Cannabis: Implications for Physical and Occupational Therapy

*Editor's note: This text-based course is a transcript of the webinar, Cannabis: Implications for Physical and Occupational Therapy, presented by Melissa Bednarek, PT, DPT, PhD, CCS.*

Please also use the handout with this text course to supplement the material.

Learning Outcomes

After this course, participants will be able to:

• Identify the various parts of the cannabis plant.
• Describe routes of administration, the mechanism of action, and the side effects of cannabis.
• Describe the implications of cannabis for physical and occupational therapy.

Introduction

Thank you for joining me for this course on cannabis and its implications for physical and occupational therapy. My name is Melissa Bednarek. I have been a physical therapist for many years and currently serve as a Professor and Program Director in the Doctor of Physical Therapy Program at Chatham University in Pittsburgh, Pennsylvania. My background is in physiology, and I have been teaching pharmacology to entry-level DPT students and providing pharmacology continuing education to licensed therapists for more than a decade. I also contribute continuing education on pharmacology through MedBridge and serve as a faculty member in the APTA Academy of Home Health Advanced Competency Program.

Cannabis is a topic I have been wanting to address for some time, and I want to start with a candid acknowledgment: this was one of the more challenging webinars I have put together. I typically organize my pharmacology presentations around multiple drug classes, so focusing an entire session on a single drug was a different exercise. But there is good reason for it. Cannabis is timely, it is confusing, and you likely have questions — or your patients do. To prepare, I actually surveyed colleagues, friends, and other therapists and asked them: if you were going to sit through a webinar on cannabis, what would you want to know? Their answers shaped this course. So over the next two hours, we are going to cover the legal landscape, the plant itself, routes of administration, the underlying physiology, the purported benefits, the risks and drug interactions, specific clinical conditions, and then — most importantly for your daily practice — the implications for physical and occupational therapy, including three hypothetical case studies that I will use to bring all of this material together.

Before we dive in, let me acknowledge a few limitations. The applicability of this content may vary depending on the geographic region in which you practice, because cannabis law differs enormously from state to state. Healthcare in this area is also rapidly evolving, and I will try to give you the most current information available as of September 2025, but things can change. And perhaps most importantly, the availability of high-quality research on cannabis is genuinely limited — not because the science is not being attempted, but because of the drug's current federal classification. We will talk about why that is as we go.

One more personal note before we begin. I know pharmacology continuing education does not always top practitioners' wish lists. But if you are here, it is because you have accepted that this information matters in your work. You know that your patients will ask you about cannabis, some are already using it, and you want to be informed enough to educate them and to recognize clinically relevant effects when you see them in your sessions. For that, I give you real credit.

The Cannabis Plant

Parts of the Plant and Key Cannabinoids

Cannabis - also known as marijuana, weed, pot, or bud - is a plant. Its commercial and clinical significance comes from the chemical compounds it contains, most notably a class of substances called cannabinoids. The cannabis plant is made up of flowers, leaves, stems, seeds, and roots, and more than 100 different cannabinoids have been identified within it. The two we are most concerned with as practitioners are delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD).

THC is the cannabinoid responsible for the psychoactive "high" associated with cannabis. CBD, on the other hand, does not produce that high and is the cannabinoid that has attracted the most interest from a medicinal standpoint. In terms of where these compounds are found within the plant, the concentration of both THC and CBD is highest in the flowers, followed by the leaves, followed by the stalks and stems. The seeds contain no cannabinoids at all - which is relevant when we talk about the various forms in which cannabis products appear.

One thing worth highlighting here is that only female plants produce flowers, and specifically unfertilized female cannabis plants contain two to five times the concentration of cannabinoids compared to male plants or fertilized females. The cultivation industry has exploited this fact to create strains with increasingly higher THC concentrations, which has real implications for the potency of products that patients may be using.

Hemp, CBD, and the Delta Variants

The word "hemp" refers to any part of the Cannabis sativa plant that contains no more than 0.3% THC by dry weight. This is the critical legal distinction: cannabis, by legal definition, contains more than 0.3% THC, while hemp contains less. CBD can be derived from both hemp and non-hemp plants, but this distinction matters significantly from a legal perspective. As of the USDA 2018 Farm Bill, CBD derived from hemp is legal at the federal level, though individual states may have their own restrictions.

You may also have heard references to Delta-8 and Delta-10 THC. These are naturally occurring cannabinoids in hemp, but they exist in such small amounts in the plant that commercially available forms are largely produced synthetically using hemp-derived CBD. In terms of potency, the hierarchy is: Delta-9 is the most potent, followed by Delta-8, followed by Delta-10. Because these compounds are technically derived from hemp, which is federally legal under the 2018 Farm Bill, there has been a legal ambiguity around them. However, many states have moved to ban Delta-8 and Delta-10 outright. When I refer to THC throughout the remainder of this course, I am referring specifically to Delta-9 THC unless otherwise noted.

Forms of CBD

CBD appears in a wide range of consumer products, and your patients may be using any of them. Cannabis seeds are used in baked goods, oils, beverages, chocolate, ice cream, and other snack foods. Hemp seed flour can serve as a gluten-free alternative to wheat flour. CBD is also commonly found in oils, tinctures, lotions, capsules, and cosmetics, including hair care products and topical formulations marketed for wound healing and dermatological conditions. Understanding these forms is important because the route of administration has significant effects on absorption, onset, and risk - which we will explore in depth when we discuss pharmacokinetics.

A Brief History

Cannabis use is not a modern invention. The use of Cannabis sativa extract can be traced back to China around 2900 BC. Western medicine began exploring it in the early 1800s. CBD was first isolated in 1940, its structure was reported in 1963, and the structure of THC was determined in 1964. Once these individual cannabinoids were identified and characterized at the molecular level, recreational interest in cannabis increased significantly through the 1960s and 1970s. More recently, Canada officially legalized cannabis for both recreational and medical use in 2018, and Mexico followed with recreational legalization in 2021. I mention Canada specifically because several of the research studies I will reference later in this course were conducted there - the legal context for that research matters.

