Cannabis Basics

Cannabis chemistry is complex. The following information is meant as a broad, elite, evidence-based overview of cannabis chemistry. Recognize that there are subtleties and nuances to the presented information that this overview cannot adequately capture. Cannabis research is rapidly evolving. The information presented is based on our current understanding and is updated accordingly. Readers are encouraged to reference the bibliography at the end for more details.

Cannabis Plant

The cannabis plant contains over 550 chemical compounds. The compounds that interest most people are as follows:

Cannabinoids

The two best-studied cannabinoids are:

Delta-9-tetrahydrocannabinol (THC)

  • Is psychoactive (works on brain chemistry) and produces much of the intoxicating effect or “the high” associated with cannabis
  • Known to contribute to various therapeutic benefits

Cannabidiol (CBD)

  • No intoxicating effect
  • Known anxiolytic and therapeutic benefits. Needs more study
  • May decrease the intoxicating effects of THC

Other cannabinoids

There are over 100 identified cannabinoids. The cannabinoids that have received most attention include:

Delta-8-tetrahydrocannabinol (▲8)
  • Psychoactive in humans
  • Synthetically derived from CBD since the 1940s
  • Regulatory status is controversial
    • Does not qualify for legal definition of marijuana under the Agriculture Improvement Act of 2018 (the “Farm Bill), but still a controlled substance as a synthetic cannabinoid
    • 14 states have blocked the sale of ▲8 due to the lack of research into the compound’s psychoactive effect
    • Quasi-legal status has increased sales, including where THC ▲9 is not permitted
  • ▲8 v. ▲9
    • Same chemical makeup with different structures (ie, THC isomers)
    • Similar pharmacology
    • Available research suggests that ▲9 may be more potent, but sufficient clinical data is lacking
Cannabigerol (CBG)
  • Non-Psychoactive
  • Not thought to act at the same receptors as THC and CBD
    • May modulate the endocannabinoid system itself
  • Potential therapeutic applications for nausea, glaucoma, and colitis. Potential anxiolytic effects.
Cannabinol (CBN)
  • A product of THC degradation/oxidation
  • Shows weak affinity to CB1-receptor, the target of THC’s effects
    • Unclear if CB2-receptor agonist or inverse agonist
  • Some mouse-model evidence in ALS, otherwise weakly psychoactive

Terpenes

Terpenes are naturally occurring organic compounds. They are responsible for the aromas and flavors in cannabis. Terpenes are also found in other plants. Research is being conducted to determine if terpenes influence the intoxicating effects of cannabinoids in whole-plant products. This is partly the reason that different cannabis products with the same THC and CBD content can have differing effects. Current research of terpenes suggests that terpenes have therapeutic properties including anti-inflammatory, analgesic, antiviral, antioxidant, and anxiolytic. However, this research regarding terpenes is in its early stages. Over 100 terpenes have been identified in cannabis. Increased studies are necessary to further understand the health impacts of terpenes.

Some commonly referenced terpenes include: b-caryophyllene, b-pinene, Humulene, Limonene, Linalool, and Myrcene.

Sativa or Indica?

These colloquial terms are used to describe the expected effects of a given product: Sativa products are purported to have energizing, uplifting, and creative effects (a “mind high”), while Indica products tend to be sedating, and relaxing physically and mentally (a “body high”). While these terms are commonly used, it is difficult to obtain a pure indica or sativa strain. This is due to the decades of hybrid breeding using original sativa and indica strains to get certain desired mental and physical effects. These breeders have been quite effective. Therefore it is necessary that research be conducted to see if it is likely that the cannabinoid and terpene profiles account for the observed differences in effects.

The degree to which a product will have energizing, intoxicating, or relaxing effects is most likely determined by the relative amounts of THC and CBD and its terpene profile.

