Associations between adolescent cannabis use and brain structure in psychosis.
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ABSTRACT:
SUBMITTER: Abush H
PROVIDER: S-EPMC5959798 | biostudies-literature | 2018 Jun
REPOSITORIES: biostudies-literature
Publications
Associations between adolescent cannabis use and brain structure in psychosis.
Abush Hila H Ghose Subroto S Van Enkevort Erin A EA Clementz Brett A BA Pearlson Godfrey D GD Sweeney John A JA Keshavan Matcheri S MS Tamminga Carol A CA Ivleva Elena I EI
Psychiatry research. Neuroimaging 20180328
Associations between cannabis use and psychotic disorders suggest that cannabis may be a contributory risk factor in the neurobiology of psychosis. In this study, we examined brain structure characteristics, total and regional gray matter density (GMD), using Voxel Based Morphometry, in psychotic individuals, stratified by history of cannabis use (total n = 109). We also contrasted GMD estimates in individual diagnostic groups (schizophrenia/bipolar I disorder) with and without history of adoles ...[more]
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Project description:AIMS:This study tested whether adolescents who used cannabis or met criteria for cannabis dependence showed neuropsychological impairment prior to cannabis initiation and neuropsychological decline from before to after cannabis initiation. DESIGN:A longitudinal co-twin control study. SETTING AND PARTICIPANTS:Participants were 1989 twins from the Environmental Risk (E-Risk) Longitudinal Twin Study, a nationally representative birth cohort of twins born in England and Wales from 1994 to 1995. MEASUREMENTS:Frequency of cannabis use and cannabis dependence were assessed at age 18. Intelligence quotient (IQ) was obtained at ages 5, 12 and 18. Executive functions were assessed at age 18. FINDINGS:Compared with adolescents who did not use cannabis, adolescents who used cannabis had lower IQ in childhood prior to cannabis initiation and lower IQ at age 18, but there was little evidence that cannabis use was associated with IQ decline from ages 12-18. For example, adolescents with cannabis dependence had age 12 and age 18 IQ scores that were 5.61 (t = -3.11, P = 0.002) and 7.34 IQ points (t = -5.27, P < 0.001) lower than adolescents without cannabis dependence, but adolescents with cannabis dependence did not show greater IQ decline from age 12-18 (t = -1.27, P = 0.20). Moreover, adolescents who used cannabis had poorer executive functions at age 18 than adolescents who did not use cannabis, but these associations were generally not apparent within twin pairs. For example, twins who used cannabis more frequently than their co-twin performed similarly to their co-twin on five of six executive function tests (Ps > 0.10). The one exception was that twins who used cannabis more frequently than their co-twin performed worse on one working memory test (Spatial Span reversed; ? = -0.07, P = 0.036). CONCLUSIONS:Short-term cannabis use in adolescence does not appear to cause IQ decline or impair executive functions, even when cannabis use reaches the level of dependence. Family background factors explain why adolescent cannabis users perform worse on IQ and executive function tests.
| S-EPMC5760333 | biostudies-other
Project description:Prior cannabis use, compared to nonuse, is reported to be associated with less cognitive impairment in schizophrenia. The age of cannabis use and the persistent influence of cannabis use on cognitive function has not been examined across the psychosis dimension. Ninety-seven volunteers with psychosis (schizophrenia, schizoaffective, or bipolar psychosis) and 64 controls were recruited at the Dallas site of the Bipolar-Schizophrenia Network on Intermediate Phenotypes consortium. Cannabis use history obtained in a semi-structured manner was used to categorize subjects into nonusers, adolescent-onset users, and late-onset users. The a priori hypothesis tested was that individuals with psychosis and a history of adolescent cannabis use (ACU) would have better global neuropsychological performance, as measured by the Brief Assessment of Cognition in Schizophrenia (BACS) battery, compared to those with psychosis and no cannabis use history. BACS Composite scores were significantly higher in individuals with psychosis with ACU compared to individuals with psychosis and no prior cannabis use. In subgroup analyses, ACU influenced global cognition in the schizophrenia/schizoaffective (SCZ) subgroup but not the bipolar psychosis subgroup. Exploratory analyses within the SCZ group, suggest that ACU was associated with better performance in specific domains compared to non-ACU groups. There are distinct associations between age of cannabis use and neuropsychological function across psychotic illnesses. Specifically, ACU is associated with better cognitive function in SCZ but not bipolar psychosis. This age-dependent and diagnosis-specific influence of cannabis may need to be factored into the design of future cognitive studies in SCZ.
