Marijuana Smoking Research Articles

PSAT327 Can Cannabis Use Lead to Central Hypothyroidism

Abstract Background Marijuana has been legalized for medical use in 36 states and for recreational use in 18 states. Its effects on thyroid function and hypothalamic-pituitary-thyroid axis in humans is not known. Clinical Case 72 years old male presented to his primary care physician with occasional difficulty swallowing. He reported fatigue for 4-5 years, trouble falling asleep for 2 months, weight gain 8 pounds over last few weeks, occasional diarrhea, and intermittent episodes of heat intolerance. His past medical history included controlled type 2 diabetes mellitus, recurrent herpes simplex infection, arthritis of hip joints, short-term memory loss, anemia, carpal tunnel syndrome and benign prostatic hyperplasia. Medications included glimepiride, lisinopril, acyclovir, tamsulosin, finasteride, escitalopram. He had been smoking marijuana regularly since he was a teenager. He denied using any other supplements. His physical exam was normal with stable vital signs and normal BMI. His labs showed a low TSH (0.096 mcIU/mL, n: 0.358-3.8 mcIU/mL), normal free T4 (0.90 ng/dL, n: 0.76-1.46 ng/dL), normal total T3 (70 ng/dL, n: 60-180 ng/dL). Review of his labs showed low TSH for last 4 years progressively getting worse with normal free T4 levels. TSH-receptor antibody and TPO Antibody level were negative. His white cell count, hemoglobin and platelets were normal. His electrolytes, kidney function and liver function tests were also normal. Thyroid Ultrasound showed 2 small sub-centimeter hypoechoic nodules in the left thyroid lobe. Two years ago, a radioactive Iodine scan showed normal iodine uptake. A recent radioactive iodine uptake scan showed generalized decreased iodine uptake with no evidence of graves’ disease or toxic multinodular goiter. Conclusion Currently there are no controlled studies on the effect of marijuana use on thyroid function in humans. A cross-sectional analysis using National Health and Nutrition Examination Survey (NHANES) from 2007 to 2012 showed recent marijuana use was significantly associated with lower levels of TSH but was not associated with thyroid dysfunction (1). This study suggests that marijuana use is associated with low TSH levels. This could be due to hypothalamic suppression of TSH or may indicate a protective role against hypothyroidism. Older studies in rodents showed that cannabis exposure may lead to suppression of TSH and hypothalamic function (2). The data related to human subjects is scarce. Therefore, pathophysiologic mechanisms are speculative, although animal data support potential mechanism of hypothalamic suppression.

ODP165 Atypical DKA? Think Cannabis!

Abstract Diabetic ketoacidosis (DKA) can be life threatening if not recognized and treated promptly. DKA is characterized by hyperglycemia, acidosis, ketosis and elevated anion gap. The presence of these metabolic derangements is essential to make the diagnosis. The use of cannabis has been associated with atypical acid-base profile in DKA which may contribute to confusion in diagnosis and treatment. Case A 20-year-old man with type 1 diabetes since age 10 presented to the emergency department with 4 days of nausea, vomiting and elevated blood glucose (BG). Emesis occurred up to 6 times daily and started 2 days prior to hyperglycemia. He was unable to correct BG with rapid acting insulin. Moderate urine ketones were present. He denied symptoms of diarrhea, fever, sore throat, runny nose or cough and reported adherence to insulin regimen. Physical exam was remarkable for dry mucous membranes and mild epigastric tenderness. Lab evaluation showed BG of 268 (70-110mg/dL), sodium 133 (135-145 mmol/L), potassium 3.6 (3.5- 5.1 mmol/L), chloride 95 (98-107 mmol/L), bicarbonate 22 (22-32 mmol/L), creatinine 0.8 (0.6–1.2 mg/dL), Anion gap 16, beta-hydroxybutyrate 3.38 (<0.27 mmol/L). He had normal white blood cell count and infectious work up was unremarkable. The patient was started on continuous IV fluids and was managed with intermittent subcutaneous rapid acting insulin in addition to basal insulin. After anion gap closure he was transitioned to his home doses of insulin. Prior to discharge, the patient discretely asked about the effects of smoking marijuana on BG and subsequently disclosed he had increased his use of marijuana recently. Discussion Diabetic keto-alkalosis may present as a result of recurrent vomiting that leads to gastric acid loss. Cannabis use has been linked to an increased risk of diabetic keto-alkalosis. The underlying mechanism is hypothesized to be related to cannabis effects on the stomach causing delayed gastric emptying and leading to cyclic nausea and vomiting. One study conducted to investigate acid-base parameters seen in atypical DKA in Type 1 Diabetes referred to this as "Hyperglycemic Ketosis due to Cannabis Hyperemesis Syndrome" (HK-CHS) recommending obtaining urine drug screen in patients with atypical DKA 1 . Attention should be drawn to this phenomenon as cannabis use has grown with its legalization in many states. Individuals with T1D presenting with ketosis but normal or elevated pH and/or serum bicarbonate may confuse clinicians and delay proper diagnosis. When the patient does not disclose cannabis use voluntarily, taking a thorough social history is critical to making the correct diagnosis. Reference: 1. Akturk HK, Snell-Bergeon J, Kinney GL, Champakanath A, Monte A, Shah VN. Differentiating diabetic ketoacidosis and hyperglycemic ketosis due to cannabis hyperemesis syndrome in adults with type 1 diabetes. Diabetes Care 2021 December 8,: dc211730 Presentation: No date and time listed

