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Racial Difference in the Long-Term Effects of Marijuana Use on Physical Health Outcomes
Abstract
Introduction:Health benefits of marijuana use have been identified for several diseases such as glaucoma, cancer, HIV-AIDS, multiple sclerosis, and Crohn’s disease. In fact, more than 100 conditions qualify for medical marijuana in California. Conversely, only a few definitive negative health effects of marijuana have been found, including respiratory problems, cardiovascular risks, and cognitive impairments. Nevertheless, few studies have prospectively examined the long-term effects of marijuana use on physical health. Even rarer are studies examining race differences in these effects, which is critical given health disparities generally favoring Whites and generally higher rates of marijuana use among Black than White adults. The purpose of this study was to examine racial differences in the effects of chronic and intensive marijuana use during adolescence and/or emerging adulthood (ages 18-25) on physical health symptoms in young adulthood (age 35).
Methods: We used data from 487 young men who were interviewed annually from the 7thgrade until age 25 and then again at age 35. Four trajectory groups of regular (approximately monthly) marijuana use between ages 12 and 25 were identified: nonusers/nonregular users, adolescence-limited, late-onset, and chronic regular marijuana users.
Results: ANCOVAs (covarying race) and Chi-square tests indicated no trajectory group differences in the number of current health problems, number of medications currently taken for physical illnesses, number of physical injuries, ever being shot by age 35, and being hospitalized in the past year. We also used regression analyses to examine the effects of marijuana use at age 25 and at age 35, race, and their interactions on these same outcomes at age 35. There were no significant effects of quantity or frequency of use in the total sample or among users only on any of the health outcomes. There were also no health differences between Blacks and Whites except that Blacks were more likely to have been shot by age 35.
Conclusions: It appears that continuous monthly marijuana use from adolescence through emerging adulthood is not a high enough threshold to lead to negative health outcomes at least by young adulthood and that frequent use in emerging or young adulthood is also not related to health outcomes. Given that there were relatively few serious illnesses in this sample by young adulthood, it is possible that negative consequences of marijuana use will become evident at later ages. Prevention programs should highlight psychosocial rather than physical health consequences.
... As marijuana use is associated with both positive and negative health outcomes, there is a continuing need to investigate the good and the bad of marijuana use (Hasin, 2018). Of note, consistent monthly marijuana use from adolescence to young adulthood is not a sufficient threshold to associate with negative health outcomes (White, Simpson, Pardini, & Finlay, 2013). In other words, monthly marijuana use among boys does not make a significant difference to 35-year-old men's health issues in general including medications, injuries, or hospitalizations, compared with those who did not consume marijuana (White et al., 2013). ...
... Of note, consistent monthly marijuana use from adolescence to young adulthood is not a sufficient threshold to associate with negative health outcomes (White, Simpson, Pardini, & Finlay, 2013). In other words, monthly marijuana use among boys does not make a significant difference to 35-year-old men's health issues in general including medications, injuries, or hospitalizations, compared with those who did not consume marijuana (White et al., 2013). However, weekly use is a key to human health. ...
The present study aims to investigate the associations of weekly marijuana use with health-related measurements, including overall, physical, and mental health, and quality of life among adults, in a single research effort with panel analysis. The two latest Waves (2014–2015 and 2015–2016) of the Population Assessment of Tobacco and Health study (PATH) were used for this work. Weekly marijuana use was defined as marijuana use at least one time per week. Propensity score matching was applied at the previous wave to control selection bias and unobservable differences. Logistic regressions were estimated to investigate the associations of weekly marijuana use with health-related measurements. The analysis also considered the interaction of race and weekly marijuana use. The majority of participants reported good health outcomes. Based on the regression models without the interaction term, weekly marijuana use was only negatively associated with mental health and overall health, but was not associated with physical health and quality of life. With the interaction effect of race in the overall sample, weekly marijuana use was negatively associated all with health measurements. However, weekly marijuana use among non-white respondents was positively associated with health outcomes (all ps < 0.01), except mental health. Further policy and research directions are discussed.
As marijuana use becomes legal in some states, the dominant public opinion is that marijuana is a harmless source of mood alteration. Although the harms associated with marijuana use have not been well studied, enough information is available to cause concern.
The link between cannabis use and psychosis comprises three distinct relationships: acute psychosis associated with cannabis intoxication; acute psychosis that lasts beyond the period of acute intoxication; and persistent psychosis not time-locked to exposure. Experimental studies reveal that cannabis, delta-9-tetrahydrocannabinol (THC) and synthetic cannabinoids reliably produce transient positive, negative, and cognitive symptoms in healthy volunteers. Case studies indicate that cannabinoids can induce acute psychosis that lasts beyond the period of acute intoxication but resolves within a month. Exposure to cannabis in adolescence is associated with a risk for later psychotic disorder in adulthood; this association is consistent, temporally related, shows a dose response, and is biologically plausible. However, cannabis is neither necessary nor sufficient to cause a persistent psychotic disorder. More likely, it is a component cause that interacts with other factors to result in psychosis. The link between cannabis and psychosis is moderated by age at onset of cannabis use, childhood abuse, and genetic vulnerability. While more research is needed to better characterize the relationship between cannabinoid use and the onset and persistence of psychosis, clinicians should be mindful of the potential risk of psychosis, especially in vulnerable populations, including adolescents and those with a psychosis diathesis.
Recent reports show that fewer adolescents believe that regular cannabis use is harmful to health. Concomitantly, adolescents are initiating cannabis use at younger ages, and more adolescents are using cannabis on a daily basis. The purpose of the present study was to test the association between persistent cannabis use and neuropsychological decline and determine whether decline is concentrated among adolescent-onset cannabis users. Participants were members of the Dunedin Study, a prospective study of a birth cohort of 1,037 individuals followed from birth (1972/1973) to age 38 y. Cannabis use was ascertained in interviews at ages 18, 21, 26, 32, and 38 y. Neuropsychological testing was conducted at age 13 y, before initiation of cannabis use, and again at age 38 y, after a pattern of persistent cannabis use had developed. Persistent cannabis use was associated with neuropsychological decline broadly across domains of functioning, even after controlling for years of education. Informants also reported noticing more cognitive problems for persistent cannabis users. Impairment was concentrated among adolescent-onset cannabis users, with more persistent use associated with greater decline. Further, cessation of cannabis use did not fully restore neuropsychological functioning among adolescent-onset cannabis users. Findings are suggestive of a neurotoxic effect of cannabis on the adolescent brain and highlight the importance of prevention and policy efforts targeting adolescents.
