Cannabis for Nausea: A Complete Medical Guide
How cannabinoids suppress the emetic reflex, FDA-approved options, CINV phase-by-phase efficacy, antiemetic comparisons, and critical contraindications including a pregnancy warning.
- FDA-approved cannabinoids: Dronabinol (Marinol, synthetic THC) approved 1985 and nabilone (Cesamet) approved 2006 for CINV unresponsive to conventional antiemetics.
- Strongest indication: Anticipatory nausea (conditioned reflex before chemotherapy) — cannabis is more effective than other antiemetics for this CINV phase.
- Mechanism: CB1 activation in the area postrema and NTS suppresses the vomiting centre; THC also reduces 5-HT release at enteric nerve terminals, complementing 5-HT3 antagonists like ondansetron.
- Cochrane evidence: Tramèr et al. 2001 meta-analysis (30 RCTs) concluded cannabinoids were more effective than placebo and comparably effective to conventional antiemetics, with higher rates of adverse effects.
- Combination therapy: Ondansetron + THC was superior to either alone in Kwiatkowska 2004, supporting a complementary mechanism strategy.
- CRITICAL CONTRAINDICATION: Cannabis is absolutely contraindicated in pregnancy, including for morning sickness. THC is teratogenic and has no safe fetal exposure threshold.
WARNING: Cannabis is CONTRAINDICATED in Pregnancy
Cannabis must never be used to treat morning sickness, hyperemesis gravidarum, or any other pregnancy-related nausea. THC crosses the placental barrier and accumulates in fetal tissue, where it disrupts neurodevelopment. Prenatal cannabis exposure is associated with impaired fetal brain development, reduced birthweight, preterm labour risk, and long-term neurobehavioural deficits in the child. There is no established safe dose of THC during pregnancy. Seek immediate medical care for severe pregnancy nausea — safe, evidence-based options are available.
Understanding Chemotherapy-Induced Nausea and Vomiting (CINV)
Chemotherapy-induced nausea and vomiting (CINV) is one of the most feared and debilitating side effects of cancer treatment, occurring in 70-80% of patients receiving emetogenic chemotherapy agents and significantly impacting quality of life, treatment adherence, and nutritional status. Despite dramatic advances in antiemetic pharmacology over the past three decades — particularly the development of 5-HT3 receptor antagonists (ondansetron, granisetron) and NK1 receptor antagonists (aprepitant) — CINV remains incompletely controlled in 30-40% of patients, particularly those receiving highly emetogenic regimens such as cisplatin-based protocols.
CINV is clinically classified into three distinct temporal phases, each with different underlying mechanisms and optimal treatment approaches:
Acute CINV occurs within the first 24 hours of chemotherapy administration and is primarily mediated by 5-HT3 receptors. Serotonin released from enterochromaffin cells in the gut mucosa (in response to chemotherapy-induced cellular damage) activates vagal afferents via 5-HT3 receptors, relaying signals to the nucleus tractus solitarius (NTS) and area postrema in the brainstem, which coordinate the emetic reflex. 5-HT3 antagonists like ondansetron are highly effective for this phase.
Delayed CINV begins 24 hours after chemotherapy and peaks at 48-72 hours, persisting for up to 5-7 days with some regimens. It is mediated primarily by substance P (SP) binding to NK1 receptors, with a lesser 5-HT3 component. NK1 antagonists (aprepitant, fosaprepitant) are the cornerstone of delayed CINV management. Cannabis has demonstrated moderate efficacy in delayed CINV as an adjunct therapy.
Anticipatory CINV is a conditioned response that develops after prior chemotherapy-associated nausea experiences. It is triggered by stimuli associated with the treatment environment (smells, sights, the oncology clinic itself) before any chemotherapy is administered — a classic Pavlovian conditioning pattern. Anticipatory nausea is particularly resistant to pharmacological antiemetics because it operates through learned neural pathways rather than acute peripheral emetic signals. This is the CINV phase where cannabis demonstrates its most superior relative efficacy compared to other antiemetic classes, likely because cannabinoids modulate conditioned fear/memory extinction via hippocampal and amygdalar CB1 receptors in addition to direct antiemetic mechanisms.
