May 18, 2026

CBD for OCD: Does It Help with Intrusive Thoughts and Compulsions? | PureCraft CBD

Important Medical Notice  |  This article is for informational and educational purposes only and does not constitute medical advice. OCD is a serious psychiatric condition requiring professional evaluation and evidence-based clinical care. CBD is not an FDA-approved treatment for OCD and should not replace prescribed medications, ERP therapy, or psychiatric care. If OCD symptoms are significantly impairing your daily functioning, please consult a qualified mental health professional. If you are in crisis, contact the 988 Suicide and Crisis Lifeline by calling or texting 988.

 

Understanding CBD's Potential Role in OCD

Obsessive-compulsive disorder affects approximately 2–3% of the global population — around 1 in 40 people — making it one of the most common and one of the most debilitating psychiatric conditions worldwide. Despite a treatment landscape that has improved significantly with ERP therapy and high-dose SSRI protocols, 40–60% of people with OCD achieve only partial response to first-line treatment, and a meaningful subgroup remains treatment-resistant.

 

CBD's relevance to OCD stems from a specific intersection: OCD is fundamentally an anxiety-spectrum disorder with a strong serotonergic component — and CBD has well-documented mechanisms in both the anxiety and serotonin systems. This doesn't make CBD an OCD treatment. But it does make the mechanistic case worth examining carefully, and it explains why a growing number of people with OCD are integrating CBD into their management approach alongside therapy and medication.

 

This post is a supporting post in PureCraft's Mental Health cluster. For the foundational mechanisms of CBD for anxiety — which underlie everything discussed here — seeCBD for Anxiety: The Complete Guide. For the depression mechanisms that overlap with OCD's mood component, seeCBD for Depression: What the Science Actually Says. For PTSD — which shares OCD's intrusive thought burden — seeCBD for PTSD.

 

What OCD Actually Is — and What It Isn't

OCD is not a personality quirk about tidiness. It is a neurobiological condition characterized by two interlocking features: obsessions — unwanted, intrusive, distressing thoughts, images, or urges that the person recognizes as senseless but cannot suppress — and compulsions — repetitive mental or behavioral acts performed to reduce the distress generated by the obsession, which provide only temporary relief and reinforce the obsession-compulsion cycle over time.

 

The critical distinction that matters for any treatment discussion: compulsions temporarily reduce anxiety but permanently strengthen the obsession. Every compulsion teaches the brain that the obsessional thought was a real threat that required action to neutralize — reinforcing the neural pathway. This is why ERP therapy (deliberately resisting compulsions while tolerating the anxiety) is the most effective OCD intervention — it breaks the reinforcement cycle at its root.

 

The Neurobiology: Serotonin, Glutamate, and the Cortico-Striato-Thalamo-Cortical Loop

OCD's neurobiology involves a specific circuit dysfunction: the cortico-striato-thalamo-cortical (CSTC) loop, which in OCD is overactive, generating repetitive thought patterns that cannot be gated by normal inhibitory mechanisms. Two neurotransmitter systems are centrally involved:

 

Serotonin:The most established pharmacological target — SSRIs at doses 2–3 times higher than used in depression produce meaningful OCD symptom reduction in 40–60% of patients. The serotonin system modulates the CSTC loop's activity and the orbitofrontal cortex's error-detection signaling that drives obsessional doubt. CBD's 5-HT1A agonism engages the serotonin system through a different receptor subtype than SSRIs — not reuptake inhibition, but direct receptor activation — and may complement SSRI partial response through this complementary mechanism.
Glutamate:Increasingly recognized as a co-driver of OCD — elevated glutamate in the caudate nucleus, thalamus, and anterior cingulate cortex is found in OCD neuroimaging studies. Drugs that modulate glutamate (memantine, riluzole, and at high doses, ketamine) show anti-OCD effects in treatment-resistant cases. CBD has modest NMDA glutamate modulating properties at higher doses — an emerging and less established mechanism that may be relevant for OCD specifically in ways it isn't for pure anxiety.
Dopamine:The dopamine system modulates the reward circuit that drives compulsion completion — the relief of performing a compulsion activates dopaminergic reward pathways, reinforcing the behavior. This is why antipsychotic augmentation (dopamine D2 blockade) helps in partial SSRI responders. CBD's indirect dopaminergic modulation through ECS mechanisms is modest and is not a primary mechanism for OCD.