The endocannabinoid system is a complex neuromodulator system that largely serves to promote homeostasis. Researchers, scientists and doctors continue to work on fully understanding the endocannabinoid system. It is thought to play a role in regulating a wide range of processes, such as:

  • Pain
  • Appetite and digestion
  • Inflammation and immune responses
  • Mood
  • Memory
  • Reproduction and fertility
  • Motor control
  • Cardiovascular function
  • Liver function
  • Bone remodeling and growth
  • Reproductive system function

The endocannabinoid system is comprised of three parts:

  1. Cannabinoid receptors
  2. Endocannabinoids (endogenous cannabinoids)
  3. Enzymes responsible for the formation and degradation of the endocannabinoids

Cannabinoid receptors

The effects of cannabinoids are primarily mediated through two receptors: cannabinoid receptor type 1 and 2 (CB1 and CB2)

CB1 receptors
  • Found in particularly high levels in the cortex, basal ganglia, hippocampus, and cerebellum
  • Also found in many extra-neural sites such as adipose tissue, liver, testis, eye vascular endothelium, and spleen
  • ▲9-tetrahydrocannabinol (▲9-THC), the main psychotropic cannabinoid of cannabis sativa, is a partial agonist at CB1
  • CB1 mediates most of the psychotropic effects of ▲9-THC
  • Cannabidiol (CBD) has many known targets. Among them, CBD is a partial inverse agonist/antagonist and negative allosteric modulator at CB1. This is why CBD is thought to potentially attenuate some of the negative effects of THC. However, findings from studies have been inconsistent, with some even showing that CBD can enhance the effects of THC.
CB2 receptors
  • Typically considered the “peripheral” cannabinoid receptor, however functional CB2 receptors are present in the central nervous system (CNS)
  • CB2 receptors are found peripherally in the circulating immune cells, the spleen, and on macrophage-derived cells including osteocytes, osteoclasts, and hepatic Kupffer cells,
  • CB2 receptors are upregulated in neuroinflammatory conditions
  • Primarily expressed postsynaptically, as opposed to the presynaptic expression of most CB1 receptors
  • ▲9-THC is a partial agonist at CB2
  • CBD is a partial inverse agonist/antagonist at CB2
  • ▲9-THC and CBD binding at CB2 is thought to lead to anti-inflammatory effects

There are other receptors that interact with endogenous and exogenous cannabinoids:

  • Transient receptor potential cation channel subfamily V member (TRPV1)
    • Involved in synaptic transmission and pain regulation
  • G protein coupled receptor 55 (GPR55)
    • Sometimes referred to as the 3rd cannabinoid receptor (CB3)
    • Expressed in the CNS and immune/gastrointestinal (GI) systems
    • Linked to bone development and cancer cell proliferation
  • Peroxisome proliferator-activated receptor family (PPAR-a, g)
    • Expressed on bone, muscle, liver, and heart
Endocannabinoid receptor signaling
  • 2-AG primarily works as a retrograde signaling molecule
    • Activation of a receptor, or increased calcium, triggers the release of 2-AG that travels to presynaptic terminals and binds to CB1 receptors
    • In most cases, presynaptic CB1 receptor then suppresses the release of neurotransmitters by inhibiting voltage gated calcium channels or inhibiting adenylyl cyclase and the cAMP/PKA pathway. In at least one case, presynaptic CB1 can enhance the release of the neurotransmitter glutamate by regulating the presynaptic secretory machinery.
  • Anandamide primarily acts as a volume transmitter, regulating the activity of cells at a short distance from its sites of production.

Endocannabinoids (endogenous cannabinoids)

Anandamide (AEA)
  • AEA is a partial agonist for CB1 receptors, with high affinity, and largely mimics THC bindings
  • Has little affinity for CB2 receptors
  • Also interacts with TRPV1 and GPR55 receptors
  • AEA is involved in the regulation of stress-coping responses, sociability, and pain.
  • CBD has been shown to inhibit the uptake of AEA and inhibit AEA degradation, and thus increase AEA levels
2-Arachidonoylglycerol (2-AG)
  • 2-AG is a full agonist at both CB1 and CB2 receptors, with moderate to low affinity
  • More abundant in the CNS than AEA
  • 2-AG is thought to be involved in a wide array of functions, such as emotion, cognition, energy balance, pain sensation, and neuroinflammation.