| S-EPMC5049522 | biostudies-literature
Project description:Observational studies have linked cannabis use to an array of negative outcomes, including psychiatric symptoms, cognitive impairment, and educational and occupational underachievement. These associations are particularly strong when cannabis use occurs in adolescence. Nevertheless, causality remains unclear. The purpose of the present study was thus to examine associations between prospectively assessed adolescent cannabis use and young-adult outcomes (psychiatric, cognitive, and socioeconomic) in three longitudinal studies of twins (n = 3,762). Twins reporting greater cumulative cannabis use in adolescence reported higher levels of psychopathology as well as poorer socioeconomic outcomes in young adulthood. However, cannabis use remained associated only with socioeconomic outcomes (i.e., educational attainment, occupational status, and income) in monozygotic-cotwin control analyses, which account fully for shared genetic and environmental confounding. Follow-up analyses examining associations between twin differences in adolescent cannabis use and longitudinal change in academic functioning during the middle- and high-school years provided a possible mechanism for these associations, indicating that greater cannabis use during this period was associated with decreases in grade point average and academic motivation as well as increases in academic problem behavior and school disciplinary problems. Our findings thus suggest that cannabis use in adolescence has potentially causal, deleterious effects on adolescent academic functioning and young-adult socioeconomic outcomes despite little evidence suggesting a strong, causal influence on adult mental health or cognitive ability.
| S-EPMC8040790 | biostudies-literature
Project description:ImportancePrior neuroimaging studies have suggested that alterations in brain structure may be a consequence of cannabis use. Siblings discordant for cannabis use offer an opportunity to use cross-sectional data to disentangle such causal hypotheses from shared effects of genetics and familial environment on brain structure and cannabis use.ObjectivesTo determine whether cannabis use is associated with differences in brain structure in a large sample of twins/siblings and to examine sibling pairs discordant for cannabis use to separate potential causal and predispositional factors linking lifetime cannabis exposure to volumetric alterations.Design, setting, and participantsCross-sectional diagnostic interview, behavioral, and neuroimaging data were collected from community sampling and established family registries from August 2012 to September 2014. This study included data from 483 participants (22-35 years old) enrolled in the ongoing Human Connectome Project, with 262 participants reporting cannabis exposure (ie, ever used cannabis in their lifetime).Main outcomes and measuresCannabis exposure was measured with the Semi-Structured Assessment for the Genetics of Alcoholism. Whole-brain, hippocampus, amygdala, ventral striatum, and orbitofrontal cortex volumes were related to lifetime cannabis use (ever used, age at onset, and frequency of use) using linear regressions. Genetic (ρg) and environmental (ρe) correlations between cannabis use and brain volumes were estimated. Linear mixed models were used to examine volume differences in sex-matched concordant unexposed (n = 71 pairs), exposed (n = 81 pairs), or exposure discordant (n = 89 pairs) sibling pairs.ResultsAmong 483 study participants, cannabis exposure was related to smaller left amygdala (approximately 2.3%; P = .007) and right ventral striatum (approximately 3.5%; P < .005) volumes. These volumetric differences were within the range of normal variation. The association between left amygdala volume and cannabis use was largely owing to shared genetic factors (ρg = -0.43; P = .004), while the origin of the association with right ventral striatum volumes was unclear. Importantly, brain volumes did not differ between sex-matched siblings discordant for use (fixed effect = -7.43; t = -0.93, P = .35). Both the exposed and unexposed siblings in pairs discordant for cannabis exposure showed reduced amygdala volumes relative to members of concordant unexposed pairs (fixed effect = 12.56; t = 2.97; P = .003).Conclusions and relevanceIn this study, differences in amygdala volume in cannabis users were attributable to common predispositional factors, genetic or environmental in origin, with little support for causal influences. Causal influences, in isolation or in conjunction with predispositional factors, may exist for other brain regions (eg, ventral striatum) or at more severe levels of cannabis involvement and deserve further study.