 

OCD Subtypes and CBD's Relevance to Each

OCD is not a single homogeneous condition — it encompasses multiple distinct presentations with different neurobiological profiles and different responses to pharmacological and behavioral intervention. CBD's relevance varies by subtype:

 

 

OCD Subtype / Presentation

Primary Obsession Theme

Compulsion Pattern

CBD Mechanism Relevant

Evidence Level

Contamination OCD

Fear of germs, illness, spreading harm to others through contact; distress from being 'unclean'

Excessive hand washing, cleaning, avoidance of public surfaces; reassurance seeking about illness risk

5-HT1A anxiolytic reduces the anxiety driving the compulsion cycle; HPA modulation lowers the cortisol baseline that amplifies threat perception

Moderate — directly overlaps with CBD's anxiety evidence base; contamination OCD has the most anxiety-prominent profile

Harm OCD

Intrusive thoughts about harming oneself or others (ego-dystonic — the person does not want to act on them); fear of 'losing control'

Avoidance of sharp objects, checking behaviors, seeking reassurance that the thought doesn't mean harm is intended

5-HT1A modulation reduces intrusive thought distress; serotonin system role in harm OCD is well-established; CBD's indirect serotonin support is directly applicable

Moderate — anxiety evidence transfers; harm OCD responds to serotonergic treatment; CBD's 5-HT1A mechanism is relevant

Pure-O OCD (Primarily Obsessional)

Intrusive thoughts without visible external compulsions — religious obsessions, sexual orientation fears, existential obsessions, relationship OCD; compulsions are mental (rumination, mental checking, prayer rituals)

Mental compulsions: reviewing memories, seeking internal reassurance, mental neutralization rituals — invisible to observers but highly time-consuming and distressing

The anxiety and serotonergic components are the same as other OCD subtypes; CBD's 5-HT1A mechanism is relevant; the mental compulsion pattern may be harder to interrupt through pharmacology than through ERP therapy

Moderate — serotonin mechanism translates; ERP therapy remains the most evidence-based intervention for Pure-O specifically

Checking OCD

Fear that something bad will happen due to negligence — gas left on, door unlocked, driving over someone; excessive responsibility fear

Repetitive checking (locks, appliances, routes driven); reassurance seeking; may take hours before leaving home

HPA cortisol modulation reduces the exaggerated sense of responsibility and catastrophic threat assessment that drives checking; 5-HT1A reduces background anxiety between checking cycles

Moderate — same anxiety/serotonin mechanisms apply; ERP therapy is critical for breaking the checking reinforcement cycle

Symmetry / 'Just Right' OCD

'Not just right' experiences — a sensory or cognitive feeling that things are not correct until a ritual is completed; may not involve fear but intense discomfort

Arranging, ordering, repeating actions until they feel 'right'; counting rituals; symmetry behaviors

Weaker fit — this OCD subtype has the strongest glutamate involvement and weakest serotonin involvement of all OCD presentations; CBD's glutamate modulation (NMDA) is emerging but less established than its serotonin mechanisms

Emerging / limited — serotonin-targeting approaches (including CBD's 5-HT1A mechanism) are less effective for this subtype; specialist OCD therapy is the primary intervention

Hoarding OCD (as OCD subtype, distinct from hoarding disorder)

Fear of discarding items needed in the future; distress from 'wasting' or losing something important

Compulsive acquisition; inability to discard; distress when items are removed

Weakest CBD fit of all OCD subtypes — hoarding has distinctive neurobiology from other OCD presentations including weaker serotonin and stronger dopamine/reward circuit involvement

Limited — this subtype is least responsive to serotonergic approaches; specialist behavioral treatment is essential

 

 

The most important insight from this table:CBD has the strongest mechanistic fit for OCD subtypes that are anxiety-prominent (contamination, harm, Pure-O, checking) — where the obsession-compulsion cycle is primarily maintained by anxiety and serotonergic distress. It has the weakest fit for subtypes with glutamate-prominent or dopamine-prominent profiles (symmetry/'just right', hoarding). This is not a failure of CBD — it reflects the genuine neurobiological diversity of OCD and the importance of matching intervention to mechanism.