Legal Aspects

Federal Classification

To understand the legal landscape surrounding cannabis in the United States, we need to start with the Comprehensive Drug Abuse Prevention and Control Act, passed in 1970. This legislation established the framework for the Controlled Substances Act and gave the Drug Enforcement Administration (DEA) authority to regulate controlled substances through a five-tiered scheduling system based on the potential for physical and psychological dependence and the presence or absence of accepted medical use.

A Schedule I substance is defined as having no currently accepted medical use and a high potential for abuse. Examples include heroin, LSD, and - yes - cannabis. Schedule II includes drugs with high abuse potential and the possibility of severe psychological or physical dependence, such as cocaine, hydromorphone, oxycodone, and fentanyl. Schedule III drugs have moderate to low dependence potential; examples include anabolic steroids and certain codeine-containing preparations. Schedule IV drugs carry a low potential for abuse and dependence, including alprazolam, lorazepam, and tramadol. Schedule V contains preparations with the lowest abuse potential among controlled substances, often used for antitussive, antidiarrheal, or analgesic purposes.

Cannabis, then, sits at the very top of this framework as a Schedule I substance - meaning the federal government has officially taken the position that it has no accepted medical use and carries a high potential for dependency. You might be thinking: that does not sound right. We will get to that tension in a moment.

It is also worth understanding the distinction between illegal and decriminalized. Decriminalization means that possession of a substance remains technically illegal, but the penalties are civil rather than criminal - typically a fine rather than jail time. When you read about different state policies, the word "decriminalized" will appear, and it is not the same as legalized.

Despite its Schedule I status, cannabis is the most commonly used federally illegal drug in the United States. According to the CDC, 61.9 million people used cannabis in 2022. Approximately 3 in 10 of those users - roughly 30% - meet the criteria for cannabis use disorder.

State-Level Legal Status

The gap between federal law and state law in this area is enormous. As of February 2024, 47 states, the District of Columbia, and three U.S. territories (Guam, Puerto Rico, and the U.S. Virgin Islands) had legalized cannabis for medical use. The three states that had not, at that time, were Idaho, Nebraska, and Kansas. For non-medical adult recreational use, 24 states, the District of Columbia, and two territories (Guam and the Northern Mariana Islands) have legalized it. The situation is not always linear - for example, South Dakota approved cannabis use in November 2020 and then had that approval struck down by the state supreme court a year later. This is a rapidly changing area. If you are uncertain about the specific laws in your state, it is worth checking current resources rather than relying on information that may have been accurate a year ago.

FDA-Approved Cannabis-Based Medications

Here is where the tension between federal classification and medical reality becomes most visible. Even as cannabis remains Schedule I at the federal level, the FDA has approved two categories of cannabis-derived medications.

The first is cannabidiol (brand name: Epidiolex), a plant-based drug containing purified CBD. It is FDA-approved to treat seizures associated with rare forms of epilepsy, specifically Lennox-Gastaut syndrome and Dravet syndrome.

The second category includes dronabinol (brand names: Marinol, Syndros) and nabilone (brand name: Cesamet), both of which are synthetic drugs that mimic THC. These are FDA-approved to treat nausea and vomiting in patients undergoing chemotherapy and to stimulate appetite in patients with AIDS-related anorexia.

The existence of these FDA-approved medications is not insignificant. It represents the government simultaneously classifying cannabis as having no accepted medical use while approving medications derived from or based on its compounds. That is the fundamental paradox of the current legal environment.

Rescheduling Efforts

Something may have crossed your radar in recent years about efforts to change cannabis's federal classification. Here is a brief timeline. In October 2022, President Biden requested that the Department of Health and Human Services (HHS) and the DEA review how marijuana is scheduled under the Controlled Substances Act. In August 2023 - the first time in more than 50 years - the HHS formally recommended to the DEA that cannabis be rescheduled from Schedule I to Schedule III. This was a genuinely significant moment, because Schedule III carries the acknowledgment that the substance has accepted medical use. In May 2024, the DEA proposed a rule that, if finalized, would transfer cannabis to Schedule III. A public comment period generated approximately 42,000 responses. A hearing was scheduled for January 2025 but was stayed, and as of September 2025, the process remains under review by the Trump administration. As of the time of this recording, cannabis remains a Schedule I substance. However, if rescheduling does occur, the downstream effects would be substantial - not just legally, but in terms of opening the door for much more robust clinical research.

Pharmacology Fundamentals

Pharmacokinetics: What the Body Does to the Drug

Before we get into the pharmacology of cannabis specifically, I want to take a few minutes to lay some foundational pharmacology concepts, because I think they make everything that follows much easier to understand. We will start with pharmacokinetics, which is by definition the study of how the body absorbs, distributes, metabolizes, and eliminates drugs. The keyword arrangement here matters: it is about what the body does with a drug.

When any drug enters the body, it first has to be absorbed. Absorption is directly tied to the route of administration. Common routes include oral (tablets, capsules, liquids), sublingual (under the tongue), topical (applied to the skin or mucous membranes), and inhalation (absorbed through the lungs). There are also parenteral routes - subcutaneous, intramuscular, and intravenous - that bypass the gastrointestinal system entirely.

Oral administration is the most common and convenient route, but it has limitations. Some drugs are inactivated by the acidic environment of the stomach. Everything absorbed from the GI system goes first to the liver through the portal vein - a process known as the first-pass effect. Some drugs are so extensively metabolized in the liver that very little ever reaches the general circulation. Interactions with food or drink can also alter how drugs behave in the gut.

