populations and genders respectively. The three major milestones were first social and/or occupational dysfunction, first psychotic episode, and first negative symptoms.
In both studies significant differences were observed. The predominant statistic was for the mean age of onset of first negative symptoms. The mean age for onset of negative symptoms in men was 26.5 years and the mean age for women was 41.6 years. This 15.2 year median age difference was associated with a confidence interval of 95%. This strong statistical evidence was further supported by the data in the user vs non-user study. The mean age of onset for first negative symptoms in cannabis users was 23.7 years as compared to 38.4 years in non-cannabis users in the study. This 14.7 year median difference in age was associated with a 95% confidence interval (p. 503-504).
The second most significant statistic was observed in the incidence of the first social and/or occupational dysfunction. First onset of these symptoms was a median of 6.7 years earlier for male than for female users of cannabis. Users vs. non-users of cannabis had a 9.3 year earlier mean age. When reviewed for first psychotic episode, the data showed that onset in men was a median of 3.2 years earlier than in women. Among users and non-users of cannabis, the onset of first psychotic episodes was a median of 7.5 years earlier for cannabis users (Veen et al., 2004, p.504).
This study shows that among Dutch male users, cannabis consumption may precipitate an earlier onset of psychotic symptoms. Additionally, the use of cannabis may speed up the onset of negative symptoms, especially in men (p. 504-505).
These studies give much credence to the theory that cannabis has an effect on the human brain that may precipitate in certain individuals a higher than the general population’s incidence of first symptoms of psychosis. Given this conclusion, it is evident that early substance abuse educational programs should be designed to be effective in deterring the first-time use of cannabis and other illicit drugs in adolescents. The protective factor of reducing adolescent drug use will have a tremendous effect in decreasing the cost of treating these individuals long into the future. These kinds of prevention programs have the potential to save hundreds of millions of dollars each fiscal year in the United States as well as abroad.
In researching this project, much anecdotal evidence exists regarding the benefits of cannabis use among the schizophrenic population. For the most part these data have no scientific basis other than personal experiential knowledge. One notable book does exist regarding this topic by Dr. Lester Grinspoon, Associate Professor Emeritus of Psychiatry at Harvard Marihuana, the Forbidden Medicine, 1928, discusses the many different diseases and disorders that cannabis may be able to treat. The high profile of the author does little to discourage the need for evidence-based practice in the treatment of these disorders. Many websites with varying degrees of credibility tout the beneficial effects of cannabis, as well as purporting a government conspiracy regarding big pharmaceutical dollars (as well as petroleum interests) as to why the drug continues to be an illegal and controlled substance.
In all of the research reviewed for this project, the substantive evidence consistently indicated a relationship between an increase of risk of mental or cognitive disorders with increased frequency and increased dose of cannabis. The National Institutes on Drug Abuse (NIDA) publishes an annual report on the effects of marijuana. This comprehensive report provides timely information on the most recent work being done in the field of substance abuse and addiction. The statistics are staggering regarding the social, cognitive, and psychological effect that cannabis consumption can have on an individual, especially youth. A multitude of studies have demonstrated the reduction in intellectual functioning in daily users of marijuana. A specific high-dose reaction to marijuana is termed as acute toxic psychosis. The syndrome includes symptoms of hallucinations, delusions, and depersonalization. Long-term cannabis use has also been shown to hasten the age related loss of hippocampal neurons; this loss causes increased difficulty with short-term memory and may not in some cases be reversible (NIDA, 2005).
It is not surprising that a correlation between earlier onset of schizophrenia and early cannabis abuse exists; given the large body of evidence regarding the negative effect this drug has on adolescent brain activity. No longitudinal studies to date have looked at the per capita levels of cannabis abuse in teens in the United States with an incidence of early onset psychotic symptoms. This would be an interesting study given the volume of data that has been collected in both subsets. A preliminary assessment of these data would presumably indicate a level-trend in first time hospitalizations per capita over the past thirty years with an initial drop in the trend from 1988 to 1993 (Child Trends Databank 2005).