How THC and CBD Suppress the Vomiting Reflex
The endocannabinoid system plays a physiologically meaningful role in regulating nausea and emesis. CB1 receptors are densely expressed in the two key brainstem structures that coordinate vomiting: the area postrema (the blood-brain barrier-deficient chemoreceptor trigger zone that samples blood for emetic toxins) and the nucleus tractus solitarius (NTS), which integrates vagal afferent signals from the gastrointestinal tract. CB1 activation in both structures inhibits downstream emetic cascade activation through Gi-coupled receptor signalling, reducing cAMP production and suppressing neural excitability in vomiting-related circuits.
At the level of the enteric nervous system, THC reduces serotonin (5-HT) release from enterochromaffin cells and enteric nerve terminals. This pre-synaptic inhibition of 5-HT release provides a mechanism that is pharmacologically complementary to 5-HT3 receptor antagonists like ondansetron, which block the 5-HT3 receptor rather than reducing 5-HT release itself. This explains the superior antiemetic effect observed when ondansetron and THC are combined versus either agent alone.
CBD contributes to antiemetic effects through a distinct, CB1-independent mechanism. Animal models demonstrate that CBD reduces nausea via 5-HT1A receptor agonism in the dorsal raphe nucleus, reducing the firing of serotonergic neurons that project to emetic brainstem circuits. This mechanism is similar to that of buspirone (a 5-HT1A partial agonist used as an anxiolytic) and provides additive antiemetic efficacy without the psychoactive effects of THC. However, human clinical evidence for CBD as a standalone antiemetic is limited compared to THC.
THCA (tetrahydrocannabinolic acid), the raw acidic precursor to THC found in unheated cannabis, also shows antiemetic activity in preclinical models at doses lower than THC, suggesting that raw cannabis preparations (juices, unheated tinctures) may have additional antiemetic utility, though human clinical data for THCA remains preliminary.
FDA-Approved Cannabinoid Antiemetics
The United States is one of the few jurisdictions where synthetic cannabinoid antiemetics have been formally approved and integrated into oncology practice guidelines. Understanding how these pharmaceutical-grade options compare to botanical cannabis is essential for patients navigating CINV management.
Dronabinol (Marinol): Synthetic delta-9-THC dissolved in sesame oil, available in 2.5 mg, 5 mg, and 10 mg gelatin capsules. FDA-approved since 1985 for two indications: (1) CINV not adequately controlled by conventional antiemetics, and (2) anorexia/weight loss in AIDS patients. The approved antiemetic dosing begins at 5 mg/m² administered 1-3 hours before chemotherapy, with additional doses every 2-4 hours as needed, to a maximum of 4-6 doses per day. A newer formulation, Syndros (oral dronabinol solution), provides a liquid option for patients with swallowing difficulties.
Nabilone (Cesamet): A synthetic bicyclic cannabinoid analogue of THC, available in 1 mg capsules. Approved in Canada in 1985 and the United States in 2006 for CINV. Nabilone has a slightly different pharmacological profile than dronabinol, with a somewhat higher CB1 receptor binding affinity. It is typically dosed at 1-2 mg twice daily, starting the day before chemotherapy and continuing for 48 hours after the last dose. Nabilone is considered slightly more potent than dronabinol with more pronounced psychoactive effects.
Both agents are Schedule III controlled substances in the United States (reclassified from Schedule II in 1999), making them more accessible for prescription than Schedule I substances while maintaining prescribing safeguards. Neither drug requires a medical cannabis card or state cannabis program enrollment to prescribe.
