Our finding that interruptions in mental health care directly linked to substance use, which in turn was linked to other negative outcomes, suggests that strategies to ensure continuity of care among this population are critical. The interruptions in care during the COVID-19 pandemic may be partly explained by loss of employment and subsequent loss of health insurance. However, given that rates of unemployment were not different among those with and without interruptions in mental health care, it is likely that these interruptions instead resulted from pandemicrelated healthcare provider cancelations of in-person services and the consequent switch to telehealth visits. Beyond limited access, to the technology required for telehealth visits including cell phone or computers and Internet connectivity , privacy concerns and limited access to confidential surroundings may also be an issue among this study population. Among participants who reported interruptions in mental health care, 20% also noted unstable housing, and less than half engaged in telehealth visits. This is supported by data from a community-based organization providing substance use treatment for HIV-affected individuals which found that all clients were unable to attend telehealth visits.Addressing the impact of COVID- 19 on healthcare delivery and, in particular, mental health care for those most vulnerable may require novel strategies that move beyond standard telehealth services. Strategies such as “task sharing” or “task shifting”—where care extenders and other nonclinical staf deliver both medical and behavioral health care—have been successfully implemented in low resource settings and may serve as a potential option in lieu of telehealth or in-person visits.The “task-sharing” model was adapted by a substance use treatment center in the USA, indoor grow shelves which used peer coaches to deliver the psychotherapy component of their substance use recovery program.
Using peer coaches, who coordinated with a program therapist, offered fexibility both in terms of time and technology requirements . This model was acceptable and showed preliminary effcacy in delivering behavioral healthcare during the COVID-19 pandemic. Among our study participants, cannabis use for the purpose of managing COVID-19 related increases in anxiety and symptoms of depression was independently associated with sexual behaviors that increase the risk of STIs, namely, number of anal sex partners. Findings related to cannabis use and sexual risk behaviors have been mixed, with prior work from mSTUDY indicating that cannabis use was in fact associated with lower STI risk behaviors and STIs.However, unique to this analysis is our focus on cannabis use specifically to manage mental health distress resulting from the COVID-19 pandemic. Social isolation caused by stay-at-home orders likely triggers both substance use, sexual compulsivity, and behaviors that increase the risk of STIs. The increase in reported sex partners raises additional concern when coupled with findings from other studies that indicate COVID-19 has reduced access to STI/ HIV testing and other prevention tools such as pre-exposure prophylaxis .Beyond the STI transmission risks, these findings also have implications in terms of SARS-CoV-2 transmission risk. For instance, a recent study of MSM in Israel found that those who reported having sex with a casual sex partner during a period when strict social-distancing mandates were in place were also more likely than those who did not have casual sex partners to report being agreeable to having sex with a person diagnosed with COVID-19. The same task-shifting strategies used to extend mental health and substance use care can be extended to provide wrap-around services including provision of self-testing kits for STIs/HIV and linkage to other HIV prevention services. These findings should be interpreted with consideration to a number of study limitations. First, our data—especially data on sexual risk behaviors and substance use—were based on self-report, which can result in an underestimation of these behaviors.
However, the use of computer-assisted self-interviews may help minimize potential response bias and reluctance in reporting behaviors that are socially stigmatized or illegal. Disentangling the temporal ordering of substance use, depressive symptoms, and anxiety is challenging; given our data, it is difficult to say whether substance use led to mental health issues and sexual risk behaviors or whether the symptoms led to substance use and subsequent sexual risk behaviors. Furthermore, the potential chronicity and persistence of the behaviors, the disruptions in mental health care, and the association with our outcome of interest make it difficult to determine which is the cause and which is the effect. However, by focusing specifically on cannabis use related to increased pandemicrelated mental distress, we hope to limit some of the challenges related to the temporal ordering of events. Finally, this study was based on participants recruited from a community-based sexual health clinic and a university-based research clinic in Los Angeles and may not be generalizable to other populations. In conclusion, interruptions in mental health care among this exceptionally vulnerable population can result in a cascade of effects that increases infectious disease risk, including STIs as well as COVID- 19. While some of the negative mental health effects regress to baseline levels within a year of the major disruptions caused by the pandemic, there exists an extended vulnerable period where many of the same socioeconomic and structural vulnerabilities that place populations at risk for STIs also increase vulnerability to infections with SARS-CoV-2, as well as other negative outcomes. Novel strategies beyond telehealth that deliver services without direct client contact are needed to bridge the care gap for marginalized and low-resourced populations and address the social determinants of health that lead to health care and mental and sexual health disparities.Cannabis and tobacco smoking frequently co-occur.A proportion of this correlation between cannabis involvement and cigarette smoking has been attributed to genetic influences , with genetic correlations ranging from 0.31 in an adolescent sample to 0.82 . One twin study also noted that while cannabis and nicotine dependence are influenced by different genetic factors, the correlation between these factors is 0.82 . Despite evidence for genetic overlap, few studies have examined whether genetic variants implicated for one substance also influence the other.