Sublingual administration takes advantage of the large blood vessels under the tongue to deliver drugs rapidly into the bloodstream. Nitroglycerin for chest pain is the classic example - you want that drug in the system fast. Topical drugs act locally at the site of application. Inhalation allows drugs to be absorbed directly through the alveoli of the lungs, which is why drugs like albuterol work so quickly.

Once a drug is absorbed, it is distributed throughout the body via the bloodstream. Some drugs are carried by plasma proteins like albumin; when bound to these proteins, the drug is effectively inactive - it is just along for the ride. The bound drug is released from the protein to maintain equilibrium as the unbound portion moves into tissues, and only the unbound drug can interact with receptors and produce effects.

Metabolism is primarily handled by the liver. A family of enzymes called cytochrome P450 (CYP) is responsible for breaking down most drugs into less active or inactive forms through a process called biotransformation. The first-pass effect I mentioned earlier is exactly this: drugs from the GI tract go straight to the liver and may be substantially broken down before they ever reach systemic circulation. Individuals with liver disease, older adults, and premature infants may process drugs more slowly, which affects dosing - this is beyond our scope to manage, but it is important context for understanding why your patients may respond differently to medications.

Finally, excretion is typically through the kidneys. Water-soluble drug metabolites can be excreted directly in urine. Fat-soluble metabolites may need to cycle back through the liver one or more times before they become water-soluble enough to be excreted. Individuals with renal disease may eliminate drugs more slowly, leading to higher circulating drug levels.

For cannabis specifically, when it is administered orally, more than 65% is excreted in feces, and about 20% is excreted in urine. These numbers reflect how the drug moves through and out of the body after oral ingestion.

Bioavailability, the proportion of a drug that actually reaches systemic circulation, varies considerably with route of administration. For THC taken orally, only 4 to 12% actually becomes bioavailable in the bloodstream. The oral bioavailability of CBD is approximately 6%. Inhalation is substantially more efficient: 10 to 35% of inhaled THC becomes bioavailable, and 11 to 45% of inhaled CBD does so. This difference in bioavailability is one reason why the route of administration matters so much clinically, and it is a key reason why patients using edibles may experience delayed or unpredictable effects.

Pharmacodynamics: What the Drug Does to the Body

Pharmacodynamics is the study of how a drug exerts its effect on the body. This is where we get into receptor interactions. An agonist is a drug or substance that binds to a receptor and activates it, producing the intended action. An antagonist or blocker binds to the receptor and prevents the agonist from binding, thereby blocking the effect. Beta blockers are a familiar clinical example: they bind to and block the beta receptors that would normally be activated by epinephrine or norepinephrine, thereby reducing heart rate and blood pressure.

Side effects are drug effects other than the intended one. Adverse effects are severe side effects that are uncommon. Every drug has both, and cannabis is no exception.

Routes of Administration

The various ways cannabis can be introduced into the body have important pharmacokinetic and clinical consequences. Cannabis can be smoked - via joints, blunts, or bongs - or vaped using devices similar to electronic cigarettes. It can be mixed into food or beverages, creating what we commonly call edibles. It can also be inhaled through oil concentrates or other extracts in a process known as dabbing. Finally, it can be applied topically in lotions, creams, and oils, or taken sublingually in tinctures.

The distinctions between these routes matter enormously in practice. Smoked or inhaled cannabis reaches the bloodstream rapidly - effects can be felt within minutes. This quick feedback loop makes overconsumption somewhat less likely because the user senses the effect before taking more. Edibles, by contrast, must be ingested, digested, absorbed through the gut, and processed through the liver before anything reaches systemic circulation. That process can take one to three hours. The clinical consequence is that a patient who takes an edible, feels nothing after thirty minutes, and takes another dose can easily end up with far more cannabis in their system than they intended. There is also no standardized dosing in foods - a homemade edible and a commercially produced one from a licensed dispensary may contain wildly different amounts of active compounds. This overconsumption risk with edibles is a real safety concern, particularly given the appeal of food-based products to children.

Topical cannabis products act locally at the site of application and generally do not enter systemic circulation in meaningful amounts. The probability of a topical product producing a positive drug test is low, though it is not zero. Anything applied to the skin that does cross into the bloodstream could, in theory, be detected. Sublingual tinctures are absorbed relatively quickly through the mucosal blood vessels under the tongue, resulting in a faster onset than oral ingestion but without the pulmonary effects of inhaled products.

The Endocannabinoid System

Overview and Function

To understand how cannabis works in the body, we need to understand the endocannabinoid system (ECS) - a naturally occurring physiological system that we all have, regardless of whether we have ever used cannabis. The ECS is responsible for central and peripheral neuromodulation and plays a regulatory role in learning and memory, emotional processing, sleep, temperature control, pain control, inflammatory responses, immune responses, and eating behavior.

That last connection helps explain the well-known phenomenon of cannabis causing the "munchies" - the drug is activating the ECS and upregulating appetite signaling. Conversely, a temporary disruption of short-term memory with high doses of cannabis also relates directly to the ECS, because this system normally plays a role in how we consolidate and process information.

CB1 and CB2 Receptors

The ECS operates through a set of receptors, naturally occurring ligands (the chemicals that bind those receptors), and enzymes that facilitate the process. The two main receptor types are CB1 and CB2.

CB1 receptors are found primarily in the brain but are also present in peripheral tissues, including adipocytes, immune cells, skeletal muscle, the exocrine pancreas, liver, and GI tract. Our bodies naturally produce compounds called endocannabinoids to stimulate these receptors. The two primary endocannabinoids are arachidonoylethanolamide (AEA) and 2-arachidonoyl-glycerol (2-AG). These molecules are structurally similar to the cannabinoids found in the cannabis plant, which is precisely why externally administered cannabis can influence this system. The activation of CB1 receptors by THC is what produces the high.