Medical Cannabis in Canadian Schools: A Scoping Review of Existing Policies.

Objective: An increasing number of children and youth in Canada are taking medical cannabis for complex medical conditions. While they deserve safe and consistent access to pharmacotherapy throughout the day, administrative policies on cannabis use in schools are inconsistent. A scoping review identified policies and publications associated with medical cannabis in Canadian schools. Methods: Five databases (Scopus, PubMed, CINAHL, EMBASE, and Web of Science) were searched to identify scientific literature. Legislation in each province and territory and Ministry of Education webpages were reviewed for pertinent laws and policies regarding cannabis use in schools. Results: The scientific search resulted in 1289 articles. The five included articles pertain to implications for school nurses in the United States, which are not relevant to the Canadian context. A search of Ministry of Education websites identified only one policy with information regarding medical cannabis in schools (from Ontario). Federal legislation (the Cannabis Act) does not specifically address medical cannabis in schools, and there is a lack of consistency in terminology and clarity within provincial and territorial laws. All provinces and territories prohibit smoking and vaping of cannabis on school property and some provinces prohibit any method of cannabis consumption. Conclusions: In Canada, there is a lack of guidance for medical cannabis administration, storage, and disposal in schools, with some policies explicitly prohibiting this type of treatment. This shifts the burden to families to individually create plans school by school. A federally harmonized approach to supporting children who take cannabis for medical purposes ought to be explored.

UHPLC-MS-MS Determination of THC, CBD, and their Metabolites in Whole Blood of Light Cannabis Smokers.

"Light cannabis" is a product legally sold in Europe with Δ9-tetrahydrocannabinol (THC) concentration lower than 0.2% and variable cannabidiol (CBD) content. In this study, we aimed to assess the time-courses of THC and metabolites (11-nor-9-carboxy-THC and 11-hydroxy-THC) and CBD and metabolites (CBD-7-oic acid, 7-hydroxy-CBD, 6α-hydroxy-CBD, and 6β-hydroxy-CBD) in whole blood of 10 healthy participants after smoking one or four light cannabis cigarettes (0.16% THC and 5.8% CBD). Blood samples were collected 0.5 to 4 h after administration. Blood analysis was performed by reversed-phase ultra-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS-MS) in multiple reaction monitoring mode, after glucuronide hydrolysis and liquid-liquid extraction in basic and acidic conditions. The method was validated following the most recent guidelines in toxicology: the method was linear, accurate, precise, and sensitive (lower limits of quantification ranged from 0.005 to 0.01 ng/mL); carryover, matrix effect, recovery, process efficiency, and dilution integrity were also assessed. As previously reported, the main metabolites of THC were THC-COOH, then 11-OH-THC, and the main metabolites of CBD were 7-OH-CBD, then 7-COOH-CBD. The time of first collection, which likely occurred after the maximal concentration of most of the analytes, and the short monitoring time, up to 4 h after smoking, limited the evaluation of the pharmacokinetic parameters.

