Δ-8-Tetrahydrocannabinol
Studies and references cited across this article, graded by evidence strength.
Data points an editor reviewed and accepted for publication.
Value Provenance
Dosing
oraltrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 5 mg | 5 mg | low |
| Low | 5–15 mg | 5–15 mg | low |
| Common | 15–40 mg | 15–40 mg | low |
| Strong | 40–80 mg | 40–80 mg | low |
| Heavy | 80+ mg | 80+ mg | low |
| Editorial | No published human dose-response data for Δ8-THC. Oral doses inferred from: (1) Mechoulam pediatric antiemetic dose of 18 mg/m² ≈ 10-30 mg; (2) consumer product serving sizes of 5-40 mg (Ray et al. 2022, noting label accuracy is unreliable); (3) structural analog inference from Δ9-THC oral doses × ~2-3x potency factor (Tagen & Klumpers 2022 estimate Δ8-THC ≈ 2/3 potency of Δ9-THC). Ranges widened conservatively to account for absent controlled data. SAFETY-CRITICAL: these are editorial proposals requiring human review. | ||
ReasoningReasoningNo published human dose-response data for Δ8-THC. Oral doses inferred from: (1) Mechoulam pediatric antiemetic dose of 18 mg/m² ≈ 10-30 mg; (2) consumer product serving sizes of 5-40 mg (Ray et al. 2022, noting label accuracy is unreliable); (3) structural analog inference from Δ9-THC oral doses × ~2-3x potency factor (Tagen & Klumpers 2022 estimate Δ8-THC ≈ 2/3 potency of Δ9-THC). Ranges widened conservatively to account for absent controlled data. SAFETY-CRITICAL: these are editorial proposals requiring human review. Evidence basis: structural_analogy | |||
vaporizedtrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Threshold | 2 mg | 2 mg | low |
| Low | 2–5 mg | 2–5 mg | low |
| Common | 5–15 mg | 5–15 mg | low |
| Strong | 15–30 mg | 15–30 mg | low |
| Heavy | 30+ mg | 30+ mg | low |
| Editorial | No published human dose-response data for Δ8-THC via inhalation. Vaporized doses inferred entirely from structural analog inference: Δ9-THC inhalation doses × ~2-3x potency factor. Johns Hopkins vaporized Δ8-THC trial (NCT05287256, Spindle et al. 2025) has been completed but full dose-response data await publication. Ranges widened conservatively. SAFETY-CRITICAL: these are editorial proposals requiring human review. | ||
ReasoningReasoningNo published human dose-response data for Δ8-THC via inhalation. Vaporized doses inferred entirely from structural analog inference: Δ9-THC inhalation doses × ~2-3x potency factor. Johns Hopkins vaporized Δ8-THC trial (NCT05287256, Spindle et al. 2025) has been completed but full dose-response data await publication. Ranges widened conservatively. SAFETY-CRITICAL: these are editorial proposals requiring human review. Evidence basis: structural_analogy | |||
Duration
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 30–120 minutes | 30–120 minutes | low |
| Editorial | Inferred from Δ9-THC oral onset profile. Δ8-THC rat PK shows Tmax ~6h for MCT oil, ~0.67-1h for nanoemulsion (Senetra et al. 2026; Tagen et al. 2023), but human subjective onset is expected to follow Δ9-THC oral kinetics. No controlled human time-course data for Δ8-THC. | ||
ReasoningReasoningInferred from Δ9-THC oral onset profile. Δ8-THC rat PK shows Tmax ~6h for MCT oil, ~0.67-1h for nanoemulsion (Senetra et al. 2026; Tagen et al. 2023), but human subjective onset is expected to follow Δ9-THC oral kinetics. No controlled human time-course data for Δ8-THC. Evidence basis: structural_analogy | |||
| Come uptrace | 30–60 minutes | 30–60 minutes | low |
| Editorial | Structural analog inference from Δ9-THC oral come-up. No human Δ8-THC time-course data published. | ||
ReasoningReasoningStructural analog inference from Δ9-THC oral come-up. No human Δ8-THC time-course data published. Evidence basis: structural_analogy | |||
| Peaktrace | 2–4 hours | 2–4 hours | low |
| Editorial | Structural analog inference from Δ9-THC oral peak duration. Active metabolite 11-OH-Δ8-THC may extend perceived peak after oral dosing. No human Δ8-THC data. | ||
ReasoningReasoningStructural analog inference from Δ9-THC oral peak duration. Active metabolite 11-OH-Δ8-THC may extend perceived peak after oral dosing. No human Δ8-THC data. Evidence basis: structural_analogy | |||
| Offsettrace | 2–4 hours | 2–4 hours | low |
| Editorial | Structural analog inference from Δ9-THC oral offset. High lipophilicity and tissue sequestration support gradual decline. No human Δ8-THC data. | ||
