The role of fathers in adolescent cannabis use disorder: Public perceptions of paternal shame and responsibility

The role of general parenting and cannabis-specific parenting practices in adolescent cannabis and other illicit drug use

Solitary cannabis use in adolescence as a correlate and predictor of cannabis problems

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

Background : Adolescent cannabis use is an established risk factor for the development of psychosis, but the premorbid vulnerability factors and specificity versus generality of the psychotic symptom domains affected in cannabis-psychosis relationships remain incompletely understood. To improve our understanding of these relationships, we used longitudinal data to examine the individual and interactive effects of preadolescent transmissible liability to substance use disorders (SUD), measured via the transmissible liability index (TLI), and adolescent cannabis use on the development of two distinct psychotic symptom domains, paranoid and schizotypal personality traits in young adulthood. Methods: We performed secondary analysis of data from the Center for Education and Drug Abuse (CEDAR) study, which longitudinally assessed offspring of men with (N = 211) and without (N = 237) lifetime history of SUD at ages 10-12, and across adolescence as they transitioned to young adulthood. TLI scores were calculated at age 10-12, self-reported cannabis use was assessed at age 16, and paranoid and schizotypal symptoms were assessed at age 19. Results: Cannabis use at age 16 and family history of SUD were significantly associated with paranoid and schizotypal symptoms at age 19, but TLI scores were not. The interactive effect of TLI x cannabis use was also not significant. Paranoid and schizotypal symptoms showed different dose-dependent sensitivities to cannabis exposure at age 16. Conclusions: These findings indicate that adolescent cannabis use and family history of SUD differentially contribute to the development of paranoid and schizotypal personality traits through mechanisms that do not include behavioral disinhibition.

Cannabis use disorder (CanUD) has increased with the legalization of the use of cannabis. Around 20% of individuals using cannabis develop CanUD, and the number of users has grown with increasing ease of access. CanUD and other substance use disorders (SUDs) are associated phenotypically and genetically. We leveraged new CanUD genomics data to undertake genetically-informed analyses with unprecedented power, to investigate the genetic architecture and causal relationships between CanUD and lifetime cannabis use with risk for developing SUDs and substance use traits. Analyses included calculating local and global genetic correlations, genomic structural equation modeling (genomicSEM), and Mendelian Randomization (MR). Results from the genetic correlation and genomicSEM analyses demonstrated that CanUD and cannabis use differ in their relationships with SUDs and substance use traits. We found significant causal effects of CanUD influencing all the analyzed traits: opioid use disorder (OUD) (Inverse variant weighted, IVW β = 0.925 ± 0.082), problematic alcohol use (PAU) (IVW β = 0.443 ± 0.030), drinks per week (DPW) (IVW β = 0.182 ± 0.025), Fagerström Test for Nicotine Dependence (FTND) (IVW β = 0.183 ± 0.052), cigarettes per day (IVW β = 0.150 ± 0.045), current versus former smokers (IVW β = 0.178 ± 0.052), and smoking initiation (IVW β = 0.405 ± 0.042). We also found evidence of bidirectionality showing that OUD, PAU, smoking initiation, smoking cessation, and DPW all increase risk of developing CanUD. For cannabis use, bidirectional relationships were inferred with PAU, smoking initiation, and DPW; cannabis use was also associated with a higher risk of developing OUD (IVW β = 0.785 ± 0.266). GenomicSEM confirmed that CanUD and cannabis use load onto different genetic factors. We conclude that CanUD and cannabis use can increase the risk of developing other SUDs. This has substantial public health implications; the move towards legalization of cannabis use may be expected to increase other kinds of problematic substance use. These harmful outcomes are in addition to the medical harms associated directly with CanUD.