Influence of personality on acute smoked cannabis effects on simulated driving.

A recent study of the impact of smoked cannabis on simulated driver behavior demonstrated a reduction in mean speed after smoked cannabis. Previous research identified an association between personality and individual differences and acute drug effects. The present study examined the impact of personality on the reduction in mean speed after smoking cannabis under single- and dual-task driving conditions originally reported by Brands et al. (2019). Sixty-one participants randomly assigned to the active drug condition completed a battery of self-report questionnaires measuring various personality constructs and subsequently operated a driving simulator before and 30 min after smoking a 12.5% Δ9-tetrahydrocannabinol (THC) cigarette. Linear regression modeling tested the influence of self-reported driving errors, lapses, and violations, driver vengeance, psychological distress, impulsivity, and sensation seeking on the reduction in speed after smoking cannabis. After adjusting for the influence of sex, blood THC concentration, and predrug mean speed, impulsivity was a significant predictor of change in speed under both single- (β = -.45, t = -3.94, p < .001) and dual- (β = -.35, t = -2.74, p = .008) task driving conditions after cannabis. Higher trait impulsivity was significantly associated with greater reductions in driving speed after cannabis use, which may reflect greater sensitivity to drug effects and a stronger compensatory response. Further multidisciplinary study, including neurochemical, genetic, and psychological components, would be beneficial in helping to better understand how impulsivity and other personality or individual differences may impact the effects of cannabis on driver behavior and performance. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

S1729 Drug-Induced Pancreatitis: Meth, Cannabis, or Meth-Laced Cannabis?,

Introduction: Drug-induced pancreatitis (DIP) is a rare entity with a 0.1 to 2% incidence of acute pancreatitis cases. Methamphetamine is a serotonergic drug used as a stimulant. It has infrequently been observed to cause pancreatic and hepatic damage due to its keen vasoconstrictive properties. Cannabis in its recreational form has also been linked with drug-induced pancreatitis. We report a 36-year-old female who presented with findings of acute pancreatitis revealing a drug-induced etiology. Case Description/Methods: The patient is a 36-year-old previously healthy female who presented with diffuse, sudden in onset abdominal pain, radiating to the back, aggravated with food without alleviating factors of 3 days duration. She reported nausea on the first day of her pain along with a single episode of nonbilious vomiting that had self-subsided. Social history was remarkable for smoking marijuana since her teenage years unremarkable for alcohol and tobacco use. She reported resorting to street, methamphetamine laced marijuana, the past month. The patient was vitally stable with a physical exam remarkable for epigastric and left lower quadrant tenderness with negative peritoneal signs. Laboratory tests showed elevated lipase, amylase, and CRP with normal liver function tests, hematocrit, BUN, bilirubin, triglycerides, and phosphocalcium balances. Ultrasound was done corroborating the absence of obstruction. Computed tomography (CT) abdomen was subsequently performed showing irregular contour of the pancreatic margins, blurring of peripancreatic fat planes, soft-tissue stranding, and trace-free fluid at the pancreatic body and tail without bile duct dilatation. Serological survey for mumps virus, cytomegalovirus (CMV), epstein barr virus (EBV), and human immunodeficiency virus (HIV) was negative. Anti-nuclear antibodies (ANA), neutrophil anti-cytoplasmic antibody (ANCA), and serum Ig G4 were also negative. She was diagnosed with mild acute pancreatitis with the culprit agent being methamphetamine-laced cannabis. The patient was followed up 3 months after agent cessation with marked symptomatic improvement and unremarkable lab work. Discussion: This case highlights that methamphetamine might also be the precipitating cause of pancreatitis in street marijuana-associated pancreatitis cases. Drug-induced pancreatitis is often challenging because there are no unique clinical characteristics to distinguish drugs from other etiologies, let alone the possibility of identifying one potential drug versus another.