This research indicates a tremendous need to build local, national and international educational programs to reduce and eliminate the incidence of marijuana abuse and abuse of other drugs in the adolescent population. There is no quick fix for modifying the current trends and attitude about drug abuse in America and internationally. On a local level, we continue to see the devastating effects of drug abuse in our teen populations through crime and other negative behaviors. Many communities choose to ignore these trends until they become overbearing or a few youth die through the neglect of a society that did not actively fight the escalating tide of drugs in the community. National policy in the United States should focus on the devastating costs associated with failure to reverse the trend of drug abuse among adolescents in our communities. Investing in the health and welfare of our teens through the development of community sports programs and recreational facilities, drug and alcohol treatment facilities and encouragement of participation in civic and religious sponsored activities can begin to address the grip that drug abuse has had on our communities.
Cannabis Abuse and Schizophrenia
From NursingWiki
Jump to: navigation, search
Question: Can a causal relationship between adolescent cannabis use and the onset of schizophrenia be inferred from the currently available research?
Answer: It is very difficult to ascertain a relationship between cannabis and the onset of schizophrenia due to many confounding factors that exist in the populations studied as well as the ethical considerations concerning performing a pure study of this relationship.
There are several studies that have attempted to establish a link between cannabis use and schizophrenia. Three notable studies are the Age, beginning and course of schizophrenia study (2000) by Martin Hambrecht and Heinz Hafner in Germany, the Dunedin multidisciplinary health and development study (2002) by Louise Arseneault et al., and the Christchurch health and development study by Fergusson et al. These three studies attempt to indicate a causal relationship between cannabis use and the onset of early psychotic symptoms. Veen et al. (2004) have contributed an important distinction regarding the understanding of this relationship and how the role of gender may influence the relationship’s causality. Other studies have shown a relationship between substance abuse and psychiatric disorders. However, only a handful of researchers have attempted to link, specifically, cannabis use prior to the onset of schizophrenia. The most important evidence so far in this link is the
Christchurch health and development study.
At the outset of this investigation, the initial question was: Does cannabis use induce symptoms of bipolar disorder? This question does not appear to be well investigated in the literature. A thorough search of CINAHL was performed using multiple search strings that included cannabis, marijuana, THC, tetrahydracannabinnol, bipolar disorder, bi-polar disorder, manic depression, affective disorder, and schizo-affective disorder. This search revealed very little regarding the initial topic. A review of those studies did reveal a significant amount of data relating to schizophrenia and cannabis. A change of focus in the question has revealed valuable literature for an understanding of this phenomenon. A subsequent search of CINAHL replacing the prior disorder with schizophrenia, psychosis, psychotic, and schizophrenoform, has revealed many studies. I have thoroughly reviewed 5 of those studied and have utilized an additional 5 studies that have pertinent information regarding understanding of this subject.
There is definitive evidence that shows a relationship between the use of cannabis at a young age and the development of schizophrenic symptoms. Arsenualt et al. (2002) performed a longitudinal study with a birth cohort of 1037 individuals born in Dunedin, New Zealand during 1972 and 1973. This study had a 96% follow up rate to age 26. The study contained data on psychotic symptoms at age 11, self-reported drug use at age 15 and 18 and a standardized psychiatric interview to obtain a DSM-IV diagnosis at age 26 (p.1212). A representative sample of 759 (n=759) individuals was extracted for complete data that fit the study’s criteria of adult psychiatric outcomes, adolescent use of illicit substances, and childhood psychotic symptoms (p.1212).
The Control group was composed of 494 (65.1%) individuals who had reported using cannabis “never,” “once,” or “twice,” at either age 15 or 18. The study groups comprised 236 (31.1%) who had reported first using “three times or more” at age 18, and 29 (3.8%) who had reported first using “three times or more” at age 15 (p.1212).
The results showed that subjects who used cannabis by age 15 and 18 exhibited more schizophrenia symptoms than the controls. These results remained significant when psychotic symptoms at age 11 were controlled for. A logistic regression analysis indicted that cannabis users at age 15 had a fourfold greater incidence of a schizophreniform disorder at age 26. The results continued to remain higher than the controls when psychotic symptoms at age 11 were accounted for. However, the risk was no longer statistically significant. Approximately 10% of the cannabis users by age 15 who did not have symptoms at age 11 developed schizophreniform disorders by age 26. This compares to approximately 3% of the remaining cohort. This study suggests that cannabis use at an early age is associated with a greater incidence of schizophrenia symptoms even when psychotic symptoms that preceded the use of cannabis are controlled for (Arsenault et al., 2002).