Clinical Evidence: Key CINV Trials
| Study | Year | Design | n | Cannabis Type | Key Finding |
|---|---|---|---|---|---|
| Tramèr et al. (Cochrane) | 2001 | Meta-analysis, 30 RCTs | 1366 | Dronabinol + nabilone vs placebo/neuroleptics | Cannabinoids superior to placebo; similar to prochlorperazine; higher adverse event rates; superior for anticipatory CINV |
| Meiri et al. | 2007 | RCT, parallel-group | 64 | Vaporised cannabis vs oral dronabinol | Comparable antiemetic efficacy; vaporised cannabis faster onset; better patient acceptability for active vomiting |
| Duran et al. | 2010 | Double-blind RCT | 16 | Sublingual THC:CBD (Sativex) vs placebo | Significant reduction in nausea NRS vs placebo (p<0.05); faster onset than oral dronabinol; good tolerability |
| Kwiatkowska et al. | 2004 | Rat model (mechanism study) | Animal | THC + ondansetron vs either alone | Combination superior to monotherapy; demonstrated 5-HT3 + CB1 complementary mechanism; informed clinical combination use |
| Ware et al. | 2010 | Survey + case series | 131 | Inhaled cannabis (CINV patients) | 74% reported significant nausea relief; 70% reduced conventional antiemetic use; anticipatory nausea best responder group |
| Machado Rocha et al. | 2008 | Systematic review | 30 studies | Dronabinol + nabilone | Both superior to placebo in CINV; nabilone slightly more effective than dronabinol for complete antiemetic response; adverse effects similar |
Cannabis Efficacy by CINV Phase
| CINV Phase | Timing | Primary Mechanism | Cannabis Efficacy | Optimal Cannabis Approach |
|---|---|---|---|---|
| Anticipatory CINV | Before chemotherapy infusion (conditioned reflex) | Pavlovian fear conditioning; hippocampal + amygdalar circuits; resistant to conventional antiemetics | Strongest — superior to other antiemetic classes | Sublingual tincture or vaporised cannabis 30-60 min before clinic visit; addresses both conditioned fear + peripheral emesis |
| Acute CINV | 0-24 hrs post-chemotherapy | 5-HT3 receptor activation (enterochromaffin 5-HT release) | Moderate — effective but 5-HT3 antagonists often stronger for this phase | Combination therapy: ondansetron + dronabinol or sublingual cannabis; use fast-onset route if vomiting active |
| Delayed CINV | 24-120 hrs post-chemotherapy | NK1 receptor (substance P); residual 5-HT3 component | Moderate — adjunct role alongside NK1 antagonists; useful for breakthrough nausea | Oral dronabinol or cannabis edibles for sustained release over multi-day delayed period; sublingual for breakthrough |
Dosing Guidelines for Cannabinoid Antiemetics
| Product | Starting Dose | Typical Therapeutic Dose | Maximum | Timing |
|---|---|---|---|---|
| Dronabinol (Marinol) oral capsule | 5 mg/m² body surface area | 5-7.5 mg/m² per dose; 1-6 doses per day | 15 mg/m² per dose; max 4-6 doses/day | 1-3 hrs before chemotherapy; every 2-4 hrs as needed |
| Nabilone (Cesamet) capsule | 1 mg twice daily | 1-2 mg twice daily | 2 mg three times daily (6 mg/day max) | Start day before chemotherapy; continue 48 hrs post last dose |
| Sublingual tincture (1:1 THC:CBD) | 2.5 mg THC / 2.5 mg CBD | 5-10 mg THC / 5-10 mg CBD | Titrate to response; avoid >20 mg THC single dose | 30-60 min before chemotherapy; repeat 4-6 hrs as needed |
| Vaporised cannabis (whole plant) | 1-2 inhalations of low-THC strain | 2-4 inhalations; 10-20% THC flower | Titrate to response; 3-6 sessions/day during active nausea | 2-10 min onset; use for active nausea/vomiting when oral route not viable |
| Oral cannabis edibles/capsules | 5 mg THC | 10-15 mg THC per dose | Titrate carefully; 2-hr rule before redosing | 1-2 hrs before chemotherapy; sustained release for delayed CINV periods |
Antiemetic Delivery Methods: When Each Works Best
One of the most practically important decisions for cannabis antiemetic therapy is matching the delivery route to the clinical situation. The key principle: when a patient is actively vomiting, oral routes fail because the drug is expelled before meaningful absorption occurs. This is why Sativex (oromucosal) and vaporised cannabis represent the most clinically rational options during acute emetic episodes.