Enzymes responsible for endocannabinoid synthesis and degradation

  • Endocannabinoids are synthesized on-demand in response to receptor activation or increased intracellular calcium concentration
  • After endocannabinoids are taken up by cells, they can be degraded via hydrolysis and/or oxidation
  • AEA is degraded by fatty acid amide hydrolase (FAAH)
  • 2-AG is primarily degraded by monoacylglycerol lipase (MAGL)

THC

The amount of THC found in a cannabis product defines its potency. Over the past several decades, the potency of cannabis has increased several-fold, from the ditch-weed of the 1970s to the current dispensary hybrids. There is no clear amount of THC that is considered a single “dose”. Some states have standardized the definition of a single dose as 5-10mg of THC. The National Institute of Health, for study and research purposes, set a dose of THC at 5mg.

Several things complicate cannabis dosing, including, variations in bioavailability across formulations and across individuals, and by the complex interaction among the different compounds present in whole plant and plant extract products. Individuals also develop tolerance with regular use which affects maximum dose. Recent consensus and expert recommendations for dosing medical cannabis for chronic pain treatment recommend a CBD-predominant variety, a starting THC dose of 0.5 to 3 mg/day, and titration to a maximum of 30 to 40 mg/day.

In studies

Nabiximols is an oromucosal spray which has been effective in improving neuropathic pain in some studies. A single dose of nabiximols contains 2.7 mg THC and 2.5 mg CBD. Participants in these studies used an average of 25 mg or less of THC over 24 hours.

Dronabinol is a synthetic form of THC that has been FDA-approved for treatment of AIDS-related cachexia, and refractory chemotherapy-induced nausea and vomiting (CINV). The recommended starting dose is 2.5 to 5 mg daily, with a maximum divided daily dose of 20 mg THC. For CINV it can be dosed up to 15 mg/m2 at 4-6 doses daily.

Calculating the dose of THC
  • Multiply the weight of the product by the percentage of THC in the product
  • According to estimates, the average joint weighs about 0.32 to 0.66 grams, A high-potency cannabis product might contain 25% THC
    • Joint is 320 mg x 0.25 = 80 mg THC/high-potency joint
    • Joint is 660 mg x 0.25 = 165 THC/high-potency joint

Routes of administration and dose

Certain formulations and routes of administration will deliver a higher effective dose (i.e., will be more potent) than others. For instance, first-pass metabolism of ingested products yields a metabolite that is more potent than THC, and dabbing delivers a very high dose of THC. Other characteristics of use such as breath-holding after cannabis inhalation can also influence the dose delivered. See the Cannabis Formulations and Routes of Administration sections below.

Overdose potential

While lethal overdose with THC is very unlikely in humans and potentially impossible via traditional routes of administration (e.g., smoking, oral, vaping), at very high doses tachycardia, acute mental defects such as psychosis, and seizures can occur, particularly in children. Because of individual variability in tolerance to THC, what is considered a threshold dose leading to these effects is unclear. In a case series of five adults who used smoked cannabis daily, they sought emergency treatment for cannabis-induced psychosis after consuming cannabis edibles with doses equating to greater than 100mg THC.

CBD

Due to its lack of psychogenic properties, less attention has been paid to potency concerns regarding CBD. In clinical trials, CBD has been used in doses ranging from anywhere , 1mg/kg to 50mg/kg per day (1mg/kg/day is equivalent to 62mg/day using global average body mass). The recommended maximum daily dose of nabiximols contains 30mg CBD, while Epidiolex (FDA-approved CBD extra) is up to 20mg/kg/day for seizure prevention. A recent US consensus recommendation for dosing medical cannabis for chronic pain treatment recommended titrating to a maximum of 40mg/day of CBD. The Australian government Therapeutic Goods Administration categorizes a low dose range as ≤1 mg/kg/day, medium as 1 to 10 mg/kg/day, and high as 10 to 50 mg/kg/day.