Even though cannabis and tobacco have unique pharmacological profiles, it is possible that pleiotropic effects may be responsible for shared aspects of their use and misuse,such as experience of reward or attenuation of negative mood states. One approach for identifying such genetic variants is to focus on those that have been repeatedly identified in meta analyses of genome wide association studies . As GWAS simultaneously examines a million or more single nucleotide polymorphisms , in these analyses only SNPs with p-values of 5 × 10−8 are considered statistically significant. Consequently, the identification of such SNPs typically necessitates large sample sizes. While there have not been such meta-analyses for cannabis involvement, three large meta analyses of cigarette smoking have identified such significant SNPs . In the present study, we selected 11 genome wide significant SNPs associated with CPD, smoking initiation and smoking cessation/current smoking and examined: whether they were associated with equivalent cigarette smoking measures in European-American subjects from an independent sample, Study of Addictions Genes and Environment ; and whether the same SNPs were associated with cannabis use, current use and DSM-IV cannabis abuse/dependence in SAGE, especially after accounting for comorbid cigarette smoking.The mean age of the sample was 38.7 [range 18–77 years]. Ever smoking even one cigarette and ever using cannabis was reported by 90.1% and 74.2% of the sample, respectively. Of those who had ever smoked, 84.5% reported smoking 100 or more cigarettes . Current smokers and cannabis users comprised 67.3% and 30.1% of those who had smoked 100 or more cigarettes and ever used cannabis, respectively. Of those who had ever used cannabis , 822 met criteria for DSM-IV cannabis abuse/dependence. In addition, for tobacco smoking, of those who had smoked 100 or more cigarettes, 1030, 530 and 223 individuals reported smoking ≥10, 11–20 and 21–30 CPD, respectively, with the remainder reporting smoking >30 cigarettes. Of those who had initiated smoking , 39.4% were nicotine dependent by the Fagerström Test for Nicotine Dependence criteria . Among those who had ever used cannabis, 96.7% ever smoked cigarettes and 90.6% reported smoking initiation . Of those who reported current cannabis use, 85% were also current tobacco users . CPD scores and FTND were also correlated with DSM-IV cannabis abuse/dependence. Table 2 presents association results for the tobacco smoking and cannabis involvement measures. After correction for multiple testing, the data confirmed previously reported associations between rs6265 and smoking initiation and between rs16969968 , rs1051730 and rs1451240 with CPD. For cannabis, rs6265 was associated with lifetime cannabis use while rs1451240 was associated with DSM-IV cannabis abuse/dependence. To examine whether the associations for cannabis involvement were attributable to the comorbidity between smoking initiation and ever using cannabis and between nicotine dependence and DSMIV cannabis abuse/dependence , analyses were repeated while including the tobacco measures as covariates. In both instances, while effect sizes remained consistent ,indoor garden table the p-values were no longer significant .
Regardless of adjustment for tobacco smoking, rs6265 and rs1451240 explained only modest proportions of variance in cannabis use and abuse/dependence respectively.These analyses suggest that the association between cannabis involvement and SNPs previously associated with tobacco smoking in three large meta-analyses is modest and, quite likely, not specific to cannabis involvement. Additionally, while the association between rs16969968/rs1051730 and tobacco smoking is well-replicated ,these SNPs were not associated with cannabis involvement . In contrast, our own prior study has found support for the association between rs1451240 and FTND. This SNP is a proxy for rs13280604 in CHRNB3 which was associated at genome wide significant levels with CPD in one prior meta-analysis and has been implicated in studies of nicotine dependence as well as subjective reactions to nicotine . The present study finds support for a similar protective association for the same allele of this variant and cannabis abuse/dependence. Being intronic, the functional significance of this SNP is unknown. This SNP has also been linked to alcohol consumption indicating its putatively pleiotropic role across a host of substance-related behaviors. Similarly, rs6265 in BDNF, a missense SNP , was associated with smoking initiation and with lifetime cannabis use. In the TAG meta-analysis, rs6265 was one of several genome wide significant SNPs associated with smoking initiation, however, its genome wide significance level was achieved only after sample sizes exceeded 143,000. In this context, the significant p-value in our sample served as replication. Carriers of the A allele were less likely to smoke 100 or more cigarettes during their lifetime, which is consistent with the meta-analysis which reported that the alternate G allele was associated with a 6% increase in relative risk for smoking initiation. This SNP has been implicated in a wide array of psychopathology, most notably affective disorders, with meta-analyses suggesting that the Met allele is associated with increased risk for major depressive disorder,schizophrenia and eating disorders but decreased risk for substance use disorders. We see a similar protective effect of the Met allele on cannabis use in this study and this decreased risk is consistent with neurobiological models of stress response that implicate this variant in blunted dopamine activity during reward processing .It is also possible that the effect of rs6265 reflects Mendelian randomization, in which the association between genotype and an outcome relates to individuals being “randomized” at birth to a higher likelihood of environmental exposure . If carriers of the G allele of rs6265 are more likely to initiate cigarette smoking, and cigarette smoking, in turn, increases the likelihood of cannabis initiation via environmental pathways, then the association between rs6265 and cannabis use may reflect an environmental process rather than evidence for genetic overlap. Due to the rather general biological role of rs6265, these processes are difficult to disentangle. Importantly, for both rs1451240 and rs6265, when smoking initiation and FTND were included as covariates, the associations with the cannabis measures were no longer statistically significant. While this might imply that the associations observed with cannabis involvement are not independent of the associations between these SNPs and tobacco-related outcomes, it is worth noting that the point estimates for and variance explained by each SNP remained relatively unchanged even after accounting for tobacco smoking. Therefore, it is possible that power to detect their specific/independent effects on cannabis involvement was attenuated in this sample that is enriched for nicotine dependence.