| Delivery Method | Onset | Duration | Bioavailability | Best CINV Phase | Practical Note |
|---|---|---|---|---|---|
| Vaporised cannabis | 2-10 min | 1-3 hrs | 20-56% | Acute & anticipatory; active vomiting episodes | Bypasses GI tract; essential when patient cannot retain oral medications; requires vaporiser device |
| Sublingual tincture / Sativex spray | 15-45 min | 3-6 hrs | 12-35% (sublingual) | Anticipatory & acute; practical alternative to vaporisation | Hold under tongue 60-90 sec before swallowing for maximum sublingual absorption; precise dosing possible |
| Oral dronabinol capsule | 30-120 min | 4-6 hrs (metabolite 11-OH-THC: up to 12 hrs) | 10-20% (first-pass metabolism) | Delayed CINV; prophylactic use before chemotherapy when nausea not yet active | Variable first-pass extraction (6-fold variation between individuals); 11-OH-THC 4-5x more potent at CNS than THC |
| Oral cannabis capsule/edible | 45-120 min | 4-8 hrs | 4-20% | Delayed CINV; sustained overnight coverage | Same first-pass variability as dronabinol; must be taken before nausea activates; cannot use if actively vomiting |
| Rectal suppository (THC) | 30-90 min | 4-8 hrs | Up to 50-70% (bypasses first-pass partially) | Active vomiting when oral + inhalation not possible; palliative CINV | Underutilised; highly effective bioavailability profile; limited commercial availability; patient acceptance variable |
Cannabinoids vs. Conventional Antiemetics: Head-to-Head
| Antiemetic | Class | Onset | CINV Efficacy | Anticipatory CINV | Key Side Effects | Relative Cost |
|---|---|---|---|---|---|---|
| Ondansetron (Zofran) | 5-HT3 antagonist | 30-60 min (oral); 15-30 min (IV) | Excellent (acute phase) | Poor (not mechanism-relevant) | Constipation, headache, QT prolongation at high doses | Low-Medium (generic) |
| Aprepitant (Emend) | NK1 antagonist | 60-120 min | Excellent (delayed phase) | Poor | Fatigue, hiccups, CYP3A4 drug interactions (warfarin, dexamethasone) | High |
| Dronabinol (Marinol) | Synthetic CB1 agonist | 30-120 min | Moderate (all phases) | Good | Dizziness, dysphoria (elderly), tachycardia, sedation | Medium-High |
| Nabilone (Cesamet) | Synthetic CB1 agonist | 60-90 min | Moderate-Good (all phases) | Good | Similar to dronabinol; slightly more pronounced psychoactivity | High |
| Vaporised cannabis | Phytocannabinoid mix (CB1/CB2/5-HT1A) | 2-10 min | Moderate (all phases) | Strong (fastest onset + conditioned fear component) | Psychoactivity, airway irritation, product variability | Low-Medium |
| Metoclopramide (Reglan) | D2 antagonist / prokinetic | 30-60 min | Moderate | Poor | Tardive dyskinesia (long-term), restlessness, sedation | Low |
Beyond CINV: Other Nausea Indications
Opioid-Induced Nausea (OIN)
Opioid-induced nausea is a common adverse effect in patients receiving opioid analgesics for cancer pain or chronic pain management, affecting 25-40% of opioid-naïve patients initiating therapy. The mechanism involves mu-opioid receptor activation in the area postrema, vestibular system sensitisation, and reduced GI motility. Emerging preclinical evidence suggests a CB1/mu-opioid receptor crosstalk mechanism in the area postrema, where CB1 activation can reduce mu-opioid receptor-mediated emetic signalling. A small number of clinical reports support cannabis as useful for OIN, though dedicated RCTs are lacking. CBD’s serotonergic (5-HT1A) mechanism may provide additional benefit. Cannabis also offers the potential advantage of opioid-sparing effects — by reducing the opioid dose required for pain control, it may indirectly reduce OIN frequency and severity.
Post-Operative Nausea and Vomiting (PONV)
PONV is primarily mediated by 5-HT3, D2, H1, and muscarinic receptor pathways activated by general anaesthetic agents, opioids used perioperatively, and surgical stimulation of the gut. Limited evidence exists for preoperative cannabinoid use in PONV prevention, and practical barriers exist (anaesthetic interaction concerns, impaired preoperative assessment). Cannabinoids are not recommended as first-line PONV management, though dronabinol has been explored in small studies. The interaction between cannabis and inhalational anaesthetics (particularly in terms of altered anaesthetic requirement and awakening time) means preoperative cannabis use should always be disclosed to the anaesthetic team.
Cannabis Hyperemesis Syndrome (CHS)
It is important to note that paradoxical vomiting can be caused by cannabis itself in a condition known as Cannabis Hyperemesis Syndrome (CHS). CHS is a cyclical vomiting syndrome occurring in long-term, heavy cannabis users (typically daily use for years), characterised by recurrent episodes of nausea, vomiting, and abdominal cramping that are temporarily relieved by hot bathing (a hallmark feature). The mechanism is incompletely understood but may involve desensitisation of hypothalamic CB1 receptors that normally regulate the HPA axis stress response, combined with TRPV1 sensitisation in the gut (explaining the hot-shower relief, as heat activates TRPV1 and may override emetic signalling). CHS resolves with cannabis cessation. Medical providers should be aware that patients presenting with intractable cyclical vomiting and regular cannabis use may have CHS rather than a condition amenable to cannabis treatment.