While there is increasing evidence on the association between cannabis use and psychotic outcomes, it is still unclear whether this also applies to depression. We aim to assess whether risk of depression and other affective outcomes is increased among cannabis users.
A cohort study of 45 087 Swedish men with data on cannabis use at ages 18-20. Diagnoses of unipolar disorder, bipolar disorder, affective psychosis and schizoaffective disorder were identified from inpatient care records over a 35-year follow-up period. Cox proportional hazard modeling was used to assess the hazard ratio (HR) of developing these disorders in relation to cannabis exposure.
Only subjects with the highest level of cannabis use had an increased crude hazard ratio for depression (HR 1.5, 95% confidence interval (CI), 1.0-2.2), but the association disappeared after adjustment for confounders. There was a strong graded association between cannabis use and schizoaffective disorder, even after control for confounders, although the numbers were small (HR 7.4, 95% CI, 1.0-54.3).
We did not find evidence for an increased risk of depression among those who used cannabis. Our finding of an increased risk of schizoaffective disorder is consistent with previous findings on the relation between cannabis use and psychosis.
Mixture modeling is a widely applied data analysis technique used to identify unobserved heterogeneity in a population. Despite mixture models' usefulness in practice, one unresolved issue in the application of mixture models is that there is not one commonly accepted statistical indicator for deciding on the number of classes in a study population. This article presents the results of a simulation study that examines the performance of likelihood-based tests and the traditionally used Information Criterion (ICs) used for determining the number of classes in mixture modeling. We look at the performance of these tests and indexes for 3 types of mixture models: latent class analysis (LCA), a factor mixture model (FMA), and a growth mixture models (GMM). We evaluate the ability of the tests and indexes to correctly identify the number of classes at three different sample sizes (n D 200, 500, 1,000). Whereas the Bayesian Information Criterion performed the best of the ICs, the bootstrap likelihood ratio test proved to be a very consistent indicator of classes across all of the models considered.
To determine the association between diabetes mellitus (DM) and marijuana use.
Cross-sectional study.
Data from the National Health and Nutrition Examination Survey (NHANES III, 1988-1994) conducted by the National Center for Health Statistics of the Centers for Disease Control and Prevention.
The study included participants of the NHANES III, a nationally representative sample of the US population. The total analytic sample was 10 896 adults. The study included four groups (n=10 896): non-marijuana users (61.0%), past marijuana users (30.7%), light (one to four times/month) (5.0%) and heavy (more than five times/month) current marijuana users (3.3%). DM was defined based on self-report or abnormal glycaemic parameters. We analysed data related to demographics, body mass index, smoking status, alcohol use, total serum cholesterol, high-density lipoprotein, triglyceride, serum 25-hydroxy vitamin D, plasma haemoglobin A1c, fasting plasma glucose level and the serum levels of C reactive protein and four additional inflammatory markers as related to marijuana use.
OR for DM associated with marijuana use adjusted for potential confounding variables (ie, odds of DM in marijuana users compared with non-marijuana users).
Marijuana users had a lower age-adjusted prevalence of DM compared to non-marijuana users (OR 0.42, 95% CI 0.33 to 0.55; p<0.0001). The prevalence of elevated C reactive protein (>0.5 mg/dl) was significantly higher (p<0.0001) among non-marijuana users (18.9%) than among past (12.7%) or current light (15.8%) or heavy (9.2%) users. In a robust multivariate model controlling for socio-demographic factors, laboratory values and comorbidity, the lower odds of DM among marijuana users was significant (adjusted OR 0.36, 95% CI 0.24 to 0.55; p<0.0001).
Marijuana use was independently associated with a lower prevalence of DM. Further studies are needed to show a direct effect of marijuana on DM.
We examined developmental trajectories of marijuana use among a cohort of urban African Americans followed from first grade to mid adulthood. We compared risk factors in childhood and adolescence and consequences in mid adulthood across trajectory groups.
Using semiparametric group-based mixture modeling, five marijuana trajectories for men (n=455) and four trajectories for women (n=495) were identified extending from adolescence to young adulthood (age 32). We labeled the four trajectory groups similar for men and women "abstainers," "adolescent only users," "early adulthood decliners," and "persistent users." We named the unique fifth group for men "late starters."
Multivariate multinomial logistic regressions show that childhood problem behaviors, adolescent family involvement, and dropping out of high school differentiated trajectory membership. Analyses comparing the trajectory groups on behavioral, social, and health outcomes at age 42 revealed that for both men and women, those in the persistent trajectory had the most problems, and those in the early adult decliner group also had specific problems. Male late starters also had poor outcomes.
The findings point to the value of identifying specific patterns of substance use over the life course and understanding the differences in their correlates and consequences. The implications of these findings are discussed.
To determine whether use of cannabis in adolescence increases the risk for psychotic outcomes by affecting the incidence and persistence of subclinical expression of psychosis in the general population (that is, expression of psychosis below the level required for a clinical diagnosis).
Analysis of data from a prospective population based cohort study in Germany (early developmental stages of psychopathology study).
Population based cohort study in Germany.
1923 individuals from the general population, aged 14-24 at baseline.
Incidence and persistence of subthreshold psychotic symptoms after use of cannabis in adolescence. Cannabis use and psychotic symptoms were assessed at three time points (baseline, T2 (3.5 years), T3 (8.4 years)) over a 10 year follow-up period with the Munich version of the composite international diagnostic interview (M-CIDI).