The mechanism by which this happens involves retrograde signaling. Rather than the traditional pre-synaptic to post-synaptic direction of neuronal communication, a signal travels backward from the post-synaptic neuron, through the synapse, back to the pre-synaptic neuron, interacting with CB1 receptors and triggering changes in neurotransmitter release. This is the neuromodulation at the heart of cannabis's effects on the brain.

CB2 receptors are primarily located in immune tissues, including the spleen, thymus, peripheral immune cells, and mast cells. When activated, they can modulate intestinal inflammation, contraction, and pain in inflammatory bowel conditions. Importantly, CB2 receptor activation does not appear to produce the same psychoactive high as CB1 activation.

Where CBD Fits In

CBD has a weak affinity for both CB1 and CB2 receptors - it does not bind them strongly in the way THC does. Instead, CBD primarily inhibits enzymes that normally break down the body's naturally occurring endocannabinoids. By preventing that breakdown, CBD effectively prolongs and amplifies the body's own endocannabinoid signaling. This is how CBD can produce physiological effects without producing the THC-associated high.

Cannabis and Opioids

Different Systems, Different Mechanisms

A common question - and a common source of confusion - is how cannabis and opioids relate to each other. They are both controlled substances, and they are both discussed in the context of pain management, but they operate through entirely different systems.

Cannabis interacts with the cannabinoid receptors - CB1 and CB2 - as I just described. Opioids interact with opioid receptors: mu, delta, and kappa. Opioids - whether naturally occurring as endorphins, derived from the opium plant, or synthetically manufactured - relieve pain by binding to these receptors in the brain and blocking ascending pain impulses. A strong mu agonist such as morphine carries a high potential for abuse, reflecting the characteristics of that particular receptor type. The different receptor subtypes account for the differing abuse potentials and side effect profiles across the opioid class.

Non-narcotic analgesics and narcotics are sometimes combined in clinical practice - products like Percocet combine acetaminophen with oxycodone, and Lortab ASA combines aspirin with hydrocodone. The non-narcotic provides a foundation of pain relief on which a lower dose of the narcotic can build. These are two entirely separate pharmacological systems from the endocannabinoid system.

Can Cannabis Reduce Opioid Use?

The answer, based on available evidence, is yes - though with important caveats. A 2021 study published in the Journal of Pain Medicine examined this question in a physician-supervised medical cannabis program in Canada. The study enrolled 1,145 patients and found that approximately 28% were using opioids at baseline. After six months of physician-supervised medical cannabis access, opioid use dropped to 11% of participants. The mean daily opioid dose decreased from 152 milligrams of morphine equivalent at baseline to 32.2 milligrams at six months - a 78% reduction. This is a substantial reduction and suggests that cannabis can, in some contexts, meaningfully reduce dependence on opioid medications. The ongoing debate, of course, is whether we are simply substituting one drug dependency for another. I will leave that as an open question rather than offering a definitive view, but it is a legitimate concern raised in the literature.

A 2025 study published in the Journal of Cannabis Research by Lent and colleagues looked at cannabis use specifically in people with opioid use disorder (OUD) and chronic pain. This observational study was conducted in Philadelphia with 47 adults who were taking buprenorphine or naloxone for their OUD and who were offered access to a THC/CBD capsule over a three-month period. The outcomes were encouraging: participants experienced reductions in pain severity and pain interference, no significant change in opioid use, and improvements in sleep quality and overall quality of life. The study used urine drug screening to verify self-reported data, which strengthens the reliability of those findings.

Benefits of Cannabis

Challenges in the Evidence Base

Before reviewing the evidence for cannabis's benefits, I need to address why that evidence is often frustratingly limited. Because cannabis remains a Schedule I substance at the federal level, institutional review boards - the bodies that approve human subjects research - face an inherent conflict. A Schedule I classification says there is no accepted medical use and high addiction potential. It is very difficult for an IRB to approve a rigorous, well-designed study with human participants using a drug that the government has declared to have no medical use. As a result, much of the strongest research has come from Canada, where legalization occurred in 2018, and clinical trials can proceed with fewer regulatory barriers. This is why I will be noting where many of these studies were conducted.

Established and Emerging Benefits

The evidence base, limited though it may be, does suggest several areas where cannabis or its compounds may be beneficial.

From an antimicrobial standpoint, both THC and CBD have demonstrated bacteriostatic and bactericidal activity against Gram-positive bacteria, with implications for infection control in clinical settings.

In the oncology space, cannabinoids have been found to have anti-cancer properties, though the precise mechanism remains unclear. Research has examined their potential role in breast, lung, liver, and bladder cancers. Separately from any direct anti-tumor effects, the anti-nausea and anti-vomiting properties of cannabis are well enough established that they form the basis for the FDA-approved medications dronabinol and nabilone, which I mentioned earlier.

Cannabis has demonstrated anti-seizure properties, as evidenced by the FDA approval of Epidiolex for rare epilepsy syndromes. Research has also found correlations between the endocannabinoid system and Parkinson's disease, particularly in the basal ganglia - the brain region involved in Parkinson's pathophysiology and also one of the areas where endocannabinoid activity is most concentrated. Finally, because the ECS is present throughout the GI tract and plays a role in controlling digestive processes, cannabis may have beneficial effects on GI motility, inflammation, and immune response in conditions such as irritable bowel syndrome.

Adverse Effects of Cannabis

Central Nervous System Effects

The adverse effects of cannabis span multiple organ systems, and understanding them is essential for monitoring your patients. Beginning with the central nervous system, short-term cannabis use can impair cognition, memory, alertness, coordination, balance, and reaction time. From a therapy perspective, impaired coordination and balance directly increase fall risk - particularly in older adults or those with existing neuromusculoskeletal conditions. Cannabis also impairs the ability to think and react quickly, raising concerns about driving and other activities requiring sustained alertness. These are not abstract concerns; they are clinically relevant to patients attending therapy sessions.