Cannabis use disorder (CUD) is strongly influenced by genetic factors; however the mechanisms underpinning this association are not well understood. This study investigated whether a polygenic risk score (PRS) based on a genome-wide association study for CUD in adults predicts cannabis use in adolescents and whether the association can be explained by inter-individual variation in structural properties of brain white matter or risk-taking behaviors. Longitudinal and cross-sectional analyses using data from the IMAGEN cohort, a European longitudinal study integrating genetic, neuroimaging and behavioral measures. We measured associations between PRS for CUD, novelty and sensation seeking traits and fractional anisotropy (FA) of white matter tracts. Mediation modeling explored whether novelty seeking and FA mediated the association between the PRS and cannabis use. Participants were assessed at 14 (n = 1762), 19 (n = 1175) and 23 (n = 1139) years old. European School Survey Project on Alcohol and Other Drugs, substance use risk profile scale, Fagerstrom Test for Nicotine Dependence, temperament and character inventory, Kirby Monetary Questionnaire, diffusor tensor imaging and CUD-PRS. CUD-PRS was associated with adolescent total cannabis exposure [P < 0.001, beta = 0.098 (95% confidence interval = 0.059, 0.137)] as well as with other substance use measures [alcohol P = 0.002, beta = 0.058 (0.020, 0.096); cigarettes smoked P < 0.001, beta = 0.086 (0.044, 0.128); fargestrom score P < 0.001, beta = 0.062 (0.028, 0.096); drug score P < 0.001, beta = 0.106 (0.065, 0.147)]. CUD-PRS was also associated with impulsivity, risk-taking behaviors [impulsivity P < 0.001, beta = 0.106 (0.060, 0.142); sensation seeking P < 0.001, beta = 0.094 (0.0523, 0.1357); novelty seeking P < 0.001, beta = 0.105 (0.064, 0.146); discounting task P < 0.001, beta = 0.051 (0.013, 0.089)] and average FA [P < 0.001, beta = -0.010 (-0.015, -0.005)]. Longitudinal mediation models showed that these behaviors and brain measures could mediate the association of PRS with cannabis use [overall indirect effect for novelty seeking P < 0.001, beta = 0.048 (0.028, 0.068); impulsivity P = 0.016, beta = 0.019 (0.004, 0.035); sensation seeking P < 0.001, beta = 0.034 (0.017, 0.05)]. The genetic risk of adult cannabis use disorder appears to be associated with substance use behavior and white matter structure as early as age 14. The observed mediation effect is consistent with the notion that genetic risk increases novelty seeking in a way that leads to more cannabis use in adolescents.

To estimate the strength of association between psychiatric disorders and substance use disorders (SUD), and cannabis use and cannabis use disorder (CUD)during early pregnancy. Observational study. Kaiser Permanente Northern California, USA. 299 496 pregnancies from 227 555 individuals screened for cannabis use by self-report and a urine toxicology test at entrance to prenatal care in Kaiser Permanente Northern California during January 2011-December 2021 (excepting year 2020). The sample was 62.5% non-White, with a mean (standard deviation) age of 31.1 (5.5) years; 6.8% used cannabis; 0.2% had a CUD. Exposure variables included electronic health record-based psychiatric diagnoses of attention deficit hyperactivity, anxiety, bipolar, depressive, personality, posttraumatic stress and psychotic disorders; and alcohol, opioid, stimulant and tobacco use disorders, during the two years prior to pregnancy up to the day before the prenatal substance use screening date. Outcome variables were any cannabis use, frequency of self-reported cannabis use and CUD during early pregnancy. Psychiatric disorder prevalence ranged from 0.2% (psychotic) to 14.3% (anxiety), and SUD ranged from 0.3% (stimulant/opioid) to 3.8% (tobacco). Psychiatric disorders were associated with cannabis use and CUD, with the strongest association for any use found for bipolar disorder (adjusted odds ratio [aOR] = 2.83; 95% confidence interval [CI] = 2.53-3.17) and the strongest association for CUD found for psychotic disorders (aOR = 10.01, 95% CI = 6.52-15.37). SUDs were associated with cannabis use and CUD, with the strongest association for any use found for tobacco use disorder (aOR = 4.03, 95% CI = 3.82-4.24) and the strongest association for CUD found for stimulant use disorder (aOR = 21.99, 95% CI = 16.53-29.26). Anxiety, bipolar, depressive disorders and tobacco use disorder were associated with greater odds of daily than monthly or less cannabis use. Psychiatric disorders and substance use disorders appear to be associated with elevated odds of any and frequent cannabis use as well as cannabis use disorder during early pregnancy. In most cases, the associations with cannabis outcomes were stronger for substance use disorders than other psychiatric disorders.