ReasoningReasoningStructural analog inference from Δ9-THC oral offset. High lipophilicity and tissue sequestration support gradual decline. No human Δ8-THC data. Evidence basis: structural_analogy | |||
| Totaltrace | 4–8 hours | 4–8 hours | low |
| Editorial | Structural analog inference from Δ9-THC oral total subjective duration. Reflects onset through offset only — does not include aftereffects or pharmacological elimination. No human Δ8-THC time-course data. | ||
ReasoningReasoningStructural analog inference from Δ9-THC oral total subjective duration. Reflects onset through offset only — does not include aftereffects or pharmacological elimination. No human Δ8-THC time-course data. Evidence basis: structural_analogy | |||
| After effectstrace | 2–12 hours | 2–12 hours | low |
| Editorial | Structural analog inference from Δ9-THC. Wide range reflects variable individual metabolism and lipophilic tissue redistribution. Residual sedation and mild appetite effects may persist. No human Δ8-THC data. | ||
ReasoningReasoningStructural analog inference from Δ9-THC. Wide range reflects variable individual metabolism and lipophilic tissue redistribution. Residual sedation and mild appetite effects may persist. No human Δ8-THC data. Evidence basis: structural_analogy | |||
vaporized
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 1–5 minutes | 1–5 minutes | low |
| Editorial | Structural analog inference from Δ9-THC inhalation onset. Rapid pulmonary absorption bypasses first-pass metabolism. No human Δ8-THC time-course data, though Johns Hopkins vaporized trial (Spindle 2025) is completed. | ||
ReasoningReasoningStructural analog inference from Δ9-THC inhalation onset. Rapid pulmonary absorption bypasses first-pass metabolism. No human Δ8-THC time-course data, though Johns Hopkins vaporized trial (Spindle 2025) is completed. Evidence basis: structural_analogy | |||
| Come uptrace | 5–10 minutes | 5–10 minutes | low |
| Editorial | Structural analog inference from Δ9-THC inhalation come-up. No human Δ8-THC data. | ||
ReasoningReasoningStructural analog inference from Δ9-THC inhalation come-up. No human Δ8-THC data. Evidence basis: structural_analogy | |||
| Peaktrace | 15–45 minutes | 15–45 minutes | low |
| Editorial | Structural analog inference from Δ9-THC inhalation peak. Less first-pass metabolite contribution than oral route. No human Δ8-THC data. | ||
ReasoningReasoningStructural analog inference from Δ9-THC inhalation peak. Less first-pass metabolite contribution than oral route. No human Δ8-THC data. Evidence basis: structural_analogy | |||
| Offsettrace | 1–2 hours | 1–2 hours | low |
| Editorial | Structural analog inference from Δ9-THC inhalation offset. No human Δ8-THC data. | ||
ReasoningReasoningStructural analog inference from Δ9-THC inhalation offset. No human Δ8-THC data. Evidence basis: structural_analogy | |||
| Totaltrace | 1–4 hours | 1–4 hours | low |
| Editorial | Structural analog inference from Δ9-THC inhalation total subjective duration. Shorter than oral due to absence of sustained first-pass metabolite generation. No human Δ8-THC data. | ||
ReasoningReasoningStructural analog inference from Δ9-THC inhalation total subjective duration. Shorter than oral due to absence of sustained first-pass metabolite generation. No human Δ8-THC data. Evidence basis: structural_analogy | |||
| After effectstrace | 1–6 hours | 1–6 hours | low |
| Editorial | Structural analog inference from Δ9-THC inhalation aftereffects. Lipophilic redistribution from tissue stores may produce residual sedation. No human Δ8-THC data. | ||
ReasoningReasoningStructural analog inference from Δ9-THC inhalation aftereffects. Lipophilic redistribution from tissue stores may produce residual sedation. No human Δ8-THC data. Evidence basis: structural_analogy | |||
Safety
Toxicity Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Acute | low | low | medium |
| Chronic | low | low | medium |
| Organs Affected | CNS, cardiovascular | CNS, cardiovascular | medium |
| Editorial | Work-notes specify acute: low, chronic: low-to-moderate. Applying evidence discount rule: chronic downgraded from 'low-to-moderate' to 'low' because organ damage evidence is absent for the pure compound — the elevated chronic concern (product contamination) is a product-level risk, not pharmacology-level. Acute toxicity supported by FAERS case series (Simon et al. 2023) and CDC poison control data (2,362 exposures). No LD50 data, no human fatalities, very high therapeutic index by class. | ||