 

The Endocannabinoid System in OCD: What Research Tells Us

The relationship between the ECS and OCD is less thoroughly documented than the ECS-PTSD connection — but it is mechanistically coherent and growing. The ECS plays a modulatory role in the serotonin and glutamate systems that drive OCD, and CB1 receptors are expressed in the orbitofrontal cortex, striatum, and thalamus — all nodes in the CSTC circuit that is overactive in OCD. For foundational ECS science, seeWhat Is the Endocannabinoid System? A Complete Guide.

 

The most directly relevant research: a2020 study in Frontiers in Behavioral Neuroscience found that CBD administration in an animal model of OCD significantly reduced compulsive marble-burying behavior — a well-validated preclinical model of OCD compulsivity — and that this effect was blocked by 5-HT1A receptor antagonists, confirming that the anti-compulsive effect was mediated through CBD's 5-HT1A mechanism. A2016 study in Psychopharmacology similarly found that CBD reduced compulsive behaviors in animal OCD models through 5-HT1A-mediated mechanisms. These are not human trials — but the precision of the mechanistic finding (5-HT1A-dependent anti-compulsive effect) is meaningful and has directly guided subsequent research interest.

 

Human research on CBD specifically for OCD remains limited. A small number of case reports and observational studies describe OCD symptom improvement with CBD use, but controlled trials are not yet published. The honest position: the animal model evidence is specific and encouraging; the human evidence is preliminary and anecdotal; the mechanism is coherent. CBD is not an evidence-based OCD treatment — it is a supplement with a plausible mechanistic rationale that may serve a complementary role alongside first-line care.

 

CBD and Intrusive Thoughts: What the Mechanism Suggests

The question most commonly asked about CBD for OCD — does it reduce intrusive thoughts — requires an honest and nuanced answer. Intrusive thoughts themselves are not the disorder. Everyone has intrusive thoughts; the OCD brain is distinctive in its inability to dismiss them. The distress the intrusive thought generates — and the compulsive urge to neutralize that distress — is what maintains OCD. This distinction matters for how CBD might help.

 

CBD does not suppress intrusive thoughts directly. It does not block thought generation in the way a sedative might impair cognitive function. What CBD may do — through its 5-HT1A mechanism and HPA modulation — is reduce the anxiety-distress amplitude of the intrusive thought. When the intrusive thought generates less immediate distress, the compulsive urge to neutralize it is weaker. This is a modest effect — not a cure — but for people whose OCD is significantly anxiety-amplified, reducing that anxiety substrate may reduce the functional impairment of each intrusive thought cycle.

 

The critical caution:Taking CBD to immediately relieve OCD distress risks becoming its own compulsion-equivalent — a 'chemical compulsion' that temporarily reduces anxiety and reinforces the idea that the obsessional distress requires neutralization. CBD should be used consistently as a daily HPA and serotonin-support supplement, not reactively in response to obsessional spikes. Using it reactively (taking CBD when an obsession spikes in an attempt to reduce the distress quickly) is functionally similar to a compulsion and may strengthen the obsessive cycle rather than weakening it. This is a nuance that most CBD guides for OCD do not address — and it is important.

 

CBD and ERP Therapy: A Potentially Important Combination

Exposure and Response Prevention therapy is the most evidence-based OCD treatment available — outperforming medication alone in multiple head-to-head studies and producing durable remission in many people. ERP involves deliberately triggering obsessional distress (exposure) and then refraining from the compulsive response (response prevention) long enough for the anxiety to naturally subside — teaching the brain that the obsession does not require a compulsive response and that the anxiety is tolerable.

 

ERP is also difficult. The deliberate confrontation of high-distress obsessional content causes significant anxiety during sessions, and dropout rates — particularly from self-directed or inadequately supported ERP — are substantial. This is where CBD's role as a complement to ERP is most plausible.