In individuals who had no reported lifetime psychotic symptoms and no reported lifetime cannabis use at baseline, incident cannabis use over the period from baseline to T2 increased the risk of later incident psychotic symptoms over the period from T2 to T3 (adjusted odds ratio 1.9, 95% confidence interval 1.1 to 3.1; P=0.021). Furthermore, continued use of cannabis increased the risk of persistent psychotic symptoms over the period from T2 to T3 (2.2, 1.2 to 4.2; P=0.016). The incidence rate of psychotic symptoms over the period from baseline to T2 was 31% (152) in exposed individuals versus 20% (284) in non-exposed individuals; over the period from T2 to T3 these rates were 14% (108) and 8% (49), respectively.
Cannabis use is a risk factor for the development of incident psychotic symptoms. Continued cannabis use might increase the risk for psychotic disorder by impacting on the persistence of symptoms.
A number of studies have found that the use of cannabis and other psychoactive substances is associated with an earlier onset of psychotic illness.
To establish the extent to which use of cannabis, alcohol, and other psychoactive substances affects the age at onset of psychosis by meta-analysis.
Peer-reviewed publications in English reporting age at onset of psychotic illness in substance-using and non-substance-using groups were located using searches of CINAHL, EMBASE, MEDLINE, PsycINFO, and ISI Web of Science.
Studies in English comparing the age at onset of psychosis in cohorts of patients who use substances with age at onset of psychosis in non-substance-using patients. The searches yielded 443 articles, from which 83 studies met the inclusion criteria.
Information on study design, study population, and effect size were extracted independently by 2 of us.
Meta-analysis found that the age at onset of psychosis for cannabis users was 2.70 years younger (standardized mean difference = -0.414) than for nonusers; for those with broadly defined substance use, the age at onset of psychosis was 2.00 years younger (standardized mean difference = -0.315) than for nonusers. Alcohol use was not associated with a significantly earlier age at onset of psychosis. Differences in the proportion of cannabis users in the substance-using group made a significant contribution to the heterogeneity in the effect sizes between studies, confirming an association between cannabis use and earlier mean age at onset of psychotic illness.
The results of meta-analysis provide evidence for a relationship between cannabis use and earlier onset of psychotic illness, and they support the hypothesis that cannabis use plays a causal role in the development of psychosis in some patients. The results suggest the need for renewed warnings about the potentially harmful effects of cannabis.
Anxiety reactions and panic attacks are the acute symptoms most frequently associated with cannabis use. Understanding the relationship between cannabis and anxiety may clarify the mechanism of action of cannabis and the pathophysiology of anxiety. Aims of the present study were to review the nature of the relationship between cannabis use and anxiety, as well as the possible clinical, diagnostic and causal implications.
Systematic review of the Medline, PsycLIT and EMBASE literature.
Frequent cannabis users consistently have a high prevalence of anxiety disorders and patients with anxiety disorders have relatively high rates of cannabis use. However, it is unclear if cannabis use increases the risk of developing long-lasting anxiety disorders. Many hypotheses have been proposed in an attempt to explain these relationships, including neurobiological, environmental and social influences.
The precise relationship between cannabis use and anxiety has yet to be established. Research is needed to fully clarify the mechanisms of such the association.
Cannabis has been reported as a likely risk factor for the development of psychosis, and a gene × environment interaction with the catechol-O-methyltransferase (COMT) gene has been proposed. Moreover, COMT has been separately linked to affective symptoms in psychosis. Despite a high rate of cannabis abuse and affective symptoms in African Americans, no studies exploring a relationship between COMT and psychosis in this group have been reported. An existing database of psychotic patients with and without adolescent cannabis use/affective symptoms was examined, and chi-square analyses for independence were applied separately for both Caucasians and African-Americans to examine genotype associations with adolescent cannabis use and affective symptoms (past or present). The two subject groups did not differ with respect to the prevalence of adolescent cannabis abuse or presence of affective symptoms. Further study is needed, with non-psychotic controls and larger samples.
The association between level of cannabis consumption and development of schizophrenia during a 15-year follow-up was studied in a cohort of 45,570 Swedish conscripts. The relative risk for schizophrenia among high consumers of cannabis (use on more than fifty occasions) was 6.0 (95% confidence interval 4.0-8.9) compared with non-users. Persistence of the association after allowance for other psychiatric illness and social background indicated that cannabis is an independent risk factor for schizophrenia.
The links between drug use and psychosis are of major aetiological and prognostic significance. Psychosis and drug dependence frequently co-occur within the prison population, providing the opportunity to study this link more closely.
To explore the relationship between psychosis and drug dependence in a sample of prisoners.
A total of 3142 prisoners were surveyed nationally, and structured clinical data were obtained from a subsample of 503 respondents. Psychiatric assessment was based on the Schedules for Clinical Assessment in Neuropsychiatry (version 1.0). Measures of amphetamine, cannabis, cocaine and heroin use and dependence were obtained through self-report.
Logistic regression analyses indicated that first use of amphetamines or cocaine before the age of 16 years and severe cannabis or cocaine dependence were related to an increased risk of psychosis. In contrast, severe dependence on heroin was associated with a reduced risk of this classification.
Severe dependence on cannabis and psychostimulants is associated with a higher risk of psychosis and is in contrast to severe dependence on heroin, which has a negative relationship with psychosis.
The Children in the Community Study is a prospective longitudinal study investigating the association between early drug use (childhood, adolescence, and early 20s) and later psychiatric disorders (in the late 20s).
Using data from a community-based sample of 736 adults (50% female) from upstate New York, the subjects were interviewed at the mean ages of 14, 16, 22, and 27 years. Psychiatric disorders, measured by age-appropriate versions of the University of Michigan Composite International Diagnostic Interview, and participant's drug use were assessed.