ReasoningReasoningWork-notes specify acute: low, chronic: low-to-moderate. Applying evidence discount rule: chronic downgraded from 'low-to-moderate' to 'low' because organ damage evidence is absent for the pure compound — the elevated chronic concern (product contamination) is a product-level risk, not pharmacology-level. Acute toxicity supported by FAERS case series (Simon et al. 2023) and CDC poison control data (2,362 exposures). No LD50 data, no human fatalities, very high therapeutic index by class. Evidence basis: published_case_series | |||
Dependence Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Physical | low | low | medium |
| Psychological | moderate | moderate | medium |
| Compulsive Redosing | low | low | medium |
| Dose Escalation | moderate | moderate | medium |
| Editorial | Physical dependence demonstrated substance-specifically in rodents (Vanegas et al. 2022: rimonabant-precipitated withdrawal after Δ8-THC ≥10 mg/kg BID × 6 days). Psychological dependence and CUD criteria inferred from Δ9-THC literature via structural analogy. Work-notes specify physical: low-to-moderate, psychological: moderate; physical rounded to 'low' per evidence discount (rodent data only, no human characterization). | ||
ReasoningReasoningPhysical dependence demonstrated substance-specifically in rodents (Vanegas et al. 2022: rimonabant-precipitated withdrawal after Δ8-THC ≥10 mg/kg BID × 6 days). Psychological dependence and CUD criteria inferred from Δ9-THC literature via structural analogy. Work-notes specify physical: low-to-moderate, psychological: moderate; physical rounded to 'low' per evidence discount (rodent data only, no human characterization). Evidence basis: animal_study | |||
Withdrawal Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Severity | mild | mild | low |
| Symptoms | Irritability, Sleep disturbance, Decreased appetite, Dysphoria, Jumping (rodent), Paw tremors (rodent), Altered marble-burying behavior (rodent) | Irritability, Sleep disturbance, Decreased appetite, Dysphoria, Jumping (rodent), Paw tremors (rodent), Altered marble-burying behavior (rodent) | low |
| Fatal | No | No | low |
| Medical Supervision | Not required | Not required | low |
| Editorial | Somatic withdrawal signs demonstrated in rodents with rimonabant-precipitated withdrawal (Vanegas et al. 2022). Human withdrawal symptoms (irritability, sleep disturbance, decreased appetite, dysphoria) and timeline (onset 1-2 days, duration 1-2 weeks) are entirely inferred from Δ9-THC cannabis withdrawal literature. Severity downgraded from 'mild-to-moderate' to 'mild' per evidence discount — no human clinical characterization exists for Δ8-THC-specific withdrawal. | ||
ReasoningReasoningSomatic withdrawal signs demonstrated in rodents with rimonabant-precipitated withdrawal (Vanegas et al. 2022). Human withdrawal symptoms (irritability, sleep disturbance, decreased appetite, dysphoria) and timeline (onset 1-2 days, duration 1-2 weeks) are entirely inferred from Δ9-THC cannabis withdrawal literature. Severity downgraded from 'mild-to-moderate' to 'mild' per evidence discount — no human clinical characterization exists for Δ8-THC-specific withdrawal. Evidence basis: animal_study | |||
Tolerance Profiletrace
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Buildup | moderate | moderate | medium |
| Half-life | 7 days | 7 days | medium |
| Full Reset | 21 days | 21 days | medium |
| Cross-tolerances | Δ9-THC, WIN 55,212-2, Synthetic cannabinoids (CB1 agonists) | Δ9-THC, WIN 55,212-2, Synthetic cannabinoids (CB1 agonists) | medium |
| Editorial | Tolerance buildup is substance-specific (Vanegas et al. 2022: tolerance to tetrad endpoints in mice). Half-life and full reset values are inferred from Δ9-THC class data — no human tolerance timeline data exist for Δ8-THC. Cross-tolerance confirmed substance-specifically for WIN 55,212-2; Δ9-THC cross-tolerance inferred from shared CB1 mechanism and discriminative stimulus substitution. | ||
ReasoningReasoningTolerance buildup is substance-specific (Vanegas et al. 2022: tolerance to tetrad endpoints in mice). Half-life and full reset values are inferred from Δ9-THC class data — no human tolerance timeline data exist for Δ8-THC. Cross-tolerance confirmed substance-specifically for WIN 55,212-2; Δ9-THC cross-tolerance inferred from shared CB1 mechanism and discriminative stimulus substitution. Evidence basis: animal_study | |||
Effects & Profile