Long-term cannabis use is associated with decreased concentration and loss of interest in activities. Because of the current Schedule I classification, the long-term effects have been difficult to study rigorously - most of what we know comes from individuals who have used cannabis recreationally over many years in largely uncontrolled circumstances. Emerging signals in the literature also suggest links between long-term use and increased symptoms of psychosis, depression, and other psychiatric disorders, particularly in individuals who are already predisposed to these conditions. Children and adolescents are especially vulnerable, both to the mental health effects and to the effects of cannabis on the developing central nervous system. The same concern applies to cannabis use during pregnancy.

Cardiovascular Effects

In the short term, cannabis can produce tachycardia, elevated blood pressure, and increased myocardial oxygen consumption - effects that appear to be mediated by the sympathetic nervous system. This has direct implications for your therapy practice. If you are working with a patient in a setting where aerobic exercise is part of the treatment plan, and that patient has used cannabis recently, they may already be starting at an elevated heart rate and blood pressure before you even begin the session. Adding aerobic exercise on top of that is going to push their cardiovascular system further.

Additionally, cannabis use has been associated with an elevated risk of acute myocardial infarction - likely due to coronary artery vasospasm - particularly in the first hour after smoking. There is also evidence linking cannabis use to an increased risk of acute ischemic stroke, particularly in younger adults in their twenties, thirties, and forties. These are not common events, but they are clinically important to be aware of, especially in settings where patients may be using cannabis without medical supervision.

Pulmonary Effects

The pulmonary adverse effects of cannabis are primarily associated with the smoked route of administration. Smoking cannabis irritates the airways and can decrease airflow. Long-term smoking can cause airway inflammation, airway obstruction, wheezing, coughing, and increased respiratory secretions - a symptom profile similar to that seen with excessive cigarette smoking. This is another reason why route of administration matters clinically. A patient using a topical CBD product poses very different pulmonary concerns than one who is smoking cannabis daily.

Gastrointestinal Effects

Cannabis can cause nausea and vomiting, which presents a genuine paradox, given that some of the strongest evidence for cannabis's therapeutic effects relates to its antiemetic properties. The truth is that the relationship between cannabis and nausea is bidirectional and context-dependent. For some individuals in some circumstances - particularly those undergoing chemotherapy - cannabis can reduce nausea. In other individuals or at other doses, it can provoke nausea. This complexity is one of the reasons why high-quality, controlled research in this area is so difficult to conduct.

Risks: Overconsumption, Contamination, and Drug Interactions

Beyond the organ-system effects, several broader risks deserve attention. As I noted when discussing routes of administration, edibles carry a particularly high risk of overconsumption because the delayed onset - sometimes one to three hours - leads individuals to take additional doses before the first has fully taken effect. There is no standard dosing in cannabis-containing foods, and the visual appeal of products like gummies makes them a particular safety concern when children are in the household.

Contamination of cannabis products with other substances, including pathogens that can cause foodborne illness, is another risk. And then there is the issue of adverse drug interactions, which I want to cover in some detail because it is directly relevant to the patients you are seeing every day.

Drug Interactions

The CYP3A4 Connection

The key to understanding cannabis's drug interactions lies in the family of enzymes I mentioned earlier - the cytochrome P450 (CYP) enzymes. A specific enzyme within this family, CYP3A4, is responsible for metabolizing THC in the liver. Here is where it gets clinically important: cannabis can also inhibit the action of CYP3A4. That means cannabis is both a substrate of CYP3A4 - it is broken down by it - and an inhibitor of CYP3A4 - it reduces that enzyme's ability to break down other things.

If CYP3A4 is inhibited, drugs that normally rely on it for metabolism will accumulate to higher-than-expected levels in the body. This can push a patient's blood levels of a drug from therapeutic into toxic territory. The risk is especially high for drugs with what pharmacologists call a narrow therapeutic index - drugs where the window between an effective dose and a toxic dose is very small. Warfarin (Coumadin) is the classic example. Patients on warfarin require frequent INR monitoring precisely because the margin between therapeutic and toxic is narrow. If a patient using warfarin begins using cannabis, THC inhibits CYP2C9 (the specific enzyme that breaks down warfarin), warfarin levels rise, the INR becomes elevated, and the risk of bleeding increases significantly.

Prescription Drug Interactions

The list of prescription medications affected by cannabis through CYP enzyme interactions includes many drugs you encounter regularly in your patients' medication lists. Calcium channel blockers such as amlodipine and nifedipine are metabolized by CYP3A4. If a patient on a calcium channel blocker for blood pressure is also using cannabis, the calcium channel blocker may accumulate to higher levels, resulting in excessive blood pressure reduction. Macrolide antibiotics such as erythromycin, benzodiazepines such as alprazolam and lorazepam, and certain statins such as atorvastatin and rosuvastatin also rely on CYP3A4 for metabolism and are similarly affected. HIV protease inhibitors and various corticosteroids round out the list of clinically important prescription drug interactions.

When you consider how many of your patients are simultaneously managing one or more of these conditions and may be using cannabis - sometimes without reporting it to their medical team - the relevance of this pharmacology to your practice becomes quite concrete.

Over-the-Counter and Supplement Interactions

The drug interaction picture also extends to over-the-counter medications and herbal supplements, which patients are even less likely to think of as drugs with real pharmacological effects. NSAIDs used in combination with cannabis can increase the risk of GI bleeding. Antihistamines taken with cannabis can amplify drowsiness. St. John's Wort has an interesting bidirectional interaction - it tends to increase the breakdown of THC, which may lead patients to use higher doses of cannabis to achieve desired effects without realizing the interaction is responsible.