RECREATIONAL NITROUS OXIDE INHALATION AS AN UNUSUAL CAUSE OF SPONTANEOUS PNEUMOMEDIASTINUM AND PNEUMORRHACHIS SECONDARY TO BAROTRAUMA

RECREATIONAL NITROUS OXIDE INHALATION AS AN UNUSUAL CAUSE OF SPONTANEOUS PNEUMOMEDIASTINUM AND PNEUMORRHACHIS SECONDARY TO BAROTRAUMA

S547 Rising Inpatient Utilization and Costs of Cannabis Hyperemesis Syndrome Hospitalizations in Massachusetts Following Cannabis Legalization

Introduction: As cannabis legalization has become widespread, we sought to describe the demographics, inpatient utilization, and cost of services among patients hospitalized for cannabinoid hyperemesis syndrome (CHS) predating and postdating cannabis legalization in Massachusetts. Methods: We performed a retrospective cohort study of patients admitted to Tufts Medical Center in Boston, Massachusetts (MA) with CHS pre- and post-Dec 15, 2016, the date of cannabis legalization in MA. We examined the demographic and clinical characteristics of admitted patients as well as utilization of hospital services including length of stay, laboratory services, antiemetic drugs, intravenous fluids, endoscopies, imaging, gastroenterology consulting services and intensive care requirements both pre- and post- legalization. We also estimated inpatient cost pre- and post- legalization. Results: We identified 63 patients admitted between 2012-2020 with CHS across 72 hospitalizations, with more admissions post-legalization (n=57) than pre-legalization (n=15). Patient demographics were similar pre- and post- cannabis legalization, with a mean age of 33, 52% identifying as female, and the majority smoking cannabis as the primary route of administration. Utilization of hospital resources increased post-legalization for CHS, with increased length of stay (3 days vs 1 day, p< .005) and increased anti-emetic use (3 days vs 1 day, p< 0.05) compared to pre-legalization, with multivariate linear regression confirming that post-legalization admissions were independently associated with increased length of stay (B=5.35, p< 0.05). The mean cost of hospitalization per patient post-legalization was significantly higher than for pre-legalization ($18,714 vs $7,460, p< .0005), with intravenous fluid administration and endoscopy costs significantly increased post-legalization (p< 0.05). On multivariate linear regression, hospitalization for CHS during post-legalization significantly predicted increased costs (B=10,131.25, p< 0.05). (Table) Conclusion: In the post-legalization era of cannabis in Massachusetts, we found increased hospitalizations due to CHS, with a concomitant increase length of hospital stay and total cost per patient. As cannabis use increases, the recognition, measurement, and cost of the deleterious effects are necessary to incorporate into future practice strategies and public health policy development. Table 1. - Demographics Pre-legalization (n=12 patients) Post-legalization(n=51patients) p-value Number of hospital admissions 15 57 NA Female gender n, (frequency) 4 (33.3) 29 (50.9) 0.25 Age mean, (st dev) 35.5 (11.5) 32.9 (13.5) 0.32 Cannabis type used n, (frequency) Smoking 6 (50.0) 31 (60.8) 0.53 Vaping 0 2 (3.9) - Edibles 0 2 (3.9) - More than one type 0 1 (2.0) - Not reported 6 (50.0) 15 (29.4) - Cannabis use frequency n, (frequency) Less than daily 0 9 (17.6) 0.19 At least daily 3 (25.0) 24 (47.1) 0.21 Multiple times daily 3 (25.0) 8 (15.7) 0.42 Unknown 6 (50.0) 10 (19.6) - Utilization of Services Pre-legalization (n=15 hospitalizations) Post-legalization (n=57 hospitalizations) p-val Length of inpatient stay, days median, (IQR) 1.0 (1.0-2.0) 3.0 (1.0-4.0) < 0.005 Cannabis urine screen positivity n, (frequency) 10 (66.7) 37 (64.9) 1.0 Cannabis urine screen not performed n, (frequency) 4 (26.7) 16 (28.1) 1.0 Basic metabolic panel, days median, (IQR) 2 (1.0-2.8) 2.0 (0.25-3.0) 0.79 Antiemetics, days median, (IQR) 1.0 (1.0-2.5) 3.0 (2.0-4.0) < 0.05 Intravenous fluids, days median, (IQR) 1.0 (1.0-2.0) 1.0 (1.0-2.0) 0.32 Endoscopies performed n, (frequency) 3.0 (20.0) 14.0 (24.5) 1.00 Imaging studies performed n, (frequency) 12.0 (80.0) 43.0 (75.4) 1.00 GI consults n, (frequency) 5.0 (33.3) 26.0 (45.6) 0.57 ICU-level care needed days median, (IQR) 0.0 9.0 (15.8) 0.19 Cost of Services Pre-legalization (n=15 hospitalizations) Post-legalization (n=57 hospitalizations) p-value Mean inpatient charge $7460 $18,714 < 0.0005 IVF charges, mean $551 $745 < 0.05 Endoscopy charges, mean $1512 $2360 < 0.05