Contraindications
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| psychiatric History of psychotic disorderstrace | absolute | absolute | low |
| Editorial | Class inference from Δ9-THC. CB1 agonism is the established mechanism for cannabis-induced psychosis. Δ8-THC shares this mechanism with ~6-fold lower CB1 affinity but sufficient agonist activity to produce psychoactive effects. | ||
ReasoningReasoningClass inference from Δ9-THC. CB1 agonism is the established mechanism for cannabis-induced psychosis. Δ8-THC shares this mechanism with ~6-fold lower CB1 affinity but sufficient agonist activity to produce psychoactive effects. | |||
| cardiovascular Cardiovascular diseasetrace | relative | relative | low |
| Editorial | Class inference from Δ9-THC. CB1-mediated cardiovascular effects are well-documented for Δ9-THC and expected to apply to Δ8-THC given shared receptor pharmacology. | ||
ReasoningReasoningClass inference from Δ9-THC. CB1-mediated cardiovascular effects are well-documented for Δ9-THC and expected to apply to Δ8-THC given shared receptor pharmacology. | |||
| pregnancy breastfeeding Pregnancy and lactationtrace | absolute | absolute | low |
| Editorial | Class inference from Δ9-THC. Lipophilicity (Vd = 108 L/kg in rats) ensures extensive tissue distribution including placental and mammary transfer. CB1 agonism during development is a recognized teratogenic risk factor. | ||
ReasoningReasoningClass inference from Δ9-THC. Lipophilicity (Vd = 108 L/kg in rats) ensures extensive tissue distribution including placental and mammary transfer. CB1 agonism during development is a recognized teratogenic risk factor. | |||
| other Anticoagulant therapy (warfarin)trace | relative | relative | medium |
| Editorial | CYP profile inferred from Δ9-THC structural analogy (Nachnani et al. 2024). Warfarin interaction is a narrow-therapeutic-index safety concern warranting relative contraindication despite indirect evidence. | ||
ReasoningReasoningCYP profile inferred from Δ9-THC structural analogy (Nachnani et al. 2024). Warfarin interaction is a narrow-therapeutic-index safety concern warranting relative contraindication despite indirect evidence. | |||
| hepatic Hepatic impairmenttrace | relative | relative | low |
| Editorial | Class inference from Δ9-THC and Δ8-THC rodent PK data showing extensive first-pass metabolism (oral bioavailability ~3%, clearance 5.6 L/h/kg). Hepatic impairment would predictably alter exposure. | ||
ReasoningReasoningClass inference from Δ9-THC and Δ8-THC rodent PK data showing extensive first-pass metabolism (oral bioavailability ~3%, clearance 5.6 L/h/kg). Hepatic impairment would predictably alter exposure. | |||
| age Pediatric populationstrace | absolute | absolute | high |
| Editorial | Substance-specific evidence from CDC HAN 00451 (2,362 exposures, 41% pediatric), Babalonis et al. 2021 (LOC in children), and Garay et al. 2025 (toxic doses in children <6). This is the highest-confidence contraindication for Δ8-THC. | ||
ReasoningReasoningSubstance-specific evidence from CDC HAN 00451 (2,362 exposures, 41% pediatric), Babalonis et al. 2021 (LOC in children), and Garay et al. 2025 (toxic doses in children <6). This is the highest-confidence contraindication for Δ8-THC. | |||
Timeline Phases
oral
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 1800–7200 sec(i=0.10) | 1800–7200 sec(i=0.10) | low |
| Editorial | All oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. | ||
ReasoningReasoningAll oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. Evidence basis: structural_analogy | |||
| Come uptrace | 1800–3600 sec(i=0.40) | 1800–3600 sec(i=0.40) | low |
| Editorial | All oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. | ||
ReasoningReasoningAll oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. Evidence basis: structural_analogy | |||
| Peaktrace | 7200–14400 sec(i=1.00) | 7200–14400 sec(i=1.00) | low |
| Editorial | All oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. | ||
ReasoningReasoningAll oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. Evidence basis: structural_analogy | |||
| Resolutiontrace | 7200–14400 sec(i=0.50) | 7200–14400 sec(i=0.50) | low |
| Editorial | All oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. | ||
ReasoningReasoningAll oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. Evidence basis: structural_analogy | |||
| Afterglowtrace | 7200–43200 sec(i=0.15) | 7200–43200 sec(i=0.15) | low |