Adolescent and young adult tobacco use was significantly associated with an increased risk of alcohol dependence and substance use disorders at a mean age of 27 years, but not with new episodes of major depressive disorder. Earlier alcohol use significantly predicted later major depressive disorder, alcohol dependence, and substance use disorders in the late 20s, as did early marijuana use and other illicit drug use. Except for the effect of tobacco use on major depressive disorder, early drug use was significantly related to later psychiatric disorders, even after statistically controlling for age, sex, parental educational level, family income, and prior episodes of major depressive disorder and substance use disorders.
Our results suggest that early drug use is associated with and predicts later psychiatric disorders. Preventive implications stem from the importance of studying a range of psychiatric disorders in the context of substance use assessed over a wide age range.
To determine whether cannabis use in adolescence predisposes to higher rates of depression and anxiety in young adulthood.
Seven wave cohort study over six years.
44 schools in the Australian state of Victoria.
A statewide secondary school sample of 1601 students aged 14-15 followed for seven years.
Interview measure of depression and anxiety (revised clinical interview schedule) at wave 7.
Some 60% of participants had used cannabis by the age of 20; 7% were daily users at that point. Daily use in young women was associated with an over fivefold increase in the odds of reporting a state of depression and anxiety after adjustment for intercurrent use of other substances (odds ratio 5.6, 95% confidence interval 2.6 to 12). Weekly or more frequent cannabis use in teenagers predicted an approximately twofold increase in risk for later depression and anxiety (1.9, 1.1 to 3.3) after adjustment for potential baseline confounders. In contrast, depression and anxiety in teenagers predicted neither later weekly nor daily cannabis use.
Frequent cannabis use in teenage girls predicts later depression and anxiety, with daily users carrying the highest risk. Given recent increasing levels of cannabis use, measures to reduce frequent and heavy recreational use seem warranted.
Various lines of evidence suggest an association between cannabis and psychosis. Five years ago, the only significant case-control study addressing this question was the Swedish Conscript Cohort. Within the last few years, other studies have emerged, allowing the evidence for cannabis as a risk factor to be more systematically reviewed and assessed. Using specific search criteria on Embase, PsychINFO and Medline, all studies examining cannabis as an independent risk factor for schizophrenia, psychosis or psychotic symptoms, published between January 1966 and January 2004, were examined. Additional studies were also reviewed from references found in retrieved articles, reviews, and a cited reference search (ISI-Web of Science). Studies selected for meta-analysis included: (i) case-control studies where exposure to cannabis preceded the onset of schizophrenia or schizophrenia-like psychosis and (ii) cohort studies of healthy individuals recruited before the median age of illness onset, with cannabis exposure determined prospectively and blind to eventual diagnosis. Studies of psychotic symptoms were also tabulated for further discussion. Eleven studies were identified examining the relationship between cannabis use and psychosis. Seven were included in the meta-analysis, with a derived odds ratio (fixed effects) of 2·9 (95% confidence interval = 2.4-3.6). No evidence of publication bias or heterogeneity was found. Early use of cannabis did appear to increase the risk of psychosis. For psychotic symptoms, a dose-related effect of cannabis use was seen, with vulnerable groups including individuals who used cannabis during adolescence, those who had previously experienced psychotic symptoms, and those at high genetic risk of developing schizophrenia. In conclusion, the available evidence supports the hypothesis that cannabis is an independent risk factor, both for psychosis and the development of psychotic symptoms. Addressing cannabis use, particularly in vulnerable populations, is likely to have beneficial effects on psychiatric morbidity.
Current marijuana use rates are the highest they have been in the past decade and are not likely to decrease given the legalization of marijuana for medicinal and recreational use. Concurrently, the nation is facing epidemic levels of obesity, cardiovascular disease, and diabetes mellitus; but, little is known about the intersecting relationships of marijuana use and cardiometabolic health. The objective of this study was to explore emerging issues in context with the intersection of cardiometabolic risk and marijuana use. This topic has potential important implications for our nation's health as we relax our approach to marijuana but continue to have unacceptable rates of cardiometabolic illnesses.
Cannabis (marijuana) smoke and tobacco smoke contain many of the same potent carcinogens, but a critical-yet unresolved-medical and public-health issue is whether cannabis smoking might facilitate the development of lung cancer. The current study aimed to assess the risk of lung cancer among young marijuana users.
A population-based cohort study examined men (n = 49,321) aged 18-20 years old assessed for cannabis use and other relevant variables during military conscription in Sweden in 1969-1970. Participants were tracked until 2009 for incident lung cancer outcomes in nationwide linked medical registries. Cox regression modeling assessed relationships between cannabis smoking, measured at conscription, and the hazard of subsequently receiving a lung cancer diagnosis.
At the baseline conscription assessment, 10.5 % (n = 5,156) reported lifetime use of marijuana and 1.7 % (n = 831) indicated lifetime use of more than 50 times, designated as "heavy" use. Cox regression analyses (n = 44,284) found that such "heavy" cannabis smoking was significantly associated with more than a twofold risk (hazard ratio 2.12, 95 % CI 1.08-4.14) of developing lung cancer over the 40-year follow-up period, even after statistical adjustment for baseline tobacco use, alcohol use, respiratory conditions, and socioeconomic status.
Our primary finding provides initial longitudinal evidence that cannabis use might elevate the risk of lung cancer. In light of the widespread use of marijuana, especially among adolescents and young adults, our study provides important data for informing the risk-benefit calculus of marijuana smoking in medical, public-health, and drug-policy settings.
