How it actually works
Cannabinoid science is unusually prone to overstatement online. Here's the honest version: what THC and CBD do, the endocannabinoid system, where terpenes stand, how dosing works — and the popular myths, corrected.
Last reviewed 15 June 2026 · Education, not medical advice
Your body's homeostatic “dimmer switch”
Receptors
CB1 (mostly in the nervous system, behind THC's psychoactive effects) and CB2 (mainly immune cells, generally anti-inflammatory).
Endocannabinoids
Anandamide and 2-AG — made 'on demand' and released backwards across the synapse to dampen neurotransmitter release.
What it regulates
Pain, mood, appetite, memory, motor control, sleep and immune responses — acting as a homeostatic balancer.
THC, CBD and the minor cannabinoids
THC
IntoxicatingTetrahydrocannabinol
A partial agonist at CB1 and CB2 receptors; its CB1 action in the brain drives the intoxicating 'high'. Effects include euphoria, relaxation and increased appetite — but at higher doses, or in vulnerable people, anxiety, paranoia and cognitive impairment. It is dose-limiting and titrated in small steps.
Evidence · Approved use (antiemetic); moderate for pain & spasticity
CBD
Non-intoxicatingCannabidiol
Non-intoxicating, with the strongest evidence of any cannabinoid (purified CBD for rare childhood epilepsies). Myth correction: CBD is NOT a direct CB1 agonist — it works through a 'promiscuous' set of more than 65 targets, including 5-HT1A and TRPV1, and acts as a CB1 negative allosteric modulator that can blunt some THC effects.
Evidence · Strong (rare epilepsies); mixed elsewhere
CBG
Non-intoxicatingCannabigerol
The biosynthetic 'mother cannabinoid' from which others form. Weak, mixed CB1/CB2 activity; notable as a potent α2-adrenoceptor agonist in the lab. No approved human uses — claims are preclinical.
Evidence · Preclinical only
CBN
Non-intoxicatingCannabinol
A degradation product of THC. The popular belief that 'CBN is strongly sedating' is largely a myth — it traces to anecdotes and a roughly 50-year-old rat study, with essentially no human data.
Evidence · Preclinical; sedation claim is largely a myth
CBC
Non-intoxicatingCannabichromene
Non-intoxicating, acting largely independently of CB1/CB2 (mainly via TRPA1/TRPV1). Interesting in the lab, but unproven in people.
Evidence · Preclinical only
THCV
Dose-dependentTetrahydrocannabivarin
Dose-dependent: at low doses it acts as a CB1 neutral antagonist — the basis for appetite suppression, the opposite of THC. Studied for metabolic effects, but mostly preclinical.
Evidence · Mostly preclinical
Aromatic compounds — mostly preclinical
For almost every “terpene benefit” promoted online, the supporting data is preclinical (test-tube or rodent). Treat strong therapeutic claims as hypotheses, not established medicine.
| Terpene | Proposed effects | Actual evidence |
|---|---|---|
| Myrcene | Sedation, analgesia | Animal/preclinical only. The 'myrcene = couch-lock' rule has no peer-reviewed basis. |
| Limonene | Anxiolytic, mood | Strongest human signal of any terpene: vaporised D-limonene reduced THC-induced anxiety in a small RCT. |
| Pinene | Anti-inflammatory, 'protects memory' | In-vitro / animal. The 'pinene protects memory' claim is not supported by human data. |
| Linalool | Sedative, anxiolytic | Mostly animal/in-vitro; lavender aromatherapy has some human anxiety data. |
| β-Caryophyllene | Anti-inflammatory, analgesic | Clearest mechanism — a dietary cannabinoid and selective CB2 agonist — but human proof still lacking. |
| Humulene | Anti-inflammatory | In-vitro / animal only; no human efficacy data. |
“Start low, go slow”
Begin at a very low dose and increase in small steps at spaced intervals, watching for benefit and side effects, to find the lowest effective dose. THC has biphasic effects — low doses can calm, higher doses can provoke anxiety — and reaching a “high” is not required for symptom control. Dosing is individual and set by your prescriber.
| Route | Onset | Duration | Bioavailability |
|---|---|---|---|
| Inhaled / vaporised | Seconds–minutes | 2–4 h (up to 6–7 h) | THC ~30% (technique-dependent) |
| Oromucosal spray / sublingual | In plasma ~15 min, peak ~45–120 min | Comparable to oral | Higher than swallowed (partly bypasses first-pass) |
| Swallowed oil / capsule | 1–3 h | 6–12 h (up to 24 h per NZ guidance) | THC ~6–20% (variable) |
| Topical | Minutes–~1 h, local | A few hours locally | Minimal systemic |
| Transdermal patch | Slow (hours) | Many hours to >24 h | Low without permeation enhancers |
Where cannabis is inhaled, vaporising (around 180–210°C) is preferred over smoking, which produces tar and other toxicants.
What you'll hear online vs the evidence
“CBD activates your CB1 receptors like THC does.”
No. CBD is not a direct CB1 agonist. It works through a wide set of other targets and can actually blunt some of THC's effects as a CB1 negative allosteric modulator.
“CBN is a powerful sleep aid.”
Largely a myth. It traces to old anecdote and a single ageing rat study, with essentially no human evidence.
“Indica vs sativa / myrcene tells you the effect.”
The 'myrcene = couch-lock indica' rule has no peer-reviewed basis — it traces to an uncited blog post. Cannabinoid ratio and dose matter far more.
“The entourage effect is proven.”
Biologically plausible and interesting, but there are no clinical trials designed to validate it. The term is often used for marketing.
“CBD always cancels out THC.”
An oversimplification. The 'THC-sparing' effect is dose- and route-dependent; one controlled edibles study found CBD did not reliably reduce — and on some measures increased — THC's adverse effects.
“A prescription means I can drive normally.”
No. A prescription does not exempt you from roadside oral-fluid testing or the 12-hour ban, and it is always illegal to drive while impaired. See the Driving & the law page.
This is general information, not medical advice. Only a registered New Zealand doctor can decide whether medicinal cannabis is right for you.