| S-EPMC4624286 | biostudies-literature
Project description:Parental cannabis use disorder (CUD) and low positive parenting (monitoring, support, and consistency) are risk factors for adolescent cannabis use. However, it is unclear whether parental cannabis use without CUD is sufficient to increase risk for low positive parenting and adolescent cannabis use. Additionally, parents may not treat each of their adolescents the same, and risk for adolescent cannabis use may increase as a result of low levels of positive parenting in families or low positive parenting unique to each adolescent. The current study prospectively tested low positive parenting as a mediator of the relation between parental cannabis use history (with parental cannabis use and CUD considered separately) and adolescent cannabis use at the family level and individual level. Participants were 363 adolescents from a multigenerational longitudinal study who reported on positive parenting when they were ages 9-16 (M = 11.6, SD = 1.40) and on cannabis use when they were ages 13-19 (M = 16.3, SD = 1.84). Parents reported on their own cannabis use and CUD. Results showed that parental CUD was associated with adolescent cannabis use (OR = 3.62, p = .047) but parental cannabis use without CUD was not, and only parental CUD predicted low positive parenting (B = -0.28, p < .05). Average levels of low positive parenting within a family partially mediated the association between parental CUD and offspring cannabis use. These findings suggest parental cannabis use alone may not impair parenting, but parental use that meets criteria for CUD does impair parenting. Additionally, average levels of positive parenting in families may be a mechanism underlying the intergenerational transmission of cannabis use. (PsycINFO Database Record
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Project description:Pubertal processes are associated with structural brain development, but studies have produced inconsistent findings that may relate to different measurements of puberty. Measuring both hormones and physical characteristics is important for capturing variation in neurobiological development. The current study explored associations between cortical thickness and latent factors from multi-method pubertal data in 174 early adolescent girls aged 10-13 years in the Transitions in Adolescent Girls (TAG) Study. Our multi-method approach used self-reported physical characteristics and hormone levels (dehydroepiandrosterone (DHEA), testosterone (T), and estradiol (E2) from saliva) to estimate an overall pubertal factor and for each process of adrenarche and gonadarche. There were negative associations between the overall puberty factor representing later stage and thickness in the posterior cortex, including the occipital cortices and extending laterally to the parietal lobe. However, the multi-method latent factor had weaker cortical associations when examining the adnearcheal process alone, suggesting physical characteristics and hormones capture different aspects of neurobiological development during adrenarche. Controlling for age weakened some of these associations. These findings show that associations between pubertal stage and cortical thickness differ depending on the measurement method and the pubertal process, and both should be considered in future confirmatory studies on the developing brain.
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Project description:BACKGROUND AND AIMS:Individual differences in DSM-IV personality disorders (PDs) are associated with increased prevalence of substance use disorders. Our aims were to determine which combination of PDs trait scores best predict cannabis use (CU) and cannabis use disorder (CUD), and to estimate the size and significance of genetic and environmental risks in PD traits shared with CU and CUD. DESIGN:Linear mixed-effects models were used to identify PD traits for inclusion in twin analyses to explore the genetic and environmental associations between the traits and cannabis use. SETTING:Cross-sectional data were obtained from Norwegian adult twins in a face-to-face interview in 1999-2004 as part of a population-based study of mental health. PARTICIPANTS:Subjects were 1419 twins (μage = 28.2 years, range = 19-36) from the Norwegian Institute of Public Health Twin Panel with complete PD and cannabis data. MEASUREMENTS:PD traits were assessed using DSM-IV criteria. Life-time CU and CUD were based on DSM-IV abuse and dependence criteria, including withdrawal and craving. FINDINGS:After adjusting for age and sex, antisocial [β = 0.23, 95% confidence interval (CI) = 0.19-0.28] and borderline PDs (β = 0.20, 95% CI = 0.14-0.26) were associated strongly with CU. Antisocial (β = 0.26, 95% CI = 0.21-0.31) and borderline PDs (β = 0.12, 95% CI = 0.06-0.18) were also linked strongly to CUD. Genetic risks in antisocial and borderline PD traits explained 32-60% of the total variance in CU and CUD. Dependent and avoidant PDs explained 11 and 16% of the total variance in CU and CUD, respectively. CONCLUSIONS:Individual differences in the liability to cannabis use and cannabis use disorder appear to be linked to genetic risks correlated with antisocial and borderline personality disorder traits.
| S-EPMC6043378 | biostudies-literature
Project description:METHODS:Data are from an online survey of 482 adolescents (aged 15-19 years) living in states with legalized retail cannabis. Youth were asked about their engagement with cannabis promotions, including whether they liked/followed cannabis businesses on social media (Facebook, Twitter, and Instagram), had a favorite cannabis brand, or could see themselves owning/wearing a cannabis-branded product. Youth also self-reported cannabis use in the past year. We used logistic regression with a Bonferroni correction to compare the odds of cannabis use among youth with different levels of engagement with cannabis promotions and brands after controlling for demographics. RESULTS:After adjusting for several possible confounders, youth who liked or followed a cannabis business on at least one social media platform had 5 times higher odds of past-year cannabis use (aOR = 5.00, 95% CI: 2.47, 10.09, p < 0.001). Youth who thought it was likely that they would own or wear cannabis-branded merchandise (aOR = 6.93, 95% CI: 4.45, 10.78, p < 0.001) or who had a favorite cannabis brand (aOR = 7.98, 95% CI: 4.90, 13.00, p < 0.001) had nearly 8 times greater odds of past-year cannabis use. CONCLUSION:Youth who engage with cannabis promotions and brands had higher odds of past-year cannabis use. Jurisdictions with retail cannabis may want to consider restrictions to limit youth engagement with cannabis promotions.