Animal evidence considered in determination of cannabis smoke and Δ9 -tetrahydrocannabinol as causing reproductive toxicity (developmental endpoint); Part I. Somatic development.

On December 11, 2019, California's Developmental and Reproductive Toxicant Identification Committee (DARTIC) met to consider the addition of cannabis smoke and Δ9 -THC to the Proposition 65 list as causing reproductive toxicity (developmental endpoint). As the lead state agency for implementing Proposition 65, the Office of Environmental Health Hazard Assessment (OEHHA) reviewed and summarized the relevant scientific literature in the form of a hazard identification document (HID). Here we provide reviews based on the HID: shortened, revised, and reformatted for a larger audience. While the HID included both human and animal data, this set of three reviews will highlight the animal-derived data pertaining to somatic development (Part I), neurodevelopmental effects (Part II), and proposed neurodevelopmental mechanisms of action (Part III). Endogenous cannabinoids (eCBs) and their receptors serve many critical functions in normal development. Δ9 -THC can interfere with these functions. Mechanistic studies employed techniques including: blocking Δ9 -THC binding to endocannabinoid (EC) receptors, inhibiting Δ9 -THC metabolism, and/or using animals expressing knockout mutations of EC receptors. Apical somatic effects of cannabis smoke or Δ9 -THC reported in whole animal studies included decreases in offspring viability and growth. Mechanistic studies discussed in Part I focused on Δ9 -THC effects on early embryos and implantation, immune development, and bone growth. In reaching its decision to list cannabis and Δ9 -THC as a developmental toxicant under California's Proposition 65, the DARTIC considered biological plausibility and the consistency of mechanistic information with effects reported in human and whole animal studies.

Animal evidence considered in determination of cannabis smoke and Δ9 -tetrahydrocannabinol as causing reproductive toxicity (developmental endpoint): Part III. Proposed neurodevelopmental mechanisms of action.

This review summarizes the most common potential pathways of neurodevelopmental toxicity due to perinatal exposure to Δ9 -tetrahydrocannabinol (Δ9 -THC) that lead to behavioral and other adverse outcomes (AOs). This is Part III in a set of reviews highlighting the animal-derived data considered by California's Developmental and Reproductive Toxicant Identification Committee (DARTIC) in 2019. The Hazard Identification Document (HID) provided to the DARTIC included a summary of human, whole animal, and mechanistic data on the neurodevelopmental toxicity of cannabis smoke and Δ9 -THC. The literature search for mechanistic data has been updated through 2020. We focus on mechanistic pathways relating to behavioral and other neurodevelopmental outcomes of perinatal exposure to Δ9 -THC. The endocannabinoid system (EC system) plays a crucial role in many processes involved in neurodevelopment and exposure to Δ9 -THC can alter these processes. Whole animal studies report changes in cognitive ability, behavior, and motor function after prenatal exposure to Δ9 -THC. Findings from mechanistic studies add to this evidence and further provide information regarding the pathways leading to these outcomes. Neuromechanistic studies can bridge the gaps between molecular initiating events and apical neurodevelopmental endpoints caused by a chemical. They offer insight into potential alterations in the same pathways by other chemicals that can also result in AOs. Studies of cannabinoid receptor agonist-induced molecular alterations and provide deep biological plausibility at the mechanistic level for the cognitive, behavioral, and motor impairments observed in animal studies after perinatal exposure to Δ9 -THC.

