A patient takes 10 mg of THC by mouth and feels nothing for an hour. The same 10 mg inhaled would have been unmistakable in five minutes. Nothing about the molecule changed. Only the route changed, and the route decides almost everything about timing, intensity and how much of the dose reaches the blood at all.
1. What This Article Covers, and What It Does Not
Our earlier articles Routes of Administration for Medical Cannabis (topic 1311) and Start Low, Go Slow (topic 1312) cover the delivery methods themselves, typical onset and duration, and why you should wait before redosing. This article looks at what sits underneath them: how much of a dose is absorbed, where it goes in the body, how it is broken down and how long it takes to leave.
That field has a name. Pharmacokinetics, abbreviated PK, is the study of what the body does to a drug. Pharmacodynamics is the study of what the drug does to the body. Pharmacokinetics is conventionally divided into four processes, abbreviated ADME: Absorption, Distribution, Metabolism, Excretion.
This matters clinically because a prescriber adjusting a dose also has to decide when to judge the result. Judge an oral dose too early and you may conclude it does not work. Judge an inhaled dose too early and you may be reading a peak that will not last.
2. Before Absorption: Decarboxylation
Raw cannabis contains mostly the acid precursors THCA and CBDA rather than active THC and CBD. Heat converts them through decarboxylation: in a vaporiser this happens at the moment of use, and in an oral product it must already have happened during manufacture. How this works, and why a lab report’s “total THC” is not the same as active THC, is covered in topics 1316 and 1318.
3. Absorption: Two Very Different Curves
Inhalation
Inhaled cannabinoids pass from the lung into the bloodstream almost immediately. THC and CBD are highly lipophilic (fat-soluble), and the lung offers a very large absorptive surface with only a thin membrane between air and blood.
In Huestis’s 2007 review of human cannabinoid pharmacokinetics in Chemistry & Biodiversity, plasma THC after smoking peaked at around nine minutes, at mean concentrations of roughly 84–162 ng/mL depending on dose.
Bioavailability is the fraction of a dose that reaches the general circulation, and here the honest figures are uncomfortable. Huestis reports a range of 2 to 56% for smoked THC across studies, with one estimate of systemic availability at about 8–24%. Single central figures circulate widely, but quoting one without the range hides the main point. Two people inhaling the same amount can absorb very different doses, depending on how deeply and how long they inhale, how long they hold their breath, and how much is lost in sidestream smoke. Vaporisation removes the combustion losses but not the individual variation.
Oral
Swallowed cannabinoids take a longer road. They are absorbed from the small intestine and carried to the liver in the portal circulation, where much of the dose is metabolised before it reaches the general circulation. This is first-pass metabolism, and it is why oral bioavailability is low: about 4–12% in most estimates, with some studies up to 20%. Huestis cites an estimate of about 6% (Ohlsson et al.) and 10–20% (Wall et al.). A 2025 review in Pharmaceutics by Caicedo and colleagues gives roughly 5–20% and puts the low figure down to erratic absorption as well as first-pass metabolism.
Plasma timing is just as variable. In the studies Huestis reviews, the oral plasma peak usually comes at 1–2 hours, sometimes as late as 4–6 hours, and at much lower concentrations than after smoking.
Plasma Peak and Effect Peak Are Not the Same Event
Blood concentration and felt effect do not rise and fall together. After inhalation, blood levels peak before the effect does, because the drug still has to move from the blood into brain tissue. After oral dosing the link is even looser, because an active metabolite formed in the liver (section 4) adds its own effect on its own timetable.
The practical consequence: with an oral dose, feeling no effect at 45 minutes tells you very little. Redosing at that point stacks a second dose on top of a first that has not fully arrived, and this is a common cause of oral overshoots.
4. The Metabolite That Changes the Picture
In the liver, THC is converted mainly by CYP2C9 into 11-hydroxy-THC (11-OH-THC). This metabolite is psychoactive itself. It is then broken down further into the inactive THC-COOH (11-nor-9-carboxy-THC), which is what drug tests look for.