Plant

  • Other Terms: Flower, bud
  • Development: The highest concentration of cannabinoids are found in the flower, not the leaf, of the female plant; topical preparations and rectal suppositories can be made with dry flower or plant extract
  • Route of Administration:

    Smoking, Vaporization, Topical Rectal

Edibles

  • Other Terms: Brownies, cookies, candy, beverages
  • Development: Typically butter or oil used to extract cannabinoids and put into a variety of edible products including beverages
  • Route of Administration:

    Oral

Tincture

  • Other Terms: Golden dragon, green dragon
  • Development: Alcohol or glycerin used to extract active ingredients*
  • Route of Administration:

    Oral, Suboral, Oromucosal

Oil

  • Other Terms: Vape cartridges, droppers
  • Development: CO2 or organic solvents used to extract active ingredients, or live resin
  • Route of Administration:

    Vaporization, Sublingual, Topical 

Resin

  • Other Terms: Hash, dry, sift, kief
  • Development: Concentrate made by mechanically separating trichomes (hair like protrusions on flower with high concentration of cannabinoids) from the plant
  • Route of Administration:

    Smoking, Vaporization

Rick Simpson Oil

  • Other Terms: RSO
  • Development: Alcohol used to make highly viscous concentrated extract
  • Route of Administration:

    Oral, Topical, Suppository

Nabiximols

  • Other Terms: Sativex™
  • Development: Pharmaceutically prepared whole plant extract in spray form; 1:1 THC:CBD concentration; approved for prescription use in many countries outside the US
  • Route of Administration:

    Oromucosal

Dab

  • Other Terms: Wax, shatter, butane hash oil (BHO)
  • Development: Ultraconcentrated extract made with solvents such as butane; very high levels of THC
  • Route of Administration:

    Dabbing (concentrate placed on very hot metal rod and inhaled)

Pharmaceutical Cannabinoids

  • Other Terms: Dronabinol (Marinol™; Syndros™), Nabilone (Cesamet™), Epidiolex™
  • Development: Dronabinol and nabilone are synthetic THC (FDA-approved for chemotherapy induced nausea/vomiting and AIDS-related cachexia); Epidiolex is a highly purified CBD plant extract (FDA-approved for the treat of two rare epilepsy syndromes
  • Route of Administration:

    Oral

*Some dispensaries have been known to sell oils extracted using CO2 or other chemicals as tinctures

Smoking

Description: Combustion of dried cannabis flower using several methods: cigarettes (joints, spliffs), pipes, water pipes (bongs)

Pharmacology

Rapid onset and peak

  • Time to peak effect (THC): 2-30 minutes (usually within 10)
  • Duration (THC): 45-180 minutes (dose dependent)
  • Distribution (THC): 90% plasma protein bound, 10% bound to red blood cells, 1% gets into the brain
  • Bioavailability:

    THC 10-40% (average 35%), CBD 11-45% (average 31%)

Cautions: Bronchial irritation; cough; sputum; production contains carcinogens; potential for adverse effects on lung function with heavy use over many years 

Vaporization (“Vaping”)

Description: Vaporization is used to heat dried flower to concentrated extract (oil, resin) and the resultant vapor is inhaled

Pharmacology

Rapid onset, peak, and duration similar to smoking

  • Time to peak effect (THC): Similar to smoking
  • Duration (THC): Similar to smoking
  • Bioavailability:

    Similar to smoking, although THC levels can vary depending on product (e.g., oil, dab, vape, cartridge

Cautions: Substantially higher blood THC concentrations achieved at a given dose than with smoking; higher risk of adverse effects in novice users; long-term lung safety is unknown; need for potentially costly equipment; potentially fatal vaping-related pulmonary illness†

Oral/Edibles

Description: Variety of edibles available; often sold in multi-dose/serving packages; beverages also fall in this category

Pharmacology

No inhalation; broad range of products; slower onset (liquids likely to be absorbed more quickly) and longer duration of action

  • Time to peak effect (THC): 1-6 hours (usually 2-4)
  • Duration (THC): Duration 3-8 hours (dose dependent)
  • Bioavailability:

    THC 4-12%, CBD 13-19%, Overall 6-20%

Cautions: Onset and peak are delayed, and effects can last many hours which makes it more difficult to titrate dose; oral metabolite of THC (11-OH-THC) may have four-fold more powerful psychoactive effect; risk of overdose; caution especially in novice users.