Frequent Cannabis Smoking and Association with Prediabetes and Diabetes in Early Adulthood

Background: Cannabis use in young adulthood has been linked with increased risk of prediabetes later in life. However, many previous studies have only used fasting blood samples to determine risk for type 2 diabetes (T2D), which may not detect early changes in glucose homeostasis. The objective of this study was to determine the association between cannabis use and risk for prediabetes and T2D in young adults using several measures of glucose homeostasis, including an oral glucose tolerance test (OGTT). Methods: The Meta-CHEM study is a subset (N=84) of overweight and obese young adults aged 22–25 years from the Children&amp;#x27;s Health Study (CHS). Participants underwent a single clinical visit which included a 2-hour OGTT and questionnaire about cannabis smoking habits in the past year. Participants were classified as non-smokers, light cannabis smokers (smoke &amp;#x3c;once a week), and heavy cannabis smokers (smoke &amp;#x3e;once a week). Those smoking more than one cigarette in the past week were excluded from the study. Participants were classified as having prediabetes or T2D if they had a HbA1c &amp;#x3e;5.6%, fasting glucose &amp;#x3e;99 mg/dL, and/or 2-hour OGTT glucose &amp;#x3e;139 mg/dL. Logistic regression was used to assess the associations between cannabis smoking habits and metabolic outcomes after adjusting for age, sex, education, body mass index, Hispanic ethnicity, physical activity, and alcohol consumption. Results: 52 (62%) participants were non-diabetic, 28 (33%) had pre-diabetes, and 4 (0.05%) had T2D. 25 (30%) participants were nonsmokers, 47 (56%) were light cannabis smokers, and 12 (14%) were heavy cannabis smokers. The odds of having prediabetes or T2D was 7.3 times higher among heavy smokers (95% CI: 0.94, 7.7), and 1.5 times higher among light smokers (CI: 0.43, 6.0) than nonsmokers (P-value for trend = 0.03). Conclusion: Cannabis use in overweight and obese young adults was significantly associated with risk of having prediabetes or T2D.

Animal evidence considered in determination of cannabis smoke and Δ9 -tetrahydrocannabinol (Δ9 -THC) as causing reproductive toxicity (developmental endpoint); Part II. Neurodevelopmental effects.

This review focuses on neurodevelopmental effects observed in animal studies of cannabis smoke and Δ9 -THC. Effects in offspring after preconceptional, prenatal, or perinatal exposure to cannabis smoke or Δ9 -THC were considered. Locomotor and exploratory behavior effects were noted in rats. Cognitive effects observed included impairment of memory and learning, attention deficits, time taken to complete tasks (rats) and alterations in response to visual stimuli (rats/monkeys). Emotionality was observed in rodents as an increase in separation-induced ultrasonic vocalizations, reduced social interaction and play behavior, and increased generalized anxiety. Increased rate of acquisition of morphine self-administration and/or enhanced sensitivity towards the rewarding effects of morphine or heroin were observed in adult rats prenatally exposed to Δ9 -THC. Expression of cannabinoid receptors was examined in rodent studies along with behavioral parameters. Altered mRNA levels of genes relevant to synaptic plasticity in the nucleus accumbens (the brain region associated with compulsivity, addiction vulnerability, and reward sensitivity) were noted. Findings in zebrafish supported effects in mammalian models. Neurochemical effects on specific brain regions and neurotransmitter systems seen in these animal studies appear to impact cognitive function, motor activity, and drug sensitivity. Mechanistic studies provided evidence for the biological plausibility of effects observed. Observations from animal studies of changes in motor behavior, cognitive performance, emotionality and susceptibility to drug sensitivity later in life were among the findings from animal and human studies considered by California's Developmental and Reproductive Toxicant Identification Committee, in concluding that cannabis smoke and Δ9 -THC are developmental toxicants.

Adverse Effects of Cannabinoids and Tobacco Consumption on the Cardiovascular System: A Systematic Review.