Recommended Strains for Nausea Management
Strain selection for nausea management should prioritise moderate THC content, balanced or CBD-containing profiles (for reducing psychoactive adverse effects), and terpene profiles rich in myrcene and caryophyllene. Very high-THC cultivars may exacerbate anxiety and dysphoria in patients already distressed by illness and chemotherapy. The following strains are commonly recommended in clinical cannabis programs for CINV management.
| Strain | Type | THC % | CBD % | Key Terpenes | Why for Nausea |
|---|---|---|---|---|---|
| Harlequin | Sativa-dominant Hybrid | 7-10% | 10-15% | Myrcene, caryophyllene, pinene | High CBD:THC ratio reduces psychoactive risk; myrcene contributes antiemetic + sedative effects; ideal for daytime nausea management |
| Cannatonic | Hybrid | 6-9% | 12-17% | Myrcene, ocimene, caryophyllene | Near 1:1 to 2:1 CBD:THC mirrors Sativex ratio; broad entourage effect; low anxiety risk; gentle appetite stimulation |
| Blue Dream | Sativa-dominant Hybrid | 17-21% | 1-2% | Myrcene, pinene, caryophyllene | Gentle euphoric onset; reduces anticipatory anxiety component of CINV; myrcene sedative support; widely available |
| Granddaddy Purple | Indica | 17-23% | <1% | Myrcene, caryophyllene, linalool | Deep sedation; evening nausea + sleep disruption; appetite stimulation (munchies effect); linalool anxiolytic for anticipatory CINV |
| Cherry Pie | Indica-dominant Hybrid | 16-20% | <1% | Myrcene, caryophyllene, pinene | Mood elevation reduces CINV-associated anxiety; moderate body relaxation supports GI calm; palatable terpene profile for sensitive patients |
| ACDC | CBD-dominant Hybrid | 1-6% | 14-20% | Myrcene, pinene, caryophyllene | For patients who cannot tolerate any psychoactivity; CBD 5-HT1A antiemetic mechanism; safe for paediatric oncology (with physician guidance) |
Risks, Contraindications, and Special Populations
Pregnancy (Absolute Contraindication): As detailed in the warning box above, cannabis is absolutely contraindicated for nausea in pregnant individuals. The contrast between the legitimate therapeutic benefit of cannabis for CINV and the absolute prohibition during pregnancy cannot be overstated. Obstetricians report increasing rates of cannabis use for morning sickness — this is a significant patient safety concern requiring clear professional guidance.
Paediatric Oncology: Children receiving chemotherapy have specific considerations. Dronabinol has been used off-label in paediatric CINV with some evidence of benefit. The psychoactive effects of THC may be particularly distressing for younger children. High-CBD preparations require paediatric oncologist guidance and are not a standard first-line option. If considering cannabinoid antiemetics in paediatric patients, this must be under specialist supervision with explicit parental consent and careful dose titration.
Elderly Patients: Older adults are more sensitive to THC-induced dizziness, orthostatic hypotension, and cognitive effects. Starting doses should be 50-75% lower than standard adult doses. Nabilone tends to produce more pronounced psychoactive effects than dronabinol at equivalent antiemetic doses, making dronabinol the preferable pharmaceutical-grade option in the elderly. Falls risk is a significant concern.
Cardiovascular Comorbidity: THC produces a transient increase in heart rate and blood pressure, with potential reflex bradycardia at high doses. Patients with arrhythmia, recent myocardial infarction, or uncontrolled hypertension should have cardiac assessment before initiating cannabinoid antiemetic therapy.
Cannabis Hyperemesis Syndrome (CHS): Long-term daily cannabis users with cyclical vomiting and hot-shower-seeking behaviour should be evaluated for CHS before initiating any additional cannabis therapy. Adding cannabis to CHS will worsen rather than improve the condition.