| Editorial | All oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. | ||
ReasoningReasoningAll oral timeline phases inferred from Δ9-THC oral duration profile via structural analogy. No controlled human time-course data for Δ8-THC have been published. Δ8-THC shares identical metabolic pathway (CYP3A4/2C9 → 11-OH-Δ8-THC active metabolite) and comparable lipophilicity, supporting analogous oral kinetics. Phase durations widened to reflect absent direct evidence. Evidence basis: structural_analogy | |||
vaporized
| Field | Published | AI Proposed | Confidence |
|---|---|---|---|
| Onsettrace | 60–300 sec(i=0.30) | 60–300 sec(i=0.30) | low |
| Editorial | All vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. | ||
ReasoningReasoningAll vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. Evidence basis: structural_analogy | |||
| Come uptrace | 300–600 sec(i=0.70) | 300–600 sec(i=0.70) | low |
| Editorial | All vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. | ||
ReasoningReasoningAll vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. Evidence basis: structural_analogy | |||
| Peaktrace | 900–2700 sec(i=1.00) | 900–2700 sec(i=1.00) | low |
| Editorial | All vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. | ||
ReasoningReasoningAll vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. Evidence basis: structural_analogy | |||
| Resolutiontrace | 3600–7200 sec(i=0.40) | 3600–7200 sec(i=0.40) | low |
| Editorial | All vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. | ||
ReasoningReasoningAll vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. Evidence basis: structural_analogy | |||
| Afterglowtrace | 3600–21600 sec(i=0.10) | 3600–21600 sec(i=0.10) | low |
| Editorial | All vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. | ||
ReasoningReasoningAll vaporized timeline phases inferred from Δ9-THC inhalation duration profile via structural analogy. No controlled human time-course data for vaporized Δ8-THC published, though Johns Hopkins trial (Spindle et al. 2025, NCT05287256) compared vaporized Δ8-THC to Δ9-THC — full data await publication. Rapid onset reflects pulmonary absorption bypassing first-pass metabolism. Evidence basis: structural_analogy | |||
Dose Tier Summaries
Minimal perceptible effects emerge as a faint shift in mood — a subtle brightening or softening of emotional tone that may take 30 minutes or more to notice via oral administration. A gentle body warmth or slight heaviness may be felt, but physical effects are barely distinguishable from baseline. Cognitive function remains largely intact. Appetite may increase marginally. Tolerant cannabis users may find threshold doses imperceptible. The experience serves primarily as a calibration point for individual sensitivity rather than a meaningful psychoactive event. Oral onset is slow (up to 2 hours). Do not redose before confirming full onset, as stacking threshold doses can produce unexpectedly strong effects.
No published human dose-response data for Δ8-THC. Threshold description inferred from Δ9-THC threshold experience profile, adjusted for Δ8-THC's ~2/3 relative potency and consumer reports of 'clearer-headed' character (Kruger & Kruger 2022).
ReasoningReasoning
No published human dose-response data for Δ8-THC. Threshold description inferred from Δ9-THC threshold experience profile, adjusted for Δ8-THC's ~2/3 relative potency and consumer reports of 'clearer-headed' character (Kruger & Kruger 2022).
Evidence basis: structural_analogy
Mild relaxation and subtle euphoria become clearly noticeable. A light body high develops — gentle warmth and slight muscle relaxation without heaviness. Appetite enhancement begins, and dry mouth may appear. The mood shift is pleasant but easily managed. Cognitive clarity is largely preserved at this level, distinguishing Δ8-THC from equivalent subjective doses of Δ9-THC. Thought deceleration is minimal. Focus suppression is slight — most tasks remain manageable. Anxiety is unlikely; anxiolytic effects are more typical. Social interaction feels natural. Duration commitment is modest (1–4 hours inhaled, 4–6 hours oral). Sleep may come more easily at the tail end of the experience.
Inferred from Δ9-THC light-dose experience, adjusted for Δ8-THC's lower CB1 affinity and consumer survey data describing 'lighter' and 'clearer-headed' effects (Kruger & Kruger 2022). No controlled human dose-response data.
