This is not an endorsement of drinking or taking drugs (please read before you proceed).
If you live with T1D and are choosing to consume drugs, please check in with your diabetes care team and have support in place. This is not medical advice.
This is Part 4 of the Partying with T1D guide. It is an honest, lived-experience, harm-reduction look at cannabis, ketamine, and classical psychedelics — and the failure modes they commonly create in T1D: appetite shifts, time distortion, dissociation, nausea/vomiting, impaired judgement, and reduced self-rescue capacity.
Make sure you’ve read Part 1: Partying with T1D (Hub + Intro) to understand the shared principles used across this system (the inverted U, set and setting, dose uncertainty, reduced self-rescue).
This page is not a recommendation or an endorsement of using any psychoactive substance. It does not provide instructions for use. It draws from lived experiences of people with T1D (people we’ve met, worked with, and supported), focusing on what tends to happen in the body and in glucose patterns, what can go wrong, and what has reduced harm in practice.
One key theme is the inverted U-curve: a little may be subjectively “pleasant”; too much can become overwhelming, dysregulating, or dangerous. For T1D, the problem is often not the drug’s direct metabolic effect — it’s the downstream behaviour (eating, insulin decisions, time loss, sleep disruption, and reduced capacity to self-correct).
Overview
Cannabis, ketamine, and hallucinogens are often described as “not really glucose drugs”. In T1D, that framing is misleading. The main risk is loss of reliable self-management: time distortion, altered perception, dissociation, impaired judgement, nausea/vomiting, and unpredictable eating patterns.
Across lived experience, the most common T1D failure modes look like this:
- Unplanned eating (munchies, snacking, “forgot I ate”) → post-event hyperglycaemia if insulin isn’t given
- Time distortion → missed boluses, missed hypo treatment, missed set changes
- Reduced self-rescue → you may recognise a problem but be unable to act cleanly
- Nausea/vomiting (especially with ketamine and mushrooms) → hypo risk + dehydration risk
- Sleep disruption → next-day insulin resistance and care fatigue
- Alcohol co-use → multiplies risk by adding sedation + delayed hypoglycaemia
Everything on this page points back to two concepts:
- The inverted U: each substance has a narrow “manageable” zone and a steep drop-off into panic, confusion, vomiting, dissociation, or unsafe behaviour.
- Dose uncertainty: with unregulated substances, potency can vary. Numbers can create false confidence if the content is not what you think it is.
The detail
Cannabis (THC) and T1D
Psychoactive cannabinoid. The main active compound is THC (tetrahydrocannabinol), which acts primarily via the endocannabinoid system (notably CB1 receptors) and alters perception, attention, mood, appetite, and time sense. Effects vary by product potency, route, and individual sensitivity.
T1D pattern: cannabis is rarely a direct “glucose mover”. The common risk is behavioural: unannounced eating (“munchies”), time loss, and reduced follow-through on bolusing and hypo treatment.
Typical exposure bands (illustrative, not prescriptive)
Because products vary massively in THC content, “dose” is best described by route. The ranges below exist to make the inverted U concept concrete — not to guide use.
| Route | Lower exposure band | Moderate exposure band | Higher exposure band |
| Edibles (gummies, brownies, drinks) | ~2.5–5 mg THC | ~5–10 mg THC | >10–20+ mg THC (often overwhelming, especially with low tolerance) |
| Inhaled (smoked/vaped) | Low exposure (a small number of inhalations) | Moderate exposure | High exposure (including high-potency products / concentrates) |
Why inhaled is hard to quantify: inhaled exposure depends on product potency and the inhalation pattern. The more useful framing is the inverted U: moving from “mild” to “too much” can happen quickly, especially when tired, anxious, dehydrated, or drinking.
Onset and duration (typical)
- Onset: inhaled within minutes; edible 30–120 minutes
- Peak: inhaled 15–45 minutes; edible 1.5–3 hours
- Total duration: inhaled ~2–4 hours; edible ~4–8+ hours
- After-effects: sedation, “hangover”, altered sleep, reduced concentration (especially after heavier exposure)
T1D considerations
- Unplanned eating can cause large post-cannabis highs if insulin isn’t taken
- Judgement may be impaired, reducing the chance of bolusing or correcting
- Closed-loop systems can struggle with repeated unannounced snacks
- At higher exposure: paranoia, anxiety, panic, and loss of control can make self-care collapse
Ketamine (Special K) and T1D
Ketamine is a dissociative anaesthetic and primarily an NMDA receptor antagonist. At recreational exposures, it can produce dissociation, altered body ownership, dream-like states, and impaired coordination. In T1D, the glucose risk is mostly indirect: dissociation can remove your ability to self-manage even if you “know” what to do.
Typical exposure bands (illustrative, not prescriptive)
The table below is illustrative, not prescriptive. It exists to explain why overshooting happens and why “a bit more” can flip the experience into immobility, vomiting, or loss of self-rescue capacity.
| Route | Lower exposure band | Moderate exposure band | Higher exposure band |
| Nasal (insufflated) | ~15–30 mg | ~30–75 mg | >75–125+ mg (risk of “K-hole”, immobility, vomiting) |
| Oral | ~40–75 mg | ~75–150 mg | >150–250+ mg (higher nausea/immobility risk) |
Oral exposures are often higher than nasal to achieve similar subjective effects because oral bioavailability is lower. With unregulated products, potency varies, which narrows the margin for error.