Dabbing

Description: Ultra -concentrated formulation placed on a hot metal implement and vapor inhaled, often through water.

Pharmacology

Can deliver very high potency with over 90% THC. Rapid onset and peak.

  • Time to peak effect (THC): Similar to smoking
  • Duration (THC): Similar to smoking
  • Distribution (THC): Similar to smoking
  • Bioavailability:

    Likely similar to smoking but no comparative data available at this time

Cautions: Very high levels of THC; risk of overdose and acute psychosis.

†In response to the outbreak of severe vaping-related pulmonary illness cases in 2019-2020, cartridges sold in dispensaries have been reformulated to remove Vitamin E Acetate, which was implicated in these cases. However, vape cartridges sold outside of dispensaries do not have the assurance and providers should advise against their use.

Cannabis-drug interactions

Cannabis has the potential to compound the sedative effects of different drug classes, including anticholinergics and CNS depressants. The sedative effect of cannabis combined with antidepressants or lithium is unpredictable.

Cannabinoids can induce or inhibit CYP enzymes and can, therefore, decrease or increase the levels of pharmacologic drugs.

For example:

  • THC may reduce levels of the following drugs: aminophylline/theophylline, clozapine, ropinirole
  • CBD may increase levels of the following drugs: clobazepam, diazepam, proton pump inhibitors, phenytoin/fosphenytoin

Since THC and CBD are substrates of different CYP enzymes, their levels can also be increased by certain drugs.

For example:

  • Boceprevir, Ritonavir, Clarithromycin, Conivaptan, Ketoconazole, Posaconazole, and Voriconazole can increase levels of CBD and THC
  • Carbamazepine, Phenobarbitol, Phenytoin, Rifampin, and St. John’s Wort can decrease levels of THC and CBD

The most important take away is that more comprehensive, thorough and specific research is necessary.

Adams, R. (1942). Marihuana: Harvey lecture, February 19, 1942. Bulletin of the New York Academy of Medicine, 18, 705-730.

Agriculture Improvement Act of 2018. U.S. Congress (2018).

Ashton CH, Moore PB, Gallagher P, Youg AH. Cannabinoids in bipolar affective disorder: a review and discussion of their therapeutic potential. J Psychopharmacol. 2005;19(3):293-300.

Australian Government; Department of Health; Therapeutic Goods Administration. Safety of low dose cannabidiol. Published 2020. Updated April 2020. Accessed Nov 23, 2022.

Bhaskar A, Bell A, Boivin M, et al. Consensus recommendation on dosing and administration of medical cannabis to treat chronic pain: results of a modified Delphi process. J Cannabis Res. 2021;3(1):22.

Boehnke KF, Clauw DJ. Cannabinoids for chronic pain: translating systematic review findings into clinical action. Annals of Internal Medicine. 2022;175(8):1191-1192.

Bowles DW, O’Bryant CL, Camidge DR, Jimeno A. The intersection between cannabis and cancer in the United States. Crit Rev Oncol Hematol. 2021;83(1):1-10.

Cuttler C, Stueder A, Cooper ZD, et al. Acute effects of cannabigerol on anxiety, stress, and mood: a double-blind, placebo-controlled, crossover, field trial. Sci Rep. 2024;14(1):16163.

El Sohly MA, Mehmedic Z, Foster S, Gon C, Chandra S, Church JC. Changes in Cannabis potency over the last 2 decades (1995-2014): analysis of current data in the United States. Biol Psychiatry. 2016;79(7):613-619.