We investigated the existence of a temporal association between age at initiation of cannabis use and age at onset of psychotic illness in 997 participants from the 2010 Survey of High Impact Psychosis (SHIP) in Australia. We tested for group differences in age at onset of psychotic illness and in the duration of premorbid exposure to cannabis (DPEC). Analyses were repeated in subgroups of participants with a schizophrenia-spectrum disorder (SSD), a diagnosis of lifetime cannabis dependence (LCD), and a comorbid SSD/LCD diagnosis. The association between age at initiation of cannabis use and age at onset of psychotic illness was linear and significant, F(11, 984) = 13.77, P < .001, even after adjusting for confounders. The effect of age at initiation of cannabis use on DPEC was not significant (mean duration of 7.8 years), and this effect was similar in participants with a SSD, LCD, and comorbid SSD/ LCD diagnosis although a shift toward shorter premorbid exposure to cannabis was noted in the SSD/LCD subgroup (mean duration of 7.19 years for SSD/LCD). A temporal direct relationship between age at initiation of cannabis use and age at onset of psychotic illness was detected with a premorbid exposure to cannabis trend of 7-8 years, modifiable by higher severity of premorbid cannabis use and a diagnosis of SSD. Cannabis may exert a cumulative toxic effect on individuals on the pathway to developing psychosis, the manifestation of which is delayed for approximately 7-8 years, regardless of age at which cannabis use was initiated.
Aims:
To examine the direction of the longitudinal association between vulnerability for psychosis and cannabis use throughout adolescence.
Design:
Cross-lagged path analysis was used to identify the temporal order of vulnerability for psychosis and cannabis use, while controlling for gender, family psychopathology, alcohol use and tobacco use.
Setting:
A large prospective population study of Dutch adolescents [the TRacking Adolescents' Individual Lives Survey (TRAILS) study].
Participants:
A total of 2120 adolescents with assessments at (mean) age 13.6, age 16.3 and age 19.1.
Measurements:
Vulnerability for psychosis at the three assessment points was represented by latent factors derived from scores on three scales of the Youth Self-Report and the Adult Self-Report, i.e. thought problems, social problems and attention problems. Participants self-reported on cannabis use during the past year at all three waves.
Findings:
Significant associations (r = 0.12-0.23) were observed between psychosis vulnerability and cannabis use at all assessments. Also, cannabis use at age 16 predicted psychosis vulnerability at age 19 (Z = 2.6, P < 0.05). Furthermore, psychosis vulnerability at ages 13 (Z = 2.0, P < 0.05) and 16 (Z = 3.0, P < 0.05) predicted cannabis use at, respectively, ages 16 and 19.
Conclusions:
Cannabis use predicts psychosis vulnerability in adolescents and vice versa, which suggests that there is a bidirectional causal association between the two.
OBJECTIVE: Although a number of studies have examined the respiratory impact of marijuana smoking, such studies have generally used convenience samples of marijuana and tobacco users. The current study examined respiratory effects of marijuana and tobacco use in a nationally representative sample while controlling for age, gender, and current asthma.
DESIGN: Analysis of the nationally representative third National Health and Nutrition Examination Survey (NHANES III).
SETTING: U.S. households.
PARTICIPANTS: A total of 6,728 adults age 20 to 59 who completed the drug, tobacco, and health sections of the NHANES III questionnaire in 1988 and 1994. Current marijuana use was defined as self-reported 100+ lifetime use and at least 1 day of use in the past month.
MEASUREMENTS AND MAIN RESULTS: Self-reported respiratory symptoms included chronic bronchitis, frequent phlegm, shortness of breath, frequent wheezing, chest sounds without a cold, and pneumonia. A medical exam also provided an overall chest finding and a measure of reduced pulmonary functioning. Marijuana use was associated with respiratory symptoms of chronic bronchitis (P=.02), coughing on most days (P=.001), phlegm production (P=.0005), wheezing (P<.0001), and chest sounds without a cold (P=.02).
CONCLUSION: The impact of marijuana smoking on respiratory health has some significant similarities to that of tobacco smoking. Efforts to prevent and reduce marijuana use, such as advising patients to quit and providing referrals for support and assistance, may have substantial public health benefits associated with decreased respiratory health problems.
Cannabis use is associated with an increased risk for psychotic disorder, yet most cannabis users do not develop psychosis, suggesting that other factors are also involved. This paper reviews the available evidence suggesting that differential sensitivity to the psychosis-inducing effects of cannabis may be related to underlying genetic liability. There is robust evidence that persons at psychometric risk for psychosis are most vulnerable to display psychotic symptoms subsequent to the use of cannabis. Multiple studies have also found that persons at familial risk for psychosis have an increased sensitivity to the effects of cannabis. Together, these findings support the concept of a biological interaction between cannabis use and one's underlying genetic vulnerability. At the molecular-genetic level, however, few (if any) interactions have been consistently replicated, although a reported interaction with variation in AKT1 is promising and deserves further follow-up. The apparent lack of consistent replication can be ascribed to problems of initial gene selection, statistical power, a bias towards positive results and insufficient attempts at true replication, leading to the conclusion that increased sample sizes, greater density of genetic markers and a stronger focus on true replication are necessary. The major challenge for molecular-genetic geneenvironment interaction research will be to combine the agnostic detection of disorder-associated genetic variants from genome-wide studies with the hypothesis-based approach from epidemiological and neurobiological studies. Possible strategies for future cannabis interaction studies are discussed.
Cigarette smoking is the major cause of lung cancer, the largest cancer killer in the world. This chapter discusses the role
of cigarette smoke carcinogens as causes of lung cancer. A general mechanistic framework is presented, in which cigarette
smoke carcinogens and their metabolically activated forms cause mutations in critical growth control genes, along with other
effects. Evidence and unresolved issues for the role of various groups of carcinogens, such as polycyclic aromatic hydrocarbons,
nitrosamines, volatile organic compounds, and metals as causes of lung cancer are discussed. An overview of inhalation studies
of cigarette smoke in laboratory animals is also presented. Collectively, the massive studies on carcinogenesis by cigarette
smoke and its constituents provide a firm base for understanding the mechanisms of human lung carcinogenesis.
Throughout the world, violence is among the leading causes of death for people age 15–44 years (Krug, Dahlberg, Mercy, Zwi,
& Lozano, 2002). Uniformly, alcohol and drug use are risk factors that are associated with violence within this age group.
In fact, alcohol use is implicated in about half the incidents of violent crime (Murdoch, Pihl, & Ross, 1990).