Inhaled THC reaches the brain before it passes through the liver, so inhalation produces relatively little 11-OH-THC. Huestis reports plasma levels after smoking of only about 6–10% of the THC level at the same time. Swallowed THC is converted in much larger amounts on its way through. So an oral dose does not feel like a smaller version of an inhaled one: it delivers a different mix of active compounds.
How much stronger 11-OH-THC is remains unsettled, and sources that give a single number are overstating what is known:
| Source | Statement |
|---|---|
| Commonly repeated in clinical summaries | Roughly twice as psychoactive as THC |
| Huestis 2007 | Described as equipotent with THC |
How receptor binding and receptor activation add up to felt potency in a whole person has not been settled by laboratory data either. The direction is not in dispute: oral dosing produces proportionally more 11-OH-THC than inhalation. Treat “twice as strong” as a rule of thumb that is repeated with more confidence than the evidence supports.
5. Distribution: Where the Drug Goes and Why It Lingers
THC is 95–99% bound to plasma proteins, mainly lipoproteins, so only a small free fraction is pharmacologically active at any moment. Its steady-state volume of distribution has been estimated at about 3.4 L/kg (Huestis 2007). That is far larger than total body water, which tells you the compound leaves the blood and is stored in tissue.
That tissue is mainly fat. THC builds up in adipose tissue, and more so with frequent and long-term use. It moves back from fat into the blood only slowly, and that slow release controls how fast it is eliminated.
Patients often misread three consequences of this:
- Elimination is slow, and slower with regular use. Huestis reports a terminal plasma half-life of THC of about 4.1 days in chronic users.
- Drug testing measures history, not impairment. The reported plasma half-life of THC-COOH averages around 5–6 days, with wide individual variation, so metabolites can stay detectable for days after use and for weeks in frequent users. A positive test is not proof of being under the influence. In Thailand, driving under the influence of intoxicants is an offence under traffic law, and a positive test may still be used against a driver who is no longer impaired.
- Levels build up with repeated dosing. On a regular regimen, THC and its metabolites accumulate in tissue and blood over days. How that shows up as effect is complicated by tolerance, which develops to the psychoactive effects in regular users. MacCallum and Russo (2018) advise titrating any cannabis preparation slowly, over as long as two weeks. When to judge whether a regimen works is a decision for the prescriber.
6. Metabolism and Why It Creates Interaction Risk
Cannabinoids are metabolised mainly by the liver’s cytochrome P450 (CYP) enzymes.
- THC is oxidised by CYP2C9, CYP2C19 and CYP3A4, with CYP2C9 mainly responsible for forming 11-OH-THC. It is then conjugated with glucuronic acid. Huestis notes that more than 100 THC metabolites have been identified.
- CBD is metabolised mainly by CYP2C19 and CYP3A4, with other CYP enzymes contributing.
- CBD also inhibits several of these enzymes, notably CYP3A4 and CYP2C19. This is the mechanism behind its documented interactions.
These interactions have real clinical consequences. Case reports describe raised INR with warfarin. Geffrey et al. (2015) followed 13 children taking both CBD and clobazam: on average, levels of the active clobazam metabolite N-desmethylclobazam rose by about 500% and clobazam itself by about 60%, and most of the children needed their clobazam dose reduced. One published case report (Leino et al. 2019) described about a 3-fold rise in dose-normalised tacrolimus levels in a patient taking high-dose CBD. Because CYP2C9 and CYP2C19 both have common genetic variants, the same dose can also give different blood levels in two people. Drug interactions need their own article. Until then, the cautious approach in Start Low, Go Slow (topic 1312) applies, and your full medication list belongs with your prescriber.
7. Excretion
THC leaves the body almost entirely as metabolites rather than unchanged. According to Huestis, 80–90% of a dose is excreted within five days: more than 65% in faeces and about 20% in urine. The main urinary metabolite is the glucuronide conjugate of THC-COOH. CBD is different: a large share of the dose is excreted unchanged in the faeces.