Gaoni, Y., & Mechoulam, R. (1966). Hashish–VII: The isomerization of cannabidiol to tetrahydrocannabinols. Tetrahedron, 22, 1481-1488.

Hall W. What has research over the past two decades revealed about the adverse health effects of recreational cannabis use? Addiction. 2015;110(1):19-35.

Herkenham M, Lynn AB, Little MD, et al. Cannabinoid receptor localization in brain. Proc Natl Acad Sci U S A. 1990;87(5):1932-1936.

Hudak M, Severn D, Nordstrom K. Edible Cannabis-induced psychosis: intoxication and beyond. AM J Psychiatry. 2015;172(9):911-912.

Kelly BF, Nappe TM/ Cannabinoid toxicity. In: StatPearls. Treasure Island (FL): StatPearls Publishing Copyright 2022, StatPearls Publishing LLC.; 2022.

Koski, L. (2021). Delta-8 THC: It’s time to regulate like cannabis. Forbes.

Kramer JL. Medical marijuana for cancer. CA Cancer J Clin. 2015;65(2):109-122.

Kruger JS, Kruger DJ. Delta-8-THC: Delta-9-THC’s nicer younger sibling? J Cannabis Res. 2022 Jan 4;4(1):4. doi: 10.1186/s42238-021-00115-8. PMID: 34980292; PMCID: PMC8725316

Layden JE, Ghinai I, Pray I, et al. Pulmonary illness related to e-cigarette use in Illinois and Wisconsin – final report. N Engl J Med. 2020;382(10):903-916.

Liktor-Busa E, Keresztes A, LaVigne J, Streicher JM, Largent-Milnes TM. Analgesic potential of terpenes derived from cannabis sativa. Pharmacol Rev. 2021;73(4):98-126.

Loflin M, Earleywine M. A new method of cannabis ingestion: the dangers of dabs? Addict Behav. 2014;39(10):1430-1433.

Lu HC, Mackie K. An Introduction to the Endogenous Cannabinoid System. Biol Psychiatry. 2016;79(7):516-525.

MacCallum CA. Russo EB. Practical considerations in medical cannabis administration and dosing. Eur J Intern Med. 2018;49:12-19.

Mariani JJ, Brooks D, Haney M, Levin FR. Quantification and comparison of marijuana smoking practices: blunts, joints, and pipes. Drug Alcohol Depend. 2011;113(2-3):249-251.

McPartland JM. Cannabis sativa and cannabis indica versus “sativa” and “indica”. In: Chandra S, Lata H, ElSohly MA, eds. Cannabis sativa L. – botany and biotechnology. Cham: Springer International Publishing; 2017:101-121.

Mechoulam R, Parker LA. The endocannabinoid system and the brain. Annu Rev Psychol. 2013;64:21-47.

Monte AA, Shelton SK, Mills E, et al. Acute illness associated with cannabis use, by route of exposure: an observational study. Ann Intern Med. 2019;170(8):531-537.

Miller OS, Elder EJ, Jr., Jones KJ, Gidal BE. Analysis of cannabidiol (CBD) and THC in nonprescription consumer products: Implications for patients and practitioners. Epilepsy Behav. Feb 2022;127:108514. doi:10.1016/j.yebeh.2021.108514

Morales P, Hurst DP, Reggio PH. Molecular targets of the phytocannabinoids: a complex picture. Prog Chem Org Nat Prod. 2017;103:103-131.

National Academies of Sciences E, Medicine, Health, et al. The National Academies Collection: Reports funded by National Institutes of Health. In: The Health effects of cannabis and cannabinoids: the current state of evidence and recommendations for research. Washington (DC): National Academies Press (US) Copyright 2017 by the National Academy of Sciences. All rights reserved.; 2017.

National Institutes of Health. Notice of Information: Establishment of a standard THC unit to be used in research (NOT-DA-21-049). Published 2021. Updated May 7, 2021. Accessed Jul 28, 2022.