| S-EPMC6878135 | biostudies-literature
Project description:Background:General obesity has been linked to dysregulation of the endocannabinoid system in humans. However, there is a lack of studies on the relationship between cannabis use and specific abdominal fat phenotypes. The aim was to investigate the associations between cannabis use and magnetic resonance imaging-derived fat phenotypes, as well as indices of insulin sensitivity and insulin secretion. Methods:In this cross-sectional study, magnetic resonance imaging was used to quantify subcutaneous fat volume (SFV), visceral fat volume (VFV), intra-hepatic fat deposition (IHFD), intra-pancreatic fat deposition (IPFD) and skeletal muscle fat deposition (SMFD) by two independent observers. Insulin sensitivity was determined based on HOMA-IS, Raynaud index and Matsuda index, whereas insulin secretion was determined based on HOMA-?, insulinogenic index 30' and insulinogenic index 60'. A validated questionnaire was used to ascertain participants' cannabis use. Linear regression models were constructed, adjusting for demographics, glycated hemoglobin, physical activity, tobacco smoking and alcohol consumption. Results:A total of 120 individuals were included. Cannabis use explained 9.2% of variance in IHFD, 4.4% in SMFD, 3.4% in VFV, 0.4% in SFV and 0.2% in IPFD. Regular cannabis users had significantly greater IHFD compared with never users, in both the unadjusted (P = 0.002) and all adjusted (P = 0.002; P = 0.008) analyses. The other fat phenotypes did not differ significantly between either regular or non-regular users compared with never users. Regular cannabis users had significantly greater insulin secretion (as defined by the insulinogenic index 60') compared with never users, in both the unadjusted (P = 0.049) and all adjusted (P = 0.003; P = 0.004) analyses. Cannabis use explained 20.3% of variance in the insulinogenic index 60', but was not significantly associated with the other indices of insulin secretion. There were no significant differences in indices of insulin sensitivity in either regular or non-regular cannabis users compared with never users. Conclusion:Regular cannabis use may be a risk factor for non-alcoholic fatty liver disease (but not IPFD) and may alter the neuromodulation of insulin secretion. Further investigations are now warranted to elucidate the mechanisms underlying these associations.
| S-EPMC7295553 | biostudies-literature
Project description:Background and aimsCannabis use disorder (CUD) during pregnancy has increased dramatically in the United States (US). This study examined the associations between prenatal CUD and adverse neonatal outcomes and heterogeneities in the associations by mothers' tobacco use status and race/ethnicity.DesignPopulation-based, retrospective cohort study.SettingCalifornia, USA.ParticipantsA total of 4.83 million mothers who delivered a live singleton birth during 2001 to 2012 and their paired infants. Data were obtained from mother-infant linked hospital discharge records and birth and death certificates. Identified by ICD-9 codes recorded at delivery, 20 237 mothers had prenatal CUD.MeasurementsNeonatal outcomes included length of gestation, preterm birth, birth weight, admission into neonatal intensive care unit, hospitalization within 1 year of birth, and death within 1 year of birth. Propensity score matching was used to balance maternal, paternal, and infant characteristics in the comparisons between infants exposed and unexposed to prenatal CUD.FindingsCUD increased from 2.8 to 6.9 per 1000 deliveries during 2001 to 2012. Multivariable regressions in matched samples estimated that prenatal CUD was associated with greater odds of being small for gestational age (OR = 1.13, 95% CI = 1.08, 1.18), preterm birth (OR = 1.06, 95% CI = 1.01, 1.12), low birth weight (OR = 1.13, 95% CI = 1.07, 1.20), and death within 1 year of birth (OR = 1.35, 95% CI = 1.12, 1.62). Compared with infants whose mothers were tobacco non-users, infants whose mothers were tobacco users had greater odds of preterm birth, low birth weight, hospitalization, and death in association with prenatal CUD. Compared with infants whose mothers were non-Hispanic White, infants whose mothers were Hispanic had greater odds of hospitalization and death and infants whose mothers were non-Hispanic Black had greater odds of being small for gestational age in association with prenatal CUD.ConclusionPrenatal cannabis use disorder appears to be associated with escalated odds of major adverse neonatal outcomes, with heterogeneities in the associations by mothers' tobacco use status and race/ethnicity.
| S-EPMC8492477 | biostudies-literature