On the other side, echinacea inhibits the enzymes that normally break down THC, resulting in higher THC levels and a more pronounced effect. Melatonin and valerian root, both popular sleep aids, can interact with cannabis to impair cognitive and motor function. As therapists, we routinely ask patients about their prescription medications, but we do not always ask about herbal supplements, teas, and over-the-counter sleep aids. In patients who are using cannabis, this expanded medication review becomes even more important.

Factors That Influence the Effects of Cannabis

The effects of cannabis in any given individual are shaped by multiple variables: the concentration of THC in the product, the frequency of use, concurrent use of other substances such as alcohol, the route of administration, and individual biological factors such as sex and genetic variation in enzyme activity. This variability is one reason why predicting cannabis's effects in a given patient is so challenging and why anecdotal reports about what worked for one person may not translate to another. It also underscores why large, well-controlled clinical trials are so needed - and so hampered by the current legal environment.

CBD-Specific Side Effects

While much of the drug interaction discussion centers on THC and its effects through the CYP system, CBD carries its own side effect profile. The FDA has identified limited safety data for CBD, but known effects include potential liver damage (particularly relevant given the liver's central role to drug metabolism), drowsiness, diarrhea, changes in appetite, and mood changes such as irritability. CBD also interacts with other medications. The CDC specifically notes that CBD is not recommended during pregnancy or while breastfeeding, because of concerns about effects on the developing central nervous system.

Specific Clinical Conditions

Spasticity

One of the most studied therapeutic applications of cannabis is in the management of spasticity, and a landmark study by Corey-Bloom and colleagues published in 2012 in the Canadian Medical Association Journal examined this directly. The study investigated the short-term effect of smoked cannabis on spasticity in individuals with multiple sclerosis. Thirty participants completed the study, which involved smoking either THC-containing cannabis or placebo cigarettes once daily for three days. To qualify, participants had to have spasticity of at least moderate severity - a score of 3 or greater on the Modified Ashworth Scale, which ranges from 0 (no increase in muscle tone) to 5 (affected parts rigid in flexion or extension). The researchers combined scores across elbow, hip, and knee measurements to yield a total possible score of 30 and established in advance that a difference of 2 or more points would represent a clinically meaningful change.

The mean baseline score was approximately 9 out of 30. After three days of smoked cannabis, participants experienced an average reduction of 2.74 points - meeting the pre-specified threshold for clinical meaningfulness. Pain, measured on a visual analog scale from 0 to 100, was also significantly reduced by an average of 5.28 points. Timed walking performance did not change, and participants did report some acute cognitive effects - consistent with the THC content of the cannabis used. What the study could not fully explain was the precise mechanism by which cannabis reduced spasticity. The endocannabinoid system is certainly involved, but the specific pathway remains an active area of investigation.

Musculoskeletal Pain

A 2024 study published in the Journal of Cannabis Research by Leroux and colleagues examined cannabis use in patients with chronic musculoskeletal pain at an orthopedic clinic in Canada. Among 629 patients surveyed, 23% - nearly one in four - reported past or current use of cannabis for their musculoskeletal pain. Of those users, 63.7% described cannabis as very or somewhat effective for their pain. The strongest predictor of cannabis use among these patients was a prior history of recreational cannabis use. Among patients who had never used cannabis, 65% expressed interest in it as a treatment option. The most commonly cited barriers were lack of knowledge about different formulations and routes of administration, concerns about side effects, access challenges, and stigma.

This study is particularly useful for us as therapists because it reflects the reality of our patient populations. Roughly one in four orthopedic patients may be using cannabis for pain, and a majority of those who are not may be considering it. These are conversations that are likely already happening in your practice, whether or not you are initiating them.

Mental Health

A 2020 systematic review by Khan and colleagues examined the therapeutic role of CBD in mental health conditions. The findings were organized by strength of recommendation. The reviewers found moderate evidence supporting CBD for schizophrenia, social anxiety disorder, autism spectrum disorder, and ADHD. They found weaker - but still positive - evidence for CBD in insomnia, anxiety, bipolar disorder, posttraumatic stress disorder, and Tourette syndrome. These are modest findings, and it is important to note that these recommendations apply specifically to CBD, not to THC-containing cannabis products. Nevertheless, this is a patient population that occupational therapists in particular frequently serve, and awareness of these emerging findings is clinically relevant.

Athletes

A 2024 study published in the Journal of Applied Physiology by Cheung and colleagues examined the effects of cannabis on exercise performance in athletes, recruiting participants from community-level cycling and rowing teams. The study enrolled 14 participants with an average age of 23 and used a semi-randomized crossover design with four conditions: smoking THC-predominant cannabis, inhaling aerosolized THC-predominant cannabis (vaporizing), inhaling aerosolized CBD-predominant cannabis, and a control condition.

Participants completed both submaximal and maximal exercise protocols, including a 20-minute time trial. With THC-predominant cannabis, heart rate at submaximal levels was significantly higher compared to CBD or control conditions. In the maximal time trial, mean power output was lower with THC-predominant cannabis - regardless of whether the THC had been smoked or vaporized, suggesting the effect was attributable to THC itself rather than the route of delivery. CBD-predominant cannabis had no significant effect on exercise response or performance compared to control.

Interestingly, the participants' ratings of perceived exertion did not differ across conditions, even though their actual power output was reduced with THC. The participants believed subjectively that they were working just as hard as in the other conditions - or even harder. This disconnect between perceived effort and actual performance is an important takeaway, especially for athletes who may believe that cannabis enhances their performance when the data suggest the opposite, at least with inhaled THC-predominant products.

Implications for Physical and Occupational Therapy

The General Framework: Education, Monitoring, and Referral

As we bring all of this pharmacology back to clinical practice, I want to start by noting something that surprised me: as of the time I researched this course, neither APTA nor AOTA has issued a formal position statement on cannabis. However, both organizations have communicated guidance that aligns with what we know about our professional scope of practice with respect to pharmacology generally.