ReasoningReasoning
Inferred from Δ9-THC light-dose experience, adjusted for Δ8-THC's lower CB1 affinity and consumer survey data describing 'lighter' and 'clearer-headed' effects (Kruger & Kruger 2022). No controlled human dose-response data.
Evidence basis: structural_analogy
Clear cannabinoid intoxication is present. Euphoria and relaxation are the dominant features — a warm, pleasant cognitive glow paired with noticeable body high and muscle relaxation. Appetite enhancement is reliable. Nausea suppression is effective at this range, consistent with Mechoulam's antiemetic findings. Cognitive effects become apparent: mild thought deceleration, short-term memory suppression, and subtle time alteration. Focus suppression makes complex tasks more difficult. These cognitive changes are consistently described as less impairing than equivalent Δ9-THC doses. Humor enhancement and music enhancement may emerge. Anxiolytic effects are typical at this tier. Motor control impairment is mild but present — driving is unsafe. Dry mouth is common. Sedation increases toward the offset phase.
Common-dose profile synthesized from Kruger & Kruger 2022 consumer survey (relaxation, euphoria, pain relief, anxiolysis as top effects; 'clearer-headed' than Δ9-THC), Mechoulam 1995 antiemetic data, and Δ9-THC common-dose class inference. Dose values themselves lack controlled human data.
ReasoningReasoning
Common-dose profile synthesized from Kruger & Kruger 2022 consumer survey (relaxation, euphoria, pain relief, anxiolysis as top effects; 'clearer-headed' than Δ9-THC), Mechoulam 1995 antiemetic data, and Δ9-THC common-dose class inference. Dose values themselves lack controlled human data.
Evidence basis: structural_analogy
Pronounced intoxication with significant sedation and strong euphoria. Body high is heavy — deep muscle relaxation and bodily heaviness dominate the physical experience. Cognitive impairment is notable: marked memory suppression, meaningful thought deceleration, and time alteration become difficult to ignore. Anxiety and paranoia become possible at this tier, particularly in predisposed individuals or those with low cannabinoid tolerance, though rates remain lower than with equivalent Δ9-THC doses. Motor control impairment is significant — coordination is visibly affected. Appetite enhancement is strong. Physical fatigue and sedation increase throughout the experience. Functional impairment is substantial; this tier commits the user to several hours of incapacity. Oral administration at this level carries risk of unexpectedly prolonged duration.
Strong-dose profile inferred from Δ9-THC strong-dose experience, CDC/FAERS adverse event data (anxiety, dizziness, confusion at high doses), and Kruger 2022 survey noting lower anxiety/paranoia rates than Δ9-THC. No controlled Δ8-THC dose-response data.
ReasoningReasoning
Strong-dose profile inferred from Δ9-THC strong-dose experience, CDC/FAERS adverse event data (anxiety, dizziness, confusion at high doses), and Kruger 2022 survey noting lower anxiety/paranoia rates than Δ9-THC. No controlled Δ8-THC dose-response data.
Evidence basis: structural_analogy
Intense sedation dominates. Confusion and disorientation are likely. Cognitive impairment is severe — memory suppression is near-total for the peak period, and thought disorganization may occur. Rare visual or auditory disturbances have been reported at this level in adverse event data, though frank hallucinations remain uncommon. Anxiety and paranoia risk is elevated, particularly in cannabis-naive individuals. Nausea may paradoxically emerge despite Δ8-THC's antiemetic properties. Dizziness is common. Tachycardia may be noticeable and distressing. Loss of consciousness has been documented in pediatric cases at high weight-adjusted doses. This tier is not recommended. The experience is unlikely to be pleasant and carries meaningful physical risk. Oral administration at heavy doses, especially with slow-onset formulations, risks hours of incapacitation with no ability to reduce intensity.
Heavy-dose profile drawn from CDC HAN 00451 adverse event data (hallucinations, vomiting, tremor, confusion, LOC in pediatric cases), FAERS data (55% required intervention), and Δ9-THC heavy-dose class inference. This tier represents adverse event territory rather than intended use.
ReasoningReasoning
Heavy-dose profile drawn from CDC HAN 00451 adverse event data (hallucinations, vomiting, tremor, confusion, LOC in pediatric cases), FAERS data (55% required intervention), and Δ9-THC heavy-dose class inference. This tier represents adverse event territory rather than intended use.
Evidence basis: structural_analogy
History
publish Oct 2, 2026 · by agent-psx
backfill Jun 4, 2026
Historical versions do not record which reviewer approved them; editorial accountability is recorded per value in the database and in the publication ledger going forward.
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