Pagano C, Navarra G, Coppola L, Avilia G, Bifulco M, Laezza C. Cannabinoids: therapeutic use in clinical practice. Int J Mol Sci. 2022;23(6).

Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br J Pharmacol. 2008;153(2):199-215.

Piomelli D, Russo EB. The cannabis sativa versus cannabis indica debate: an interview with Ethan Russo, MD. Cannabis Cannabinoid Res. (2016);1(1):44-46.

Raber JC, Elzinga S, Kaplan C. Understanding dabs: contamination concerns of cannabis concentrates and cannabinoid transfer during the act of dabbing. J Toxicol Sci. 2015;40(6):797-803. doi:10.2131/jts.40.797

Ridgeway G. Kilmer B. Bayesian inference for the distribution of grams of marijuana in a joint. Drug Alcohol Depend. 2016;165:175-180.

Rock EM, Parker LA. Constituents of cannabis sativa. Adv Exp Med Biol 2021;1264:1-13.

Sholler DJ, Moran MB, Dolan SB, et al. Use patterns, beliefs, experiences, and behavioral economic demand of indica and sativa cannabis: A cross-sectional survey of cannabis users. Exp Clin Psychopharmacol. 2022;30(5):575-583.

Spindle TR, Sholler DJ, Cone EJ, et al. Cannabinoid content and label accuracy of hemp-derived topical products available online at national retail stores.

JAMA Netw Open. Jul 1 2022;5(7):e2223019. doi:10.1001/jamanetworkopen2022.23019

Vandrey R. Raber JC, Raber ME, Douglass B, Miller C, Bonn-Miller MO. Cannabinoid dose and label accuracy in edible medical cannabis products. JAMA. 2015;313(24):2491-2493.

Volkow ND, Baler R. Emergency department visits from edible versus inhalable cannabis. Ann Intern Med. 2019;170(8):569-570.

We thank the following content experts for their extensive input and editorial suggestions:

Jacci Bainbridge, PharmD, FCCP (Professor, Department of Clinical Pharmacy at Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus)

Kendall Browne, PhD (Former Core Investigator, Center of Excellence in Substance Abuse Treatment and Education (CESATE), VA Puget Sound. Former Assistant Professor of Psychiatry and Behavioral Sciences, University of Washington)

Joseph Bubalo, PharmD, BCPS, BCOP (Assistant Professor of Medicine, Oregon Health and Science University)

Michelle Cameron, MD, PT, MCR (Associate Professor, Department of Neurology, Oregon Health and Science University Co-Director, MS Center of Excellence-West, VA Portland Health Care System)

Kim D Jones, RNC, PhD, FNP (Professor of Nursing, Oregon Health and Science University Dean, Linfield-Good Samaritan School of Nursing)

Salomeh Keyhani, MD, MPH (Core Investigator, Center for Healthcare Improvement and Medical Effectiveness (CHIME), San Francisco VA Health Care System. Professor of Medicine, University of California, San Francisco)

Mark S. Kindy, PhD, FAHA (Professor, Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida. Senior Research Career Scientist, James A. Haley VA Medical Center)

Emily Lindley, PhD (Assistant Professor, Department of Orthopedics, University of Colorado Anschutz Medical Campus)

Owen Miller, PhD (Postdoctoral Fellow, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus)

Douglas Rice, MD, PhD (Resident Physician, Department of Internal Medicine, Oregon Health and Science University)

Andrew Saxon, MD (Director, Center of Excellence in Substance Abuse Treatment and Education (CESATE), VA Puget Sound Professor of Psychiatry and Behavioral Sciences, University of Washington)

Special thanks to Lynn Kitagawa, MFA at the VA Portland Health Care System for the illustration, Daniele Piomelli, PhD for critical review of the Endocannabinoid System section, and to Julia Haskin, MA, and Alison Eckhardt, LAc, MAOM at the VA Portland Health Care System, for editorial support.

Page Last Reviewed: March 2025

Scroll to Top