In the last 15 years there has been a major shift in the laws governing medical use of cannabis in the United States. Corresponding with this change there has been escalating interest in the role that cannabis, commonly referred to as marijuana, and cannabinoids play in the care of patients with cancer. This review will examine cannabis' and cannabinoids' current and potential roles in cancer care. Specifically, we will examine five areas of cannabis medicine: (1) pharmacologic properties of cannabis; (2) its potential role in the development of human cancers, particularly smoking-related malignancies; (3) cannabinoids' potential as anti-cancer therapies; (4) cannabis and cannabinoids in the palliation of common cancer-associated symptoms; (5) current legal status of cannabis for medical purposes in the United States.
This investigation studied the association between developmental trajectories of marijuana use extending from adolescence to age 32 and later antisocial behavior at age 37. Semi-parametric group-based modeling and logistic regression analyses were used to analyze the data. Five distinct trajectories of marijuana use were identified: never-users, quitters/decreasers, occasional users, chronic users, and increasing users. Being either a chronic user or an increasing marijuana user was associated with an increase in the risk of exhibiting antisocial behavior in adulthood. Both chronic and increasing use of marijuana may serve as predictors of adult antisocial behavior. Treatment programs to prevent antisocial behavior across the life course should include a component to address earlier and concurrent marijuana use.
Although there are significant differences in prevalence of substance use between African-American and White adolescents, few studies have examined racial differences in developmental patterns of substance use, especially during the important developmental transition from adolescence to young adulthood. This study examines racial differences in trajectories of heavy drinking and regular marijuana use from adolescence into young adulthood.
A community-based sample of non-Hispanic African-American (n=276) and non-Hispanic White (n=211) males was analyzed to identify trajectories from ages 13 to 24.
Initial analyses indicated race differences in heavy drinking and regular marijuana use trajectories. African Americans were more likely than Whites to be members of the nonheavy drinkers/nondrinkers group and less likely to be members of the early-onset heavy drinkers group. The former were also more likely than the latter to be members of the late-onset regular marijuana use group. Separate analyses by race indicated differences in heavy drinking for African Americans and Whites. A 2-group model for heavy drinking fit best for African Americans, whereas a 4-group solution fit best for Whites. For regular marijuana use, a similar 4-group solution fit for both races, although group proportions differed.
Within-race analyses indicated that there were clear race differences in the long-term patterns of alcohol use; regular marijuana use patterns were more similar. Extended follow ups are needed to examine differences and similarities in maturation processes for African-American and White males. For both races, prevention and intervention efforts are necessary into young adulthood.
Cannabis use is one of the environmental factors with more solid evidence contributing to schizophrenia risk, especially in genetically susceptible individuals. One of the genes that may interact with cannabis is COMT, although available data are scarce. Here, we present a case-only study of the putative COMT-cannabis interaction in schizophrenia. Two Spanish samples from Santiago de Compostela and Valencia were screened for cannabis use. One hundred and fifty five individuals from a total of 748 patients were identified as cannabis users. Five SNPs in COMT, defining three common functional haplotypes with different enzymatic activities, were genotyped and analyzed for association at the SNP, haplotype and genotype levels. An association was detected between cannabis use and low activity variants (P<0.01) in the joint analysis and results were consistent between the two samples. Schizophrenic subjects homozygous for the Met allele at rs4680 doubled the probability of lifetime prevalence of cannabis use in comparison to Val homozygous (Mantel-Haenszel OR=2.07, 95% CI: 1.27-3.26, P=0.0031, in the combined sample). These data are in contrast to those from Caspi et al. (Biol. Psychiatry 57 (2005)1117-1127) who found association between schizophrenia/schizophreniform disorder and homozygosity at the high activity Val variant of rs4680. The results of our study are discussed in the context of previous findings, suggesting the involvement of COMT polymorphisms in the association between cannabis use and schizophrenia as well as the existence of additional factors mediating this association. However, further research is needed to confirm the COMT-cannabis interaction.
Scientific findings show that substance abuse in women yields a higher risk of a variety of health problems than substance abuse in men. Research suggests that women experience addiction telescoping when they abuse alcohol, tobacco, specific stimulants, and possibly opioids. Medical side effects also develop more rapidly in women than men when they abuse many substances. Cancer and cardiac complications, specifically, pose a significant threat for women who abuse almost all types of substances. However, the physical consequences are not the only ones women suffer when they engage in substance abuse. Research on substance abuse in women ties opioids to mood and anxiety disorders, heroin to neurological deficiencies, cocaine to immune system suppression, and alcohol to intimate partner abuse. Additionally, female substance abusers, on average, have a lower level of education and lower rates of employment. In light of these gender-specific concerns, physicians should give particular consideration to detecting substance abuse in women.
Cannabis is the most widely consumed illicit drug worldwide and the relation between cannabis smoking and lung cancer is suggestive, albeit inconclusive.
We conducted three hospital based case-control studies in Tunisia, Morocco, and Algeria, three areas of high prevalence of cannabis consumption as well as production. This paper presents the pooled analysis of these three studies restricted to men with a total of 430 cases and 778 controls.
Ninety-six percent of the cases and 67.8% of the controls were tobacco smokers and 15.3% of the cases and 5% of the controls were ever cannabis smokers. All cannabis smokers were tobacco users. Adjusting for country, age, tobacco smoking, and occupational exposure, the odds ratio (OR) for lung cancer was 2.4 (95% confidence interval [CI]: 1.6-3.8) for ever cannabis smoking. This association remained after adjustment for lifetime tobacco packyears as continuous variable, OR = 2.3 (95% CI: 1.5-3.6). The OR adjusted for intensity of tobacco smoking (cigarette/d) among current tobacco smokers and never cannabis smokers was 10.9 (95% CI: 6.0-19.7) and the OR among current tobacco users and ever cannabis smokers was 18.2 (95% CI: 8.0-41.0). The risk of lung cancer increased with increasing joint-years, but not with increasing dose or duration of cannabis smoking.