With the recent legalization of marijuana in several countries for recreational use, a controversial belief is spreading about it being "safe". In this systematic review, we decided to investigate this belief and present the adverse effects of marijuana and tobacco smoking on the cardiovascular system.We carried out an electronic search on databases including PubMed, PubMed Central, and Medline. Medical Subject Headings (MeSH) terms and different keywords were used for data collection. We included studies published in the last 10 years that were in English. All types of study subjects were accepted. Grey literature, books, case reports and case series, overlapping and duplicate studies, and studies older than 10 years were excluded.In this review, we included 18 studies, which we then separated into the "tobacco and cardiovascular disease" arm and the "cannabinoids and cardiovascular disease" arm. We had 11 and seven studies for each of the arms, respectively. The types of articles included in this review were traditional and systematic reviews and meta-analyses.After reviewing all the data included in this article, we found out that cannabinoid consumption has a more devastating effect on the cardiovascular system when compared to tobacco. The shocking fact was that in several cases, deadly adverse effects were observed in patients within a few hours after consumption or even during their first time using cannabinoids.

MTF: Cannabis use with vaping goes up, cannabis smoking down

More and more high schoolers are using marijuana by vaping, and fewer are using it by smoking, according to a recent study of the Monitoring the Future (MTF) survey conducted by the National Institute on Drug Abuse (NIDA). So the next time you hear someone say that marijuana use in teens is going down, ask them about the route of administration.

Impact of cannabis-infused edibles on public safety and regulation.

Popularity of cannabis-infused products has bloomed since legalization for recreational use of marijuana started. Consumption of cannabis edibles has steadily increased, as restrictions on recreational cannabis smoking have become tighter. This phenomenon enhanced the possibility of these products crossing the state line. The most psychoactive component of cannabis, ∆9-tetrahydrocannabinol (THC) is infused in "edibles" and linked to physiological and psychological effects. Consumers unfamiliar with these edibles may mistake them for non-THC containing products, causing unintended use or overconsumption. In addition, these cannabis-infused edibles are posing significant health risks. The FDA has recognized the potential dangers and recommended that cannabis remain as a Schedule I substance and illegal at the federal level. However, states maintain control of determining the legality of cannabis related products, and creating guidelines distinguishing cannabis edibles from the non-cannabis containing products. Recently, the State of Maine offers a blueprint for edible regulation that should be implemented in all states that are considering or have legalized marijuana.

Vaping cannabis among teens is up, smoking cannabis among teens is down

More and more high schoolers are using marijuana by vaping, and fewer are using it by smoking, according to a recent study of the Monitoring the Future (MTF) survey conducted by the National Institute on Drug Abuse (NIDA). And use of other substances, particularly nicotine and binge drinking of alcohol, is strongly associated with vaping cannabis.

When Hotel Guests Complain About Tobacco, Electronic Cigarettes, and Cannabis: Lessons for Implementing Smoking Bans.

We analyzed reviews on tripadvisor.com from a random sample of N = 477 hotels in ten large cities in the US to examine how well existing policies protect guests from exposure to tobacco, electronic cigarette, and cannabis (TEC) smoke. We examined the association between complaints per 100 reviews with hotel smoking policies, star rating, cost, brand, and location. Of all TEC complaints, 80% were associated with thirdhand smoke residue lingering in hotels from previous guests. Compared to the hotel brands with the best records, the two worst-performing brands had 3.4- and 3.6-times higher complaint rates (P < .001). Hotels with ≤2-star ratings had twice the complaints as higher-rated hotels (P < .001). Compared to 100% smokefree hotels, those offering designated smoking rooms had a 35% higher rate of complaints (P < .05). The success of some hotel brands demonstrates it is feasible to protect guests by fully committing to, implementing, and enforcing 100% smokefree building policies.

Association between ABCB1 rs2235048 Polymorphism and THC Pharmacokinetics and Subjective Effects following Smoked Cannabis in Young Adults