Hambrecht and Hafner performed a study of psychiatric hospital admissions between 1987 and 1989. The focus of this study was to examine the “clinical characteristics and temporal sequence of schizophrenia and comorbid cannabis abuse at the very onset of psychosis in order to contribute to the understanding of a possible causality between the two disorders” (Hambrecht & Hafner, 2000,). These individuals were first-time admissions for schizophrenia or paranoid disorders. The initial population contained 392 persons’, however, due either to refusal or too short a hospital stay, the final number was 267. An additional 35 patients were excluded due to discovery of prior psychotic episodes, leaving a total of 232 persons. A control group was obtained from the general population that the hospital served. This group was obtained using a random selection of municipal registrations files. The first 57 respondents who had no history of schizophrenia or paranoid disorders were selected. In the control group, 7% had a history of cannabis abuse and 12% had a history of alcohol abuse (p.470).
In this study, both patients and relatives were interviewed to report on “milestones” during the early course of schizophrenia. Assessments of patients were done using the Interview for the Retrospective Assessment of the Onset of Schizophrenia (IRAOS), Present State Exam, Scale for the Assessment of Negative Symptoms, and the Disability Assessment Schedule. Both patients’ and relatives’ reports of first psychotic episodes correlated significantly (Pearson Correlations; first symptoms 0.77, First positive symptoms 0.93, first negative symptoms 0.73) (Hambrecht & Hafner, 2000, p.470).
In this study, 90% of illicit drug users had abused cannabis at some time. 37% of the study group reported cannabis as their only substance abuse. Multiple substance abuse especially concomitant alcohol abuse was prevalent. 80% of first reported abuse involved cannabis. Group-wise comparisons were done to extract the individuals whose substance abuse involved primarily cannabis and correlated to first onset of symptoms of psychosis. These statistics were compared to both the general populations as well as non-drug abusing patients in the study (p.470-471).
This study suggests three possible interpretations of the subgroups defined. Group 1 comprised patients whose onset of cannabis abuse occurred years prior to the onset of first symptoms. Group 2 comprised patients whose onset of both cannabis abuse and signs of first symptoms were within the same time period. Group 3 comprised individuals whose onset of cannabis abuse occurred after the initial onset of first symptoms. The researchers suggest specific psychosocial and biological theories for the interpretations of these behaviors (p. 473).
Group 1 has been named the “vulnerability group.” A chronic deterioration of mental health and coping skills has been caused by cannabis abuse leading to onset of first symptoms and a reduction of the vulnerability threshold (p.473).
Group 2 has been named the “stress group.” These individuals have may have been potentially vulnerable to schizophrenia due to genetic or pre/peri natal influences. Cannabis is theorized to precipitate the onset of psychosis due to the dopaminergic stress factor attributed to cannabis (p.473).
Group 3 is called the “coping group.” These individuals consume cannabis as a “self-medication regimen” to cope with the negative symptoms of schizophrenia. These patients discover how the cannabis may appear to mask the unpleasant hypodopaminergic prefrontal state due to the dopaminergic affect of cannabis (p.473).
Within group 1 it is difficult to fully ascertain the confounding variable that may exist. Neurodevelopmental and morphological brain anomalies were not ruled out as preceding factors to the onset of schizophrenia. Additionally, subtle cognitive, perceptual, affective or social deficiencies may have contributed to the initial substance abuse. These deficiencies may also contribute to the predisposition of development of schizophrenia.
This study’s limitations, particularly the control groups’ small size and the geographical bias, limit the generalizations that can be drawn for all populations. Additionally, many confounding factors that could not be controlled for are prevalent in this study. More prospective studies as well as in depth case studies need to be performed to better understand the causality issue in the etiology of schizophrenia (Hambrecht & Hafner 2000 p.473-474).