8. What All of This Changes in Practice
| Observation | The pharmacokinetic reason | What follows |
|---|---|---|
| Inhaled effect arrives in minutes | Lung absorption, no first pass | Easier to titrate in real time; short duration means repeat dosing |
| Oral effect starts much later | Gut absorption plus hepatic first pass; plasma peak usually 1–2 h, sometimes 4–6 h | Wait before redosing; redosing is a common cause of oral overshoots |
| Oral needs more drug for the same effect | Oral bioavailability about 4–12% (some studies up to 20%) versus a wide inhaled range | An oral milligram is not an inhaled milligram |
| Oral feels qualitatively different | Proportionally more 11-OH-THC | Not simply “stronger”: a different mix of active compounds |
| Levels build up with regular use | Fat storage and a long terminal half-life | Blood levels accumulate; judge with the prescriber |
| Positive drug test long after use | Fat storage and slow release back into blood | Test result ≠ impairment, but it can still have legal consequences |
| Two patients, same dose, different result | Bioavailability ranges, CYP variants, body composition | Individual titration is not optional |
9. The Thai Context (as of October 2026)
None of the above is dosing advice, and in Thailand it cannot be acted on independently anyway. Under the Notification of the Ministry of Public Health Re: Controlled Herbs (Cannabis), B.E. 2568, issued 26 June 2025, cannabis flower is a controlled herb. It may be dispensed only against a prescription on form PT 33 from an authorised practitioner. Each prescription covers no more than 30 days and is single-use, with no refills. Flower may not be sold or advertised online, and recreational use is not permitted.
In 2026, two Ministerial Regulations B.E. 2569 tightened licensing: one on cannabis and hemp extracts (in force 26 April 2026) and one on controlled-herb licences, No. 2 (in force 30 April 2026). Neither changes the PT 33 prescription rules above. The Cannabis Control Act is still a draft: the Cabinet approved it on 22 September 2026 and sent it to the House. Topic 1330 covers the 2026 changes in more detail.
Product choice, dose and titration schedule are decisions for the prescriber, who knows the patient’s other medications and conditions. What pharmacokinetics gives a patient is not a dose. It gives them the means to have a more useful conversation: to describe what happened and when, and to understand why the prescriber may ask them to wait before deciding whether a treatment works.
If you have compared an inhaled and an oral preparation of the same product under a prescriber’s supervision, please post the timings you observed below: how long until onset, how long the effect lasted, and whether the difference matched what you were told to expect. Individual reports are not evidence of efficacy, but they are a good check on whether the standard timings describe real patients.
References
- MacCallum CA, Russo EB. Practical considerations in medical cannabis administration and dosing. Eur J Intern Med. 2018;49:12–19. doi:10.1016/j.ejim.2018.01.004
- Huestis MA. Human cannabinoid pharmacokinetics. Chem Biodivers. 2007;4(8):1770–1804. doi:10.1002/cbdv.200790152
- Caicedo DA, Pérez-Mañá C, Farré M, Papaseit E. An Overview of the Potential for Pharmacokinetic Interactions Between Drugs and Cannabis Products in Humans. Pharmaceutics. 2025;17(3):319. doi:10.3390/pharmaceutics17030319
- Geffrey AL, Pollack SF, Bruno PL, Thiele EA. Drug-drug interaction between clobazam and cannabidiol in children with refractory epilepsy. Epilepsia. 2015;56(8):1246–1251.
- Leino AD, Emoto C, Fukuda T, Privitera M, Vinks AA, Alloway RR. Evidence of a clinically significant drug-drug interaction between cannabidiol and tacrolimus. Am J Transplant. 2019;19(10):2944–2948.
This article is part of the Asiannabis Community educational series on the science of medical cannabis. It is general information, not medical advice. Dosing decisions belong to a prescriber who knows your case and your other medications.