Onset and duration (typical)
- Onset: nasal 5–10 minutes; oral 15–30 minutes
- Peak: 20–60 minutes
- Total duration: ~45–90 minutes (nasal) to ~1.5–2.5 hours (oral)
- After-effects: grogginess, impaired balance, confusion; sometimes nausea/vomiting
T1D considerations
- Not usually a direct glucose-altering substance
- Biggest risk: loss of ability to self-manage (especially at higher exposure / “K-hole” states)
- You may not recognise or treat a hypo while dissociated
- Alcohol co-use increases the risk of not treating a hypo due to combined sedation/dissociation
- Ensure at least one person knows you have T1D and what severe hypoglycaemia can look like
Hallucinogens: LSD and psilocybin (magic mushrooms) and T1D
Classical psychedelics primarily act via serotonin 5-HT2A receptors. They can radically alter perception, emotion, time sense, and the feeling of self. This can feel expansive or frightening. For anyone with T1D, the practical risk is simple: these are long-acting altered states where checking glucose, eating, bolusing, and treating hypos may become unreliable.
Common experiences include:
- Perceptual shifts in sound, colour, time, and emotion
- Sensory crossover (synesthesia)
- Euphoria and insight, or anxiety and confusion
- Altered sense of self (“ego dissolution”) at higher exposures
- High sensitivity to set and setting (environment and mental state)
LSD (Acid) and T1D
LSD is active at microgram (µg) exposures, which makes dose uncertainty and product variability a major problem in unregulated contexts.
Typical exposure bands (illustrative, not prescriptive)
- Lower exposure band: ~25–75 µg
- Moderate exposure band: ~75–150 µg
- Higher exposure band: >150–300+ µg
Onset and duration (typical)
- Onset: 30–90 minutes
- Peak: 3–5 hours
- Total duration: 8–12 hours (sometimes longer)
- After-effects: fatigue, difficulty sleeping, residual anxiety or “afterglow”
Psilocybin (Magic mushrooms) and T1D
Psilocybin is converted to psilocin in the body and shares the core psychedelic mechanism (5-HT2A signalling). People often describe it as more “earthy” and introspective than LSD, but it can still be intensely dysregulating — especially at higher exposures or in unstable settings. Nausea is commonly reported.
Typical exposure bands (illustrative, not prescriptive)
- Lower exposure band: ~0.5–1.5 g dried
- Moderate exposure band: ~1.5–3.5 g dried
- Higher exposure band: >3.5–5+ g dried
Potency varies substantially by species, strain, and preparation. This is why “grams” can create false certainty.
Onset and duration (typical)
- Onset: 20–60 minutes (often faster on an empty stomach)
- Peak: 1.5–3 hours
- Total duration: 4–6 hours
- After-effects: fatigue, emotional sensitivity, nausea; sometimes “afterglow”
T1D considerations for psychedelics
- These can be long-acting altered states: self-care can degrade for hours
- Checking glucose, eating, bolusing, and treating hypos may become unreliable
- Time distortion increases the chance of “missed insulin” failure modes
- Hypoglycaemia during a trip can be difficult to recognise and treat
- Set and setting matter more than people expect: anxiety and overstimulation increase risk of panic states
Key summary: cannabis, ketamine, hallucinogens and T1D
| Risk area | T1D-specific concern |
| Appetite shifts / unplanned eating | Large highs if insulin isn’t given; looping snacks can confuse closed loops |
| Time distortion | Missed boluses, missed hypo treatment, missed kit tasks |
| Dissociation / impaired judgement | Reduced self-rescue capacity even if you “know what to do” |
| Nausea / vomiting | Hypo risk + dehydration risk; harder to keep carbs down |
| Sleep disruption | Next-day insulin resistance, mood vulnerability, care fatigue |
| Alcohol co-use | Combined sedation + delayed hypoglycaemia risk overnight |
Practical
This is a minimum viable harm-reduction plan. It won’t make drug use “safe”, but it can reduce predictable failure modes in T1D.
Download the safety graphic here.
Key safety tips:
- Don’t go in depleted: eat beforehand, hydrate, and start with a stable glucose trend.
- Keep glucose visible: use CGM alerts where possible and consider sharing CGM data with someone you trust.
- Plan for “munchies”: assume unplanned eating is likely with cannabis. Decide in advance what you’ll do if you snack. (Closed-loop users: expect the system to lag behind unannounced eating.)
- Carry hypo treatment you can take under stress: fast carbs that don’t require appetite.
- Tell at least one person: someone should know you have T1D and what severe hypoglycaemia can look like.
- Avoid stacking variables: mixing substances (especially with alcohol) narrows the margin for error.
- Set and setting are not soft factors: panic states and confusion are common routes into self-care collapse.
- After-effects are real: sleep disruption and emotional sensitivity can linger. Expect next-day variability and lower self-care bandwidth.
What’s next
If you haven’t already, read Part 2: Alcohol and T1D and Part 3: Stimulants and T1D. For most people with T1D, the highest-risk real-world pattern is not any single drug — it’s stacking substances + sleep loss + missed insulin decisions.
Return to Part 1: Partying with T1D (Hub + Intro) for the full system map and the shared risk framework.
Navigation
- Part 1: Partying with T1D (Hub + Intro)
- Part 2: Alcohol and T1D
- Part 3: Stimulants and T1D
- Part 4: Cannabis, Ketamine and Hallucinogens