The Christchurch health and development study (CHDS) published in 2005 in the journal Society for the Study of Addiction by Fergusson et al., has attempted with tremendous rigor to control for both observable as well as non-observable confounding factors as they relate to a causal relationship between cannabis and schizophrenia. This 25 year longitudinal study contained a birth cohort of 1265 New Zealand children. A total of 1055 participants were identified who met the criteria for both cannabis use and psychotic symptoms during the study’s framework. One focus of this study that has added to the rigor is the addition of data regarding frequency of use and the incidence of psychotic symptoms at ages 18, 21 and 25 years (Ferguson et al., 2005, p.354-361).
The intense depth of modeling that has been employed in this study, coupled with the time-dynamic covariate factors and fixed covariate factors has threshed out most of the confounding factors that have plagued prior research to reveal a very solid model of causality in this relationship (p. 362-364).
The analysis shows, within all ages of the study, a clear and statistically significant trend toward increased use of cannabis with increasing rates of psychotic symptoms. A rate of 2.3 to 3.3 times higher was observed over non-cannabis users in the study. When covariate factors were adjusted for, all models showed consistent data in the range of 1.6 to 1.8 times higher incidence of psychotic symptoms compared to those who did not use cannabis (Fergusson et al., 2005, p. 362).
This study employed a reciprocal cause model that measured causality of cannabis abuse and psychotic symptoms in both directions. These models were calculated for both observed variables as well as non-observed fixed effects. In each case, the incidence of increasing cannabis use was associated with an increase in psychotic symptoms. These models also show that the effect of psychotic symptom on cannabis use was negative. This evidence implies that it is unlikely for psychotic symptoms to cause an increase in cannabis use. Rather schizophrenia may in fact have an inhibitory effect on cannabis use. This suggestion of a direction of causality has been further supported by data indicating a dose response relationship between frequency of cannabis use and rates of psychotic symptoms. Daily users of cannabis had a 1.6 to 1.8 times higher incidence of psychotic symptoms over non-cannabis users even when all confounding factors were taken into account (p. 363).
The authors of this study have suggested two causal pathways for the linkage of cannabis and psychosis. The first is that cannabis use causes biochemical changes in the brain that may lead to increased rates of psychotic symptoms amongst susceptible users. The second is that those individuals who are prone to psychotic symptoms may have a greater tendency to use cannabis as a consequence of their condition or for self-medication. This study indicates clear evidence that the latter is not likely to be supported by further study. However the data do suggest that increasing the frequency and/or the dose, of cannabis is associated with increase in onset of psychotic symptoms. Furthermore, the data suggest that, with the onset of psychotic symptoms, cannabis use is decreased. There may be a confounding factor that has not been accounted for regarding the institutional milieus these individuals have experienced. This
was not noted in the study (p.362).
One further focused retrospective study was done in the Netherlands, Cannabis use and age at onset of schizophrenia, (Veen et al., 2004) attempts to assess the independent influence of gender and cannabis on the early course of schizophrenia. Veen et al. investigated a population in which cannabis use is neither illegal nor highly stigmatized. The Comprehensive Assessment of Symptoms and History (CASH) and the IRAOS tools were used along with patient medical records to assess for early signs and symptoms of schizophrenia. A cohort of 126 patients was selected from hospital admission from April 1997 to April 1999. The gender composition of the study was male (N=97) and female (N=36). A control group of non-cannabis users was also gathered for this study from the hospitalized population. The breakdown of this cohort was cannabis users (N=70), non-users of cannabis (N=63). In both cohorts the basis for qualification as a cannabis user was based on self-reported use of cannabis “greater than four times” and that the cannabis use had preceded the onset of first symptoms. Some of these patient indicated additional use of amphetamines and or cocaine in the period preceding the first symptoms (p.502). The tools used in the study categorized milestones in the patients’ histories to compare populations and genders respectively. The three major milestones were first social and/or occupational dysfunction, first psychotic episode, and first negative symptoms.
In both studies significant differences were observed. The predominant statistic was for the mean age of onset of first negative symptoms. The mean age for onset of negative symptoms in men was 26.5 years and the mean age for women was 41.6 years. This 15.2 year median age difference was associated with a confidence interval of 95%. This strong statistical evidence was further supported by the data in the user vs non-user study. The mean age of onset for first negative symptoms in cannabis users was 23.7 years as compared to 38.4 years in non-cannabis users in the study. This 14.7 year median difference in age was associated with a 95% confidence interval (p. 503-504).