The general framework is this: our role as physical and occupational therapists involves education - not advice - monitoring for effectiveness and adverse effects, and referral to a physician when indicated. This is not actually any different from how we handle any other medication our patients are taking. If a patient asks me whether they should take a beta blocker, I would not say yes or no. I would explain what a beta blocker is, how it works, its potential side effects, and its benefits, then direct them back to their physician for a prescribing decision. Cannabis is no different.

Patients and caregivers may come to us with questions about cannabis as an alternative or adjunct for managing pain, inflammation, or spasticity. We are well-positioned to provide education - factual information about routes of administration, how cannabis works in the body, what the evidence says about effectiveness for their specific condition, and what the risks and drug interactions are. What we are not positioned to do is recommend use, recommend a specific product, or specify a route of administration. That crosses into prescribing, which is outside our scope.

Staying informed is also part of our professional responsibility. As this course makes clear, this is a space where the legal landscape, the research base, and the clinical guidance are all changing quickly. Checking in periodically with current literature and authoritative sources is simply part of staying current in this area.

Implications for Physical Therapy

If a patient is already using cannabis when you begin working with them, the primary focus shifts from education to monitoring. The key things to monitor include pain - if the patient is using cannabis to manage chronic pain, we have objective tools to assess whether it is actually helping. Are their pain scores changing over time? Are functional outcomes improving? We should track this the same way we monitor the effectiveness of any analgesic.

Fall risk deserves particular attention. Cannabis impairs coordination, balance, and reaction time - all domains that are central to our work in physical therapy, especially with older adults and those with neurological conditions. Are your outcome measures showing increased risk? Would an assistive device be appropriate? These are questions worth asking systematically, not just assuming that a patient's current functional status is unrelated to their cannabis use.

Cardiovascular monitoring is relevant in any setting where you are asking patients to exercise. If a patient has used cannabis recently, their heart rate and blood pressure may already be elevated before you begin a session. Starting aerobic exercise on top of that cardiovascular activation is something to be thoughtful about - taking a baseline set of vitals and tracking the patient's response to exercise more carefully than you might otherwise.

Mood and cognition are areas where our time with patients gives us an advantage over other providers. We often see our patients multiple times a week and develop a longitudinal view of how they are functioning. If you notice changes in mood, concentration, or cognitive function over time - particularly in a patient who is a long-term or frequent user - that observation belongs in your clinical documentation and warrants a conversation about referral.

Finally, if you observe what appears to be excessive or clinically concerning cannabis use, particularly in combination with alcohol or opioids, that also warrants referral. The goal is not to be the cannabis police but to be a clinically observant practitioner who connects the dots when patients' function may be affected by a substance.

Implications for Occupational Therapy

Occupational therapy's foundational belief is that humans are occupational beings and that engagement in occupation promotes health, well-being, and survival. I want to spend a moment on a discussion that has emerged in the OT literature, because I think it adds genuine depth to how we think about cannabis clinically.

A 2023 scoping review by Guyonnet and colleagues examined 14 studies that specifically looked at cannabis use through the lens of occupation. What the review revealed was a growing discussion in OT about "non-sanctioned occupations" - activities that may be unhealthy, socially unacceptable, or legally ambiguous, but that individuals choose to engage in as part of how they navigate daily life. Cannabis use, the authors argue, fits within this category and deserves to be understood from an occupational perspective rather than simply dismissed or pathologized.

The studies in the review found that individuals reported using cannabis to help them preserve their capacity to function - to work, to socialize, and to present themselves to the world in the way they wished to be seen. They reported that cannabis helped them endure the routine of everyday life, and some described it as enhancing creativity or spirituality in ways that felt integral to who they were. Whether or not we agree with those choices, understanding why a patient is using cannabis - what occupational function it serves for them - is consistent with the kind of person-centered, occupation-focused assessment that defines good OT practice. It opens a different kind of clinical conversation than one that begins from a place of judgment.

This does not change the fundamental role of the occupational therapist - we are still providing education rather than advice, monitoring for adverse effects, and referring when indicated. But it does suggest that the conversation with a patient who is using cannabis might be richer and more therapeutically useful if we approach it with genuine curiosity about what role it plays in their daily life and occupational identity.

Case Studies

Case Study: Mr. D

Mr. D is a 62-year-old man with a history of osteoarthritis and chronic pain who has recently undergone a right total knee replacement. He lives in Pennsylvania and reports using edibles to manage his pain.

There are several important considerations when thinking through this case. First, Pennsylvania has legalized cannabis for medical use, so Mr. D is likely obtaining his cannabis through a legal channel, but it is worth understanding whether he has a formal medical recommendation or is obtaining it through other means.

Second, his route of administration - edibles - has clinical implications we have already covered. Oral ingestion of THC produces bioavailability of only 4 to 12%, and onset can take one to three hours. There is a real risk that Mr. D, who is dealing with acute post-surgical pain, may not give the edible enough time to take effect before deciding to take more. Overconsumption leading to more severe side effects is a genuine risk to monitor.

Third, I would want to know more about his pain management history. Has he previously used opioids for his chronic pain? Is he currently using any opioids post-operatively? If so, the evidence I shared earlier about cannabis's potential to reduce opioid dependence is relevant context, but so is the need for medically supervised coordination between these two substances.

Fourth, and most immediately relevant to your therapy sessions: Mr. D's use of cannabis is going to affect his cardiovascular response to exercise. If he is using edibles for pain management, the timing of his cannabis intake relative to his therapy sessions matters. Cannabis can elevate heart rate and blood pressure. If you are beginning a session with lower-extremity strengthening and progressive ambulation in the context of a total knee replacement, you want to know whether his cardiovascular baseline is already elevated before you start. Monitoring vital signs at the start of each session takes on added importance in this context.