Adolescent substance use and educational attainment: An integrative data analysis comparing cannabis and alcohol from three Australasian cohorts

Integrated cognitive behavioral therapy for cannabis use and anxiety disorders: Rationale and development

OPINION article Front. Psychiatry, 08 December 2014Sec. Addictive Disorders https://doi.org/10.3389/fpsyt.2014.00180

Co-morbid substance use disorders (SUDs) are common but difficult to study due to the complex, interacting, and overlapping mechanisms through which they affect brain networks. Many datasets collected to investigate a specific SUD include participants with co-morbid SUDs. While most studies treat comorbid SUDs as covariates of no interest, these covariates also contain untapped information. This is particularly relevant as cannabis use disorder (CanUD) has become increasingly prevalent and co-morbid with other SUDs that have been more thoroughly studied. While treatments have been established for multiple SUDs, none have been approved for CanUD, although naltrexone (NTX) has been associated with reduced use. Here, we conducted a retrospective secondary analysis of functional magnetic resonance imaging (fMRI) data from individuals with primary opioid use disorder (OUD) with co-morbid CanUD, alcohol use disorder (AUD), or cocaine use disorder (CocUD), while controlling for opioid use. All participants underwent imaging prior to receiving a therapeutic dose of long-acting intramuscular NTX (Vivitrol®), an approved treatment for OUD and AUD but not for CocUD, and again two weeks post-administration. At baseline, OUD individuals with co-morbid CanUD, AUD, or CocUD exhibited distinct functional connectivity (FC) alterations compared to those with OUD-only. These differences were greater in younger participants and primarily involved the default mode network. Following NTX administration, FC differences between the co-morbid CanUD and OUD-only groups globally diminished. A similar FC response to NTX was observed in the parietal, subcortical, sensory, and cerebellar networks in the co-morbid AUD group. In contrast, little change in FC was observed in co-morbid CocUD. These findings, combined with prior evidence that NTX reduces cannabis use by dampening the experience of reward, suggest NTX may hold promise as a treatment for CanUD.

Using genetic information to inform policy on cannabis

Poster Abstracts from the AAAP 20th Annual Meeting and Symposium

While cigarette smoking has declined over time, it is not known whether this decline has occurred similarly among individuals with substance use disorders (SUDs) in the United States (US). The current study estimated trends in smoking from 2002 to 2014 among US individuals with and without SUDs. Linear time trends of current smoking prevalence were assessed using logistic regression models. United States; data were drawn from the 2002 to 2014 National Household Survey on Drug Use (NSDUH), an annual US cross-sectional study. A representative, population-based sample of US individuals age 12yeas and older (total analytical population: n=723 283). Past-month current smoking was defined as having smoked at least 100 lifetime cigarettes and reporting smoking part or all of at least one cigarette during the past 30days. Respondents were classified as having any SUD if they met criteria for abuse or dependence for one or more of the following illicit drugs: cannabis, hallucinogens, inhalants, tranquilizers, cocaine, heroin, pain relievers, simulants and sedatives. A second SUD variable included all drugs listed above excluding cannabis use disorder (CUD). An additional variable included respondents who met criteria for cannabis abuse or dependence. Among those with any SUD, the prevalence of smoking did not change from 2002 to 2014 (P=0.08). However, when CUDs were separated from other SUDs, a significant increase in prevalence of smoking was observed among those with SUDs excluding CUDs (P<0.001), while smoking decreased among those with CUDs (P<0.001). Smoking declined among those without SUDs (P<0.001). In 2014, smoking remained significantly more common among those with any SUD (55.48%), SUDs excluding CUDs (63.34%) and CUDs (51.34%) compared with those without these respective disorders (18.16, 18.55 and 18.64%; P<0.001). The prevalence of cigarette smoking in the United States increased from 2002 to 2014 among people with substance use disorders (SUDs) excluding cannabis use disorders (CUDs) and declined among those with CUDs and without SUDs. In 2014, the prevalence of smoking was multifold higher among those with SUDs, including CUDs, compared with those without SUDs.

Substance use disorders (SUD) are often attributed to upbringing and family dynamics, an assumption that places undue responsibility on parents. Mothers may be particularly susceptible to blame due to traditional gender norms around parenting. This qualitative study explored public perceptions of maternal responsibility and shame in the context of adolescent SUD. Participants were 80 Canadian adults recruited during a larger online survey. After reading a vignette describing a mother and her adolescent child with cannabis use disorder (CUD), participants answered two open-ended prompts exploring perceptions of maternal responsibility and shame. An inductive thematic analysis revealed mixed and complex opinions regarding maternal responsibility, with themes highlighting the nature and etiology of addiction, the mother’s role in prevention and recovery, societal tendencies to parent blame, and the detrimental effects of shame and stigma. The current findings highlight the need to challenge public beliefs regarding SUD to reduce parental blame and stigmatization.