Genetic influences on acute responses to psychoactive drugs may contribute to individual variability in addiction risk. ABCB1 is a human gene that encodes P-glycoprotein, an ATP-dependent efflux pump that may influence the pharmacokinetics of delta-9-tetrahydrocannabinol (THC), the primary psychoactive component of cannabis. Using data from 48 young adults (aged 19–25 years) reporting 1–4 days of cannabis use per week who completed a placebo-controlled human laboratory experiment, we tested the hypothesis that the rs2235048 polymorphism of ABCB1 would influence acute responses to smoked cannabis. C-allele carriers reported on average greater frequency of weekly cannabis use compared to the TT genotype carriers (TC/CC mean ± SEM = 2.74 ± 0.14, TT = 1.85 ± 0.24, p = 0.004). After smoking a single cannabis cigarette to their desired high, C-allele carriers had higher area-under-the-curve (AUC) of both THC metabolites (11-OH-THC TC/CC = 7.18 ± 9.64, TT = 3.28 ± 3.40, p = 0.05; THC-COOH TC/CC = 95.21 ± 116.12, TT = 45.92 ± 42.38, p = 0.043), and these results were impact by self-reported ethnicity. There were no significant differences in self-reported subjective drug effects except for a greater AUC of visual analogue scale rating of drug liking (TC/CC = 35,398.33 ± 37,233.72, TT = 15,895.56 ± 13,200.68, p = 0.017). Our preliminary findings suggest that further work in a larger sample should investigate whether human ABCB1 influences cannabis-related phenotypes and plays a role in the risk of developing a cannabis use disorder.

Drugs of Misuse: Focus on Vascular Dysfunction.

Common drugs of misuse, including cannabis, opioids, stimulants, alcohol, and anabolic steroids, have strikingly disparate acute and chronic vascular effects, leading to a wide range of clinical cardiovascular presentations. Acute cannabis smoking has been associated with increased risk for myocardial infarction and ischemic stroke in otherwise healthy young people. However, it remains uncertain if people who exclusively smoke cannabis have increased risk for accelerated atherosclerosis similar to that found in people who exclusively smoke tobacco cigarettes. Cocaine and methamphetamines, both stimulants, increase risk for stroke, myocardial infarction, aortic dissection, and accelerated atherosclerosis, but only methamphetamine use is strongly linked to pulmonary hypertension. Chronic alcohol use is strongly associated with chronic hypertension and hemorrhagic stroke, but perhaps confers a lower risk for myocardial infarction. Finally, anabolic steroid use, presumably through adverse effects on circulating lipids and the hematopoietic system, is associated with increased risk for accelerated atherosclerosis and myocardial infarction. Physicians, especially cardiologists, emergency medicine, and internal medicine physicians, should be familiar with the short- and long-term vascular consequences of use of these substances, thereby ensuring appropriate, specific, and informed counselling and treatment.

Outcomes of lung transplantation from donors with a history of substance abuse

ObjectiveThe study objective was to determine whether donor substance abuse (opioid overdose death, opioid use, cigarette or marijuana smoking) impacts lung acceptance and recipient outcomes. MethodsDonor offers to a single center from 2013 to 2019 were reviewed to determine if lung acceptance rates and recipient outcomes were affected by donor substance abuse. ResultsThere were 3515 donor offers over the study period. A total of 154 offers (4.4%) were opioid use and 117 (3.3%) were opioid overdose deaths. A total of 1744 donors (65.0%) smoked cigarettes and 69 donors (2.6%) smoked marijuana. Of smokers, 601 (35.0%) had less than 20 pack-year history and 1117 (65.0%) had more than 20 pack-year history. Substance abuse donors were younger (51.5 vs 55.2 P < .001), more often male (65.6 vs 54.8%, P < .001), more often White (86.2 vs 68.7%, P < .001), and had hepatitis C (8.3 vs 0.8%, P < .001). Donor acceptance was significantly associated with brain dead donors (odds ratio, 1.56, P < .001), donor smoking history (odds ratio, 0.56, P < .001), hepatitis C (odds ratio, 0.35, P < .001), younger age (odds ratio, 0.98, P < .001), male gender (odds ratio, 0.74, P = .004), and any substance abuse history (odds ratio, 0.50, P < .001), but not opioid use, opioid overdose death, or marijuana use. Recipient survival was equivalent when using lungs from donors who had opioid overdose death, who smoked marijuana, or who smoked cigarettes for less than 20 patient-years or more than 20 patient-years, and significantly longer in recipients of opioid use lungs. There was no significant difference in time to chronic lung allograft dysfunction for recipients who received lungs from opioid overdose death or with a history of opioid use, marijuana smoking, or cigarette smoking. ConclusionsDonor acceptance was impacted by cigarette smoking but not opioid use, opioid overdose death, or marijuana use. Graft outcomes and recipient survival were similar for recipients of lungs from donors who abused substances.