Drug Interactions in Oncology Patients
Oncology patients typically receive complex polypharmacy regimens, making cannabinoid drug interaction screening essential. Key interactions relevant to CINV management include:
| Co-Administered Drug | Interaction | Clinical Significance | Management |
|---|---|---|---|
| Ondansetron / Granisetron (5-HT3 antagonists) | Additive antiemetic effects; complementary mechanisms (CB1 vs 5-HT3) | Beneficial combination; supported by preclinical data (Kwiatkowska 2004) | Reduce cannabis dose when combining; monitor for additive sedation |
| Aprepitant / Fosaprepitant (NK1 antagonists) | CYP3A4 inhibition (aprepitant) may raise plasma THC/CBD concentrations; additive antiemetic | Moderate; start cannabis at lower dose when aprepitant is part of regimen | Reduce cannabinoid starting dose by 25-50%; monitor for enhanced psychoactive effects |
| Dexamethasone (standard CINV protocol component) | CYP3A4 inducer; dexamethasone may slightly reduce THC/CBD plasma levels; no adverse interaction | Low clinical significance; may slightly reduce cannabis efficacy | Standard CINV protocols can include dexamethasone alongside cannabis without major interaction concern |
| Opioid analgesics (morphine, oxycodone) | Additive CNS depression; cannabis may allow opioid dose reduction (opioid-sparing effect) | Moderate; beneficial opioid-sparing effect possible if managed carefully | Monitor sedation; if opioid dose reducing due to cannabis, do so slowly under physician supervision |
| Chemotherapy agents (cisplatin, cyclophosphamide, taxanes) | CBD inhibits CYP2C9/3A4; potential to alter chemotherapy metabolism and plasma levels | Potentially significant at high CBD doses (>300 mg/day); less concern at therapeutic antiemetic doses | Disclose all cannabis use to oncologist; avoid high-dose CBD without pharmacist review of the specific chemotherapy regimen |
Medical Disclaimer
This content is for educational and informational purposes only. It does not constitute medical advice, diagnosis, or treatment. Cannabis use for chemotherapy-induced nausea should only be initiated under the supervision of an oncologist or physician experienced in cannabis medicine and familiar with your complete treatment regimen. Cannabis is absolutely contraindicated in pregnancy — do not use cannabis for morning sickness or any pregnancy-related nausea under any circumstances. Drug interactions with chemotherapy agents can be clinically significant. Laws governing medical cannabis vary by jurisdiction — dronabinol and nabilone are federally legal by prescription in the US; botanical cannabis remains federally Schedule I. Confirm your local regulations and always disclose cannabis use to your full medical team.
Frequently Asked Questions
Is cannabis FDA-approved for chemotherapy-induced nausea?
Yes. Dronabinol (Marinol, synthetic delta-9-THC) was FDA-approved in 1985 and nabilone (Cesamet) in 2006, both specifically for CINV in patients who have not responded adequately to conventional antiemetics. These are Schedule III prescription medications available from any licensed prescriber. Whole-plant botanical cannabis remains federally Schedule I in the US, though many state medical cannabis programs list CINV as a qualifying condition.
How does THC reduce nausea at the biological level?
THC reduces nausea primarily through CB1 receptor activation in the area postrema and NTS in the brainstem, inhibiting the vomiting cascade. THC also reduces serotonin (5-HT) release at enteric nerve terminals, which is pharmacologically complementary to 5-HT3 antagonists like ondansetron. CBD contributes via 5-HT1A agonism in the dorsal raphe nucleus, reducing serotonergic neuron firing that drives emetic circuits.
Is cannabis safe for morning sickness or nausea in pregnancy?
Absolutely not. Cannabis is contraindicated in pregnancy. THC crosses the placenta and accumulates in fetal tissue. Prenatal THC exposure is associated with impaired fetal brain development, reduced birthweight, preterm labour risk, and long-term neurobehavioural deficits in the child. There is no established safe threshold. Pregnant individuals with severe nausea should consult their obstetrician about approved options.
Why is vaporised cannabis sometimes better than dronabinol pills for active nausea?
When a patient is actively vomiting, swallowing and retaining an oral capsule is practically impossible. Vaporised cannabis or sublingual tinctures bypass the GI tract entirely, with onset within 2-10 minutes (vaporised) or 15-30 minutes (sublingual). The Meiri et al. 2007 Oncology study directly compared vaporised cannabis to oral dronabinol and found comparable antiemetic efficacy with faster onset and better patient acceptability during active vomiting episodes.