Can CBD Be Addictive? Reading the Study Findings
Definition
Cannabidiol, or CBD, is one of the cannabinoids found in hemp. Whether it can be addictive has been looked at in humans only a handful of times, most often in the 2017 controlled trial by Babalonis and colleagues [1]. What follows is what that work measured, on whom, and where its scope runs out.
Where the over-reading begins
A trial can report an absence. A sentence can turn that absence into a verdict about a molecule. The distance between those two is where most of this topic goes wrong.
- The most common error in this area is easy to spot once you know it: a single controlled study gets read as a statement about the whole molecule, for everyone, at any amount.
- A finding stays bound to the study that produced it. The amounts, the population and the measures, exactly as they were used, and nothing wider than that.
- Precise reading is a requirement here, not a matter of taste [1]. Swap the route, the amount range or the group of volunteers, and the question has quietly changed.
- What Babalonis and colleagues recorded in 2017 was an absence of detected signal [1]: one study, one route, one amount range, one recruited population, one measurement window.
- An absence of detected signal is not the same thing as a null result from a design that could never have detected anything [1].
- What the design was able to deliver sets the weight of what it reported [1]. No more than that, and no less either.
- Abuse liability and dependence are two items, not one. The first is what the 2017 trial reports on [1]. The second is not establishable by a single controlled trial [1].
- Frequent cannabis users were the recruited population [1], which is a specific group with a specific history, not a general adult sample.
None of that makes the study weak. It makes it a study, with edges you can actually see.
Inside the 2017 protocol
The most cited human work on this question is that 2017 trial [1]. Its shape is worth knowing before anyone quotes its conclusion at a dinner table.
- Cannabidiol was given by mouth, which fixes the route for everything that follows [1].
- The participants were frequent cannabis users, recruited for exactly that reason [1].
- Two families of measures carry the majority of the weight in this type of study, and both were used here [1].
- The first family was self-report: what the participants stated about their own experience during the sessions [1].
- The second family was physiological readings, taken under the same controlled conditions [1].
- The other half of the design was comparison, so the readings had something to sit against rather than floating on their own [1].
- What a design can deliver is what its report can carry, and this one carried both measure families across the tested amount range [1].
- The first item in the report is an absence of detected signal on those measures [1].
- The second item, dependence after prolonged use, is not something one controlled trial can establish [1].
Read that list twice and the practical limit appears on its own. One route. One amount range. One group of people with a particular cannabis history. One window in which measurements were taken [1]. Change any of those and you are asking a fresh question, and the 2017 data cannot answer it [1]. That is not a complaint about the trial. It is what a controlled trial is for: a narrow question, answered under conditions someone else can repeat.
Two cannabinoids, kept apart
THC and cannabidiol are the two best-known cannabinoids, and the reward question reaches them from different directions, which is why the literature keeps them as separate cases [1]. Reward pharmacology driven by receptor activity is the contrast case against which cannabidiol gets assessed [2]. Pharmacokinetic work sits somewhere else again: it counts exposure, not experience [3].
| Subject | What the cited work covers | Where it stops |
|---|---|---|
| THC next to CBD | The two best-known cannabinoids, approached from different directions in the 2017 work, so they are handled as separate cases [1] | A reading of one does not transfer to the other [1] |
| Receptor-driven reward pharmacology | The contrast case used when cannabidiol is assessed, described for cannabinoids in the 2007 work by Huestis [2] | A contrast case is a reference point, not a result about cannabidiol itself [2] |
| Human pharmacokinetics | How much cannabidiol turns up in the body and for how long, compiled by Millar and colleagues in 2018 [3] | Exposure figures only, no subjective effect, so no answer on reward [3] |
| The 2017 measure set | Self-report plus physiological readings, with a comparison arm, in frequent cannabis users [1] | Bound to the oral route, the tested amounts and that recruited population [1] |
The rows sit apart on purpose. Pharmacokinetics tells you what reached the blood [3]; the controlled trial tells you what was measured on people while it was there [1]. Mixing the two produces a sentence that neither publication supports.
The 2018 review and its remit
Millar and colleagues published a systematic review of human cannabidiol pharmacokinetics in 2018 [3]. Pharmacokinetics means how much of a compound reaches the blood and how long it stays measurable there. The remit matters, because the review gets quoted for things it never set out to describe.
| Item | Status in the 2018 review | What follows |
|---|---|---|
| Purpose | A description of human exposure to cannabidiol, gathered across the published studies [3] | It answers exposure questions and was not built around discontinuation after prolonged use [3] |
| Withdrawal after long use | Not the subject of the review [3] | The silence is a gap in the literature, not a demonstration in either direction [3] |
| Reward and abuse liability | Outside a pharmacokinetic remit, since exposure numbers are not subjective effect [3] | The 2017 trial remains the human reference point on that measure set [1] |
| Design logic | An absence of a reward signal in one trial [1] and dependence over time are two questions, not one | They need separate designs, separate durations and separate endpoints [1] |
| Exposure variability | Documented across the studies the review collected [3] | The review records the spread; it does not link it to anything felt [3] |
So the review is useful and narrow at the same time. It maps what has been measured in people, publication by publication, and it leaves the question of stopping after months of use where it found it [3].
What is still open
Since 2014 we have read this kind of literature the same way: what was measured, on whom, over what window. The list below is the leftover, and the leftover is the honest part of the picture. Each row names where the question comes from, so it can be checked against the same publications.
| Open question | Where it comes from | Status |
|---|---|---|
| Do the 2017 findings hold beyond the oral route, the tested amounts and the recruited population? | The scope of the trial by Babalonis and colleagues [1] | Open, since the trial was not designed to answer it [1] |
| What would multi-cannabinoid extracts do on the same measures? | The controlled study used cannabidiol alone [1] | Open, because non-CBD compounds were never part of that protocol [1] |
| Does the exposure variability in the review line up with variability in subjective effect? | The 2018 review documents the exposure side [3] | Open, and the review itself does not draw that link [3] |
| What happens on discontinuation after prolonged use? | A gap in the human literature as reviewed in 2018 [3] | Open, and a single controlled trial cannot settle it [1] |
| What applies to your own situation? | Concerns about use [3] | A conversation with a doctor, especially alongside other medication |
That is the state of the record. One controlled trial with visible edges, one review with a defined remit, and a set of questions nobody has measured yet.
Frequently Asked Questions
4 questionsWhat did the 2017 trial actually report?
Why does the oral route matter when reading that result?
Could a full-spectrum extract behave differently on the same measures?
Does the 2018 review say anything about stopping after months of use?
About this article
Luke Sholl has been writing about cannabinoids, CBD, and the broader benefits of nature since 2011. His background includes first-hand cannabis cultivation experience spanning the full seed-to-harvest lifecycle across so
This wiki article was drafted with AI assistance and reviewed by Luke Sholl, CBD & wellness writer. Editorial oversight by Joshua Askew.
Medical disclaimer. This content is for informational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before use of any substance.
Last reviewed August 27, 2026
References (3)
- [1]Babalonis, S. et al. (2017). Drug and Alcohol Dependence. DOI: https://doi.org/10.1016/j.drugalcdep.2016.11.030
- [2]Huestis, M.A. (2007). Human Cannabinoid Pharmacokinetics. DOI: https://doi.org/10.1002/cbdv.200790152
- [3]Millar, S.A. et al. (2018). A Systematic Review on the Pharmacokinetics of Cannabidiol in Humans. DOI: https://doi.org/10.3389/fphar.2018.01365
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