From a fall risk standpoint, Mr. D may already be using an assistive device given his recent surgery, but the balance and coordination effects of cannabis warrant tracking through your standard outcome measures. Changes in mood and cognition over the course of your treatment relationship are also worth noting.

Case Study: Mrs. G

Mrs. G is a 44-year-old woman with HER2-negative breast cancer. She is currently undergoing chemotherapy with docetaxel, doxorubicin, and cyclophosphamide. She reports smoking cannabis to manage the nausea and vomiting associated with chemotherapy. She lives in California, where both medical and recreational cannabis are legal.

A brief note on why HER2-negative status matters clinically: HER2-negative breast cancer does not express the HER2 protein on its surface, which affects treatment options. Approximately 70 to 80% of breast cancers are HER2-negative, and chemotherapy is a cornerstone of treatment. Understanding why chemotherapy causes nausea and vomiting - and hair loss - actually helps make sense of the cannabis question. Chemotherapy drugs target rapidly dividing cells in the body, which include cancer cells, but also the hair follicle cells and the epithelial lining of the gastrointestinal tract. The resulting GI damage directly causes nausea and vomiting.

Mrs. G is using cannabis as an antiemetic, which is one of the best-supported therapeutic applications of cannabis compounds - supported well enough, in fact, that there are FDA-approved synthetic cannabinoid medications (dronabinol and nabilone) specifically indicated for chemotherapy-induced nausea and vomiting. So the therapeutic rationale is sound.

The clinical considerations here center on route of administration. Mrs. G is smoking cannabis, which produces rapid absorption and is less prone to the overconsumption risk associated with edibles. However, smoking has real pulmonary consequences - airway irritation, decreased airflow, and potential for airway inflammation with sustained use. In a patient who may already have compromised respiratory function related to her cancer or its treatment, this is worth considering carefully.

The paradoxical nature of cannabis and nausea is also worth noting: while cannabis can reduce chemotherapy-related nausea in many patients, it can also induce nausea in others. If Mrs. G reports that her symptoms are worsening rather than improving, it is worth raising the possibility that the cannabis itself may be contributing.

Finally, the drug interaction picture is relevant here. Her chemotherapy agents - docetaxel in particular - are metabolized through the CYP3A4 pathway. As I discussed, THC can inhibit CYP3A4. This means that Mrs. G's concurrent use of cannabis could potentially elevate circulating levels of her chemotherapy drugs, increasing both their effects and their side effect burden. This is a conversation for her oncologist, not for you to manage directly - but recognizing the interaction and flagging it as a potential concern is entirely within your role as an informed practitioner.

Case Study: Ms. T

Ms. T is a 26-year-old woman with relapsing-remitting multiple sclerosis who asks you about using cannabis to address significant spasticity. Relapsing-remitting MS is the most common form of MS, characterized by periods of new or worsening symptoms (relapse) followed by periods of partial or complete recovery (remission). Ms. T is managing significant spasticity as part of her disease course and is looking into her options.

This case is fundamentally about what our role as therapists is when a patient asks us a direct question about a medication or supplement. She is asking you - her therapist - whether cannabis might help with her spasticity.

The honest, appropriate, and evidence-informed answer begins with the fact that yes, there is evidence that cannabis can reduce spasticity in MS - the Corey-Bloom study I discussed earlier is the most directly relevant. Cannabis produced clinically meaningful reductions in both spasticity and pain in people with MS over a three-day period. That is factual information you can share. You can also provide context: you are not recommending she use cannabis; you are sharing what the evidence shows. And then you refer her back to her neurologist or primary care provider for a more detailed discussion about whether it would be appropriate for her specifically, what other medications she is on, whether the legal status in her state allows for it, and what a safe approach would look like.

What you would not do is look at her medication list, identify that she is on baclofen for spasticity and perhaps a disease-modifying agent, and attempt to evaluate how cannabis might interact with those medications in detail. That level of pharmacological management is beyond our scope. You can note that there are potential drug interactions with cannabis and encourage her to have that conversation with her prescriber.

This case also invites reflection on an important practice question: before her session today, did you know enough about this topic to have an evidence-informed conversation with her? The goal of this course is to have the answer be yes.

Conclusion

Cannabis is confusing - and that confusion is not the practitioner's fault. The legal landscape is contradictory, the research base is constrained by it, the terminology is inconsistent, and the clinical implications span pharmacology, physiology, and professional ethics. Yet our patients are using cannabis in large and growing numbers, and they will ask us about it. Some of them are already using it without telling us, and its effects are showing up in their vital signs, their balance, their cognition, and their drug interactions.

Returning to our learning outcomes, I hope you can now identify the various parts of the cannabis plant and what each part contains. I hope you can describe the major routes of administration, how the endocannabinoid system functions, and the pharmacological distinction between THC and CBD. And, most importantly, for your daily practice, I hope you have a clearer sense of the role of the physical and occupational therapist when cannabis enters the clinical picture.

That role - education, monitoring, and referral - is consistent with our professional scope, our ethical obligations, and the best interests of our patients. We do not prescribe. We do not advise on whether a specific patient should use cannabis or which product they should choose. But we do educate - sharing accurate, evidence-based information about what cannabis is, how it works, and what the research shows. We do monitor - tracking pain outcomes, fall risk, cognitive function, and cardiovascular response with the same rigor we bring to monitoring any drug's effects on our patients' function. And we do refer - because some of the questions our patients bring us are genuinely beyond our scope to answer, and connecting them with practitioners who can answer those questions is itself a form of excellent care.

Thank you for taking the time to engage with this material. The field is changing, and staying informed is not optional - it is part of being the practitioner your patients deserve.

References

See additional handout.