 

CBD before ERP sessions (60–90 min):A consistent morning CBD oil dose that reduces baseline anxiety may make ERP exposures more tolerable without blunting the habituation signal that makes ERP effective. The goal is not to eliminate distress during exposures — some distress is necessary for the habituation mechanism to work — but to reduce the peak distress from a level that causes avoidance/dropout to a level that is challenging but sustainable.
CBD does not replace ERP:The anti-compulsive effect of CBD is not a shortcut that makes compulsive responses unnecessary. The behavioral component — actually refraining from the compulsion during exposure — is essential and irreplaceable. CBD may lower the anxiety threshold, but it cannot rewire the CSTC circuit without the behavioral exposure work.
Timing matters:CBD taken reactively during an OCD spike — as a chemical neutralizer — is mechanistically problematic. CBD taken consistently as a daily baseline supplement changes the anxiety substrate within which OCD operates. The distinction between 'daily supplement' and 'reactive relief tool' is essential for people with OCD.

 

CBD and OCD Medications: Interaction Guide

 

 

Treatment

Mechanism

Evidence for OCD

Side Effect Profile

CBD's Role Alongside

SSRIs — first line (fluoxetine, fluvoxamine, sertraline, paroxetine)

Serotonin reuptake inhibition; OCD requires higher SSRI doses than depression (often 2–3× the antidepressant dose)

Strong — FDA-approved for OCD; 40–60% response rate; partial response is common and leads to augmentation strategies

Sexual dysfunction, weight changes, discontinuation syndrome on stopping; OCD doses increase side effect burden

CBD may complement partial SSRI response via 5-HT1A mechanism; CYP2D6 interaction requires physician disclosure; may reduce anxiety between OCD treatment sessions

Clomipramine (tricyclic, serotonin-specific)

Most potent serotonergic tricyclic; strong 5-HT reuptake inhibition + some norepinephrine; the most effective single OCD medication in some studies

Strong — FDA-approved; may outperform SSRIs for severe OCD but with more side effects

Cardiac conduction risk, anticholinergic effects, sedation — more side effects than SSRIs

Higher drug interaction risk with CBD (CYP1A2, CYP2D6) — physician monitoring required if combining

ERP Therapy (Exposure and Response Prevention)

Graduated exposure to obsessional triggers while preventing the compulsive response — allows anxiety to habituate without the compulsion providing temporary relief; breaks the obsession-compulsion reinforcement cycle

Strongest of all OCD interventions — equivalent to or better than medication in many studies; gold standard first-line treatment

Temporarily increases distress during exposures — requires professional guidance; not a 'side effect' in the drug sense

CBD's anxiety reduction may lower ERP dropout by reducing the peak distress during exposure exercises; taking CBD before ERP sessions (60–90 min) may make the exposure more tolerable without blunting the habituation signal

Augmentation strategies (antipsychotics — risperidone, aripiprazole)

Dopamine D2 receptor blockade added to SSRI when SSRI alone is insufficient; targets the dopamine component of OCD that SSRIs miss

Moderate — used in partial SSRI responders; 30–40% additional response rate in refractory OCD

Metabolic effects, movement disorders, sedation — significant side effect burden

Multiple interaction concerns — do not combine CBD with antipsychotics without specialist psychiatry oversight

Ketamine / glutamate approaches (investigational)

NMDA glutamate receptor blockade produces rapid (within hours) OCD symptom reduction — similar mechanism to ketamine's rapid antidepressant effect; confirms glutamate's role in OCD

Emerging — open-label studies show promise; not standard of care; administered in clinical settings only

Dissociative effects, abuse potential — clinical setting only

CBD's indirect glutamate modulation is far milder than ketamine; CBD is not a glutamate antagonist and cannot replicate ketamine's effects; mechanistically interesting direction for future research

 

 

The most important practical note: OCD typically requires SSRIs at 2–3 times the standard antidepressant dose — fluoxetine 60–80mg, sertraline 150–200mg, fluvoxamine 200–300mg. At these higher doses, the CYP2D6 interaction between CBD and SSRIs is more clinically significant than at standard antidepressant doses. Physician awareness and monitoring are more important in OCD than in depression for this reason. The full CYP450 interaction guide is atCBD and Drug Interactions: The CYP450 Guide.

 

CBD Dosage for OCD: A Practical Protocol

For OCD, the dosage framework prioritizes consistency over reactive dosing.PureCraft Nano CBD Oil is nano-optimized for approximately 90% bioavailability — these doses should not be extrapolated to standard CBD oil without adjustment.