Our results suggest that cannabis smoking may be a risk factor for lung cancer. However, residual confounding by tobacco smoking or other potential confounders may explain part of the increased risk.
The purpose of this retrospective cohort study was to examine the relationship of marijuana use to cancer incidence. The study population consisted of 64,855 examinees in the Kaiser Permanente multiphasic health checkup in San Francisco and Oakland (California, United States), between 1979-85, aged 15 to 49 years, who completed self-administered questionnaires about smoking habits, including marijuana use. Follow-up for cancer incidence was conducted through 1993 (mean length 8.6 years). Compared with nonusers/experimenters (lifetime use of less than seven times), ever- and current use of marijuana were not associated with increased risk of cancer of all sites (relative risk [RR] = 0.9, 95 percent confidence interval [CI] = 0.7-12 for ever-use in men; RR = 1.0, CI = 0.8-1.1 in women) in analyses adjusted for sociodemographic factors, cigarette smoking, and alcohol use. Marijuana use also was not associated with tobacco-related cancers or with cancer of the following sites: colorectal, lung, melanoma, prostate, breast, cervix. Among nonsmokers of tobacco cigarettes, ever having used marijuana was associated with increased risk of prostate cancer (RR = 3.1, CI = 1.0-9.5) and nearly significantly increased risk of cervical cancer (RR = 1.4, CI = 1.0-2.1). We conclude that, in this relatively young study cohort, marijuana use and cancer were not associated in overall analyses, but that associations in nonsmokers of tobacco cigarettes suggested that marijuana use might affect certain site-specific cancer risks.
The complexity of tobacco smoke leads to some confusion about the mechanisms by which it causes lung cancer. Among the multiple components of tobacco smoke, 20 carcinogens convincingly cause lung tumors in laboratory animals or humans and are, therefore, likely to be involved in lung cancer induction. Of these, polycyclic aromatic hydrocarbons and the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone are likely to play major roles. This review focuses on carcinogens in tobacco smoke as a means of simplifying and clarifying the relevant information that provides a mechanistic framework linking nicotine addiction with lung cancer through exposure to such compounds. Included is a discussion of the mechanisms by which tobacco smoke carcinogens interact with DNA and cause genetic changes--mechanisms that are reasonably well understood--and the less well defined relationship between exposure to specific tobacco smoke carcinogens and mutations in oncogenes and tumor suppressor genes. Molecular epidemiologic studies of gene-carcinogen interactions and lung cancer--an approach that has not yet reached its full potential--are also discussed, as are inhalation studies of tobacco smoke in laboratory animals and the potential role of free radicals and oxidative damage in tobacco-associated carcinogenesis. By focusing in this review on several important carcinogens in tobacco smoke, the complexities in understanding tobacco-induced cancer can be reduced, and new approaches for lung cancer prevention can be envisioned.
Taxonomies of alcoholism and antisocial behaviors based on developmental course converge on two-group classifications that emphasize early and late onset. Typologies for users of illicit drugs remain to be developed. This article proposes a developmental taxonomy of marijuana users.
Cluster analysis was applied to a representative community sample of 708 (364 male, 344 female) marijuana users followed from adolescence to age 34-35. The Ward method, followed by relocation, was used to classify marijuana users into different types based on age of onset, chronicity of heavy use and persistence of use. ANOVA and logit analyses were utilized to describe the cluster solution and examine the correlates of cluster membership.
Four marijuana use clusters were identified: early onset-heavy use, early onset-light use, mid onset-heavy use and late onset-light use. The groups differed from each other in degree of involvement in marijuana and other drugs, sociodemographic and lifestyle characteristics. The majority of those with early onset did not become heavily involved in marijuana. Unique factors were associated with membership in each group. Factors differentiating early from mid-onset heavy use included association with marijuana-using peers and having had a mental disorder. Peer delinquency was an additional factor differentiating early initiators who became heavy users from those who did not.
A simple two-type classification fails to take into account the heterogeneity of early and late onset groups. By itself, early onset into marijuana will not lead to problematic use or rapid progression into the use of other drugs. Motivation underlying use and dysfunctional behaviors are associated with the development of problematic drug use and dependence.
To examine the associations between frequency of cannabis use and psychosocial outcomes in adolescence/young adulthood.
A 21-year longitudinal study of the health, development and adjustment of a birth cohort of 1265 New Zealand children.
Annual assessments of the frequency of cannabis use were obtained for the period from age 14-21 years, together with measures of psychosocial outcomes including property/violent crime, depression, suicidal ideation, suicide attempt and other illicit drug use.
The frequency of cannabis use was associated significantly with all outcomes, and particularly other illicit drug use. Statistical control for confounding by both fixed and time-dynamic factors substantially reduced the strength of association between cannabis use and outcome measures. Nevertheless, cannabis use remained significantly (P < 0.05) associated with all outcomes and particularly other illicit drug use, after adjustment for confounding. For the measures of crime, suicidal behaviours and other illicit drug use there was evidence of age related variation in the strength of association with cannabis use, with younger (14-15 years old) users being more affected by regular cannabis use than older (20-21 years old) regular users. However, the association between cannabis use and depression did not vary with age.
Cannabis use, and particularly regular or heavy use, was associated with increased rates of a range of adjustment problems in adolescence/ young adulthood-other illicit drug use, crime, depression and suicidal behaviours-with these adverse effects being most evident for school-aged regular users. The findings reinforce public health concerns about minimizing the use of cannabis among school-aged populations.