The second most significant statistic was observed in the incidence of the first social and/or occupational dysfunction. First onset of these symptoms was a median of 6.7 years earlier for male than for female users of cannabis. Users vs. non-users of cannabis had a 9.3 year earlier mean age. When reviewed for first psychotic episode, the data showed that onset in men was a median of 3.2 years earlier than in women. Among users and non-users of cannabis, the onset of first psychotic episodes was a median of 7.5 years earlier for cannabis users (Veen et al., 2004, p.504).
This study shows that among Dutch male users, cannabis consumption may precipitate an earlier onset of psychotic symptoms. Additionally, the use of cannabis may speed up the onset of negative symptoms, especially in men (p. 504-505).
These studies give much credence to the theory that cannabis has an effect on the human brain that may precipitate in certain individuals a higher than the general population’s incidence of first symptoms of psychosis. Given this conclusion, it is evident that early substance abuse educational programs should be designed to be effective in deterring the first-time use of cannabis and other illicit drugs in adolescents. The protective factor of reducing adolescent drug use will have a tremendous effect in decreasing the cost of treating these individuals long into the future. These kinds of prevention programs have the potential to save hundreds of millions of dollars each fiscal year in the United States as well as abroad.
In researching this project, much anecdotal evidence exists regarding the benefits of cannabis use among the schizophrenic population. For the most part these data have no scientific basis other than personal experiential knowledge. One notable book does exist regarding this topic by Dr. Lester Grinspoon, Associate Professor Emeritus of Psychiatry at Harvard Marihuana, the Forbidden Medicine, 1928, discusses the many different diseases and disorders that cannabis may be able to treat. The high profile of the author does little to discourage the need for evidence-based practice in the treatment of these disorders. Many websites with varying degrees of credibility tout the beneficial effects of cannabis, as well as purporting a government conspiracy regarding big pharmaceutical dollars (as well as petroleum interests) as to why the drug continues to be an illegal and controlled substance.
In all of the research reviewed for this project, the substantive evidence consistently indicated a relationship between an increase of risk of mental or cognitive disorders with increased frequency and increased dose of cannabis. The National Institutes on Drug Abuse (NIDA) publishes an annual report on the effects of marijuana. This comprehensive report provides timely information on the most recent work being done in the field of substance abuse and addiction. The statistics are staggering regarding the social, cognitive, and psychological effect that cannabis consumption can have on an individual, especially youth. A multitude of studies have demonstrated the reduction in intellectual functioning in daily users of marijuana. A specific high-dose reaction to marijuana is termed as acute toxic psychosis. The syndrome includes symptoms of hallucinations, delusions, and depersonalization. Long-term cannabis use has also been shown to hasten the age related loss of hippocampal neurons; this loss causes increased difficulty with short-term memory and may not in some cases be reversible (NIDA, 2005).
It is not surprising that a correlation between earlier onset of schizophrenia and early cannabis abuse exists; given the large body of evidence regarding the negative effect this drug has on adolescent brain activity. No longitudinal studies to date have looked at the per capita levels of cannabis abuse in teens in the United States with an incidence of early onset psychotic symptoms. This would be an interesting study given the volume of data that has been collected in both subsets. A preliminary assessment of these data would presumably indicate a level-trend in first time hospitalizations per capita over the past thirty years with an initial drop in the trend from 1988 to 1993 (Child Trends Databank 2005).
This research indicates a tremendous need to build local, national and international educational programs to reduce and eliminate the incidence of marijuana abuse and abuse of other drugs in the adolescent population. There is no quick fix for modifying the current trends and attitude about drug abuse in America and internationally. On a local level, we continue to see the devastating effects of drug abuse in our teen populations through crime and other negative behaviors. Many communities choose to ignore these trends until they become overbearing or a few youth die through the neglect of a society that did not actively fight the escalating tide of drugs in the community. National policy in the United States should focus on the devastating costs associated with failure to reverse the trend of drug abuse among adolescents in our communities. Investing in the health and welfare of our teens through the development of community sports programs and recreational facilities, drug and alcohol treatment facilities and encouragement of participation in civic and religious sponsored activities can begin to address the grip that drug abuse has had on our communities.