 

Morning baseline dose (primary):20–30mg sublingually before coffee. This is the most important dose — daily, consistent, before the cortisol awakening response peaks. The HPA recalibration and cumulative 5-HT1A sensitization from consistent morning dosing are the mechanisms most relevant to OCD's anxiety substrate. Do not skip. Do not take reactively in response to OCD spikes.
Before ERP sessions:If using CBD before therapy sessions, take the morning oil 60–90 minutes before the session — not as an additional dose on top of the morning baseline, but timed so that the morning dose is at peak blood levels during the session. Discuss this with your ERP therapist.
Inverted-U caution for OCD specifically:CBD's inverted-U dose-response is relevant for OCD — at doses above 50mg (nano-optimized), paradoxical anxiety can emerge in susceptible individuals. Because OCD patients already experience significant anxiety, paradoxical CBD-induced anxiety worsening is more consequential here than in other conditions. Start at 20mg and increase conservatively.
Sleep support:OCD frequently disrupts sleep through nighttime obsessional activity.CBD+CBN Sleep Gummies(1 gummy 30–45 min before bed) are appropriate for OCD-related sleep disruption. The anxiety-reducing and sleep-architecture-supporting effects complement the morning oil's daytime protocol without reactive dosing concerns.
Timeline:4–6 weeks minimum before assessing anxiolytic benefit; 6–8 weeks for cumulative HPA and serotonin effects. OCD symptom change typically follows the anxiety reduction — as the anxiety substrate reduces, the compulsive urgency of each obsessional cycle should decrease modestly over this window.

 

Frequently Asked Questions

 

Can CBD reduce intrusive thoughts?

CBD does not suppress intrusive thought generation directly. What it may do is reduce the anxiety-distress amplitude that makes each intrusive thought feel catastrophic and urgent — lowering the perceived need for a compulsive response. The distinction is important: OCD is not caused by too many intrusive thoughts (everyone has them). It is caused by the distress those thoughts generate and the compulsive cycle that distress drives. CBD's 5-HT1A and HPA mechanisms address the anxiety substrate of that distress, not the thoughts themselves. Animal model studies have confirmed anti-compulsive effects through the 5-HT1A pathway, and many people with OCD report that consistent CBD use reduces the urgency of obsessional cycles without eliminating the thoughts entirely.

 

Does CBD help with compulsive behaviors?

The most specific preclinical evidence for CBD in OCD comes from compulsion research — not obsession research. The 2020 Frontiers in Behavioral Neuroscience study found that CBD reduced compulsive behaviors in an OCD animal model through a 5-HT1A-dependent mechanism. This suggests CBD's primary mechanism in OCD may be anti-compulsive (reducing the compulsive response urgency) rather than anti-obsessional. In practical terms: CBD may make it somewhat easier to resist compulsions during ERP — not because the obsessional distress is gone, but because the anxiety-driven compulsive urgency is modestly reduced. This is a supporting role for ERP therapy, not a standalone treatment.

 

What's the best CBD dose for OCD?

For OCD, 20–30mg of nano-optimized CBD oil daily (PureCraft) is the evidence-aligned starting range — taken consistently every morning, not reactively during OCD spikes. The consistent daily baseline is the mechanism; reactive dosing is potentially counterproductive. If the morning dose produces no meaningful reduction in anxiety substrate after 6 weeks, a gradual increase to 35–40mg can be trialed. The ceiling for most people with OCD should be around 40–50mg of nano-optimized CBD; above this, paradoxical anxiety becomes a meaningful concern. OCD patients on high-dose SSRIs should start at 15–20mg and increase slowly due to the CYP2D6 interaction. See our full dosage framework:CBD Dosage Guide.

 

Can CBD make OCD worse?

Two scenarios where CBD may worsen OCD: First, at supraoptimal doses (above 50mg of nano-optimized oil for most people), paradoxical anxiety can emerge — this is the inverted-U dose-response that applies across anxiety and OCD, and it is more consequential for OCD patients where additional anxiety directly worsens obsessional severity. Second, if CBD is used reactively as a 'chemical compulsion' — taken specifically in response to OCD spikes to neutralize distress — it may function as a new compulsion-equivalent and reinforce rather than reduce the obsessive cycle. CBD used consistently as a daily baseline supplement does not have this risk. Using it reactively does.

 

Is CBD safe with OCD medications?

CBD can be combined with most OCD medications with physician oversight, but the interaction profile is more complex for OCD than for most conditions