Purpose:
To examine the developmental relationship between adolescent substance use and risky sexual behavior in young adulthood. A gender-balanced, ethnically diverse urban sample of 808 children in Seattle was surveyed at age 10 years in 1985 and followed prospectively to age 21 years in 1996. Semiparametric group-based modeling was used to determine trajectory groups of binge-drinking, cigarette smoking, marijuana use, and the use of other illicit drugs. Negative binomial regressions and logistic regressions were used to examine whether these trajectory groups predicted the number of sex partners and condom use at age 21 years. Specific forms of adolescent substance use significantly predicted risky sexual behavior at age 21 years, after other substance use and early measures of sexual behavior were controlled. Early binge-drinkers had significantly more sex partners than nonbinge-drinkers. Late onset binge-drinkers and marijuana users had significantly more sex partners and were less likely to use condoms consistently than those who did not binge drink or use marijuana. Experimenters in cigarette smoking, who did not escalate smoking, were more likely to use condoms consistently than nonsmokers. In contrast, the use of other illicit drugs in adolescence did not predict risky sexual behavior at age 21 years. The effects of adolescent substance use on risky sexual behavior at age 21 years differed for youths with developmentally different substance use trajectories in this urban sample disproportionately drawn from high crime neighborhoods. To prevent risky sexual behavior among young adults, attention should be paid to binge-drinking and marijuana use during adolescence.
This review describes what is known about effects of marijuana and cannabinoids in relation to human physiological and disease outcomes. The acute physiological effects of marijuana include a substantial dose-dependent increase in heart rate, generally associated with a mild increase in blood pressure. Orthostatic hypotension may occur acutely as a result of decreased vascular resistance. Smoking marijuana decreases exercise test duration in maximal exercise tests, increases the heart rate at submaximal levels of exercise. Tolerance develops to the acute effects of marijuana smoking and delta9-tetrahydrocannibol (THC) over several days to a few weeks. The cardiovascular responses that occur in response to THC are mediated by the autonomic nervous system, with recent findings also demonstrating that the human cannabinoid receptor system plays a role in regulating the cardiovascular response. Although several mechanisms exist by which marijuana use might contribute to the development of chronic cardiovascular conditions or acutely trigger cardiovascular events, there are few data regarding marijuana/THC use and cardiovascular disease outcomes. A large cohort study showed no association of marijuana use with cardiovascular disease hospitalization or mortality. However, acute effects of marijuana use include a decrease of the time until the onset of chest pain in patients with angina pectoris; one study has shown that marijuana may trigger the onset of myocardial infarction. Patients who have coronary heart disease or are at high risk for the development of CHD should be cautioned about the potential hazards of marijuana use as a precipitant for clinical events. Research directions might include more studies of cardiovascular disease outcomes and relationships of marijuana with cardiovascular risk factors, studies of metabolic and physiologic effects of chronic marijuana use that may affect cardiovascular disease risk, increased understanding of the role of the cannabinoid receptor system in cardiovascular regulation, and studies to determine if there is a therapeutic role for cannabinoids in blood pressure control or for neuroprotection after stroke.
Papers pp 1195, 1199
The strongest evidence that cannabis use may be a risk factor for later psychosis comes from a Swedish cohort study which found that heavy cannabis use at age 18 increased the risk of later schizophrenia sixfold. 1 2 This study could not establish whether adolescent cannabis use was a consequence of pre-existing psychotic symptoms rather than a cause. We present the first prospective longitudinal study of adolescent cannabis use as a risk factor for adult schizophreniform disorder, taking into account childhood psychotic symptoms3 antedating cannabis use.
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Association between cannabis use in adolescence and schizophrenia and depressive symptoms and disorders at age 26 (n=759), controlling for childhood psychotic symptoms and use of other drugs in adolescence
The Dunedin multidisciplinary health and development study (a study of a general population birth cohort of 1037 individuals born in Dunedin, New Zealand, in 1972-3)4 has a 96% follow up rate at age 26. It obtained information on psychotic symptoms at age 11 and drug use at ages 15 and 18 from self reports and assessed …
Cannabis is the most widely used illegal drug in the U.S. population. Surveys have estimated that the lifetime prevalence rate for cannabis dependence is approximately 4%. Though the presence of a psychiatric disorder increases the likelihood of developing substance dependence, the field lacks data regarding the association between mental disorders and cannabis dependence. The aim of this study is to describe the prevalence of psychiatric disorders among individuals with cannabis dependence. The National Comorbidity Survey was used to obtain these data. We found that 90% of respondents with cannabis dependence had a lifetime mental disorder, compared to 55% without cannabis dependence. Alcohol dependence, antisocial personality disorder, and conduct disorder had the strongest associations with cannabis dependence, followed by anxiety and mood disorders. A large proportion of respondents with internalizing disorders developed mood or anxiety disorders prior to onset of their first cannabis dependence symptom. Data regarding the prevalence of comorbid mental disorders underscore the importance of thorough and systematic evaluation of patients seeking treatment for cannabis dependence. The failure to identify comorbidity may lead to inadequate treatment, and a poorer prognosis.
To examine the evidence on the association between cannabis and depression and evaluate competing explanations of the association.
A search of Medline, Psychinfo and EMBASE databases was conducted. All references in which the terms 'cannabis', 'marijuana' or 'cannabinoid', and in which the words 'depression/depressive disorder/depressed', 'mood', 'mood disorder' or 'dysthymia' were collected. Only research studies were reviewed. Case reports are not discussed.
There was a modest association between heavy or problematic cannabis use and depression in cohort studies and well-designed cross-sectional studies in the general population. Little evidence was found for an association between depression and infrequent cannabis use. A number of studies found a modest association between early-onset, regular cannabis use and later depression, which persisted after controlling for potential confounding variables. There was little evidence of an increased risk of later cannabis use among people with depression and hence little support for the self-medication hypothesis. There have been a limited number of studies that have controlled for potential confounding variables in the association between heavy cannabis use and depression. These have found that the risk is much reduced by statistical control but a modest relationship remains.
Heavy cannabis use and depression are associated and evidence from longitudinal studies suggests that heavy cannabis use may increase depressive symptoms among some users. It is still too early, however, to rule out the hypothesis that the association is due to common social, family and contextual factors that increase risks of both heavy cannabis use and depression. Longitudinal studies and studies of twins discordant for heavy cannabis use and depression are needed to rule out common causes. If the relationship is causal, then on current patterns of cannabis use in the most developed societies cannabis use makes, at most, a modest contribution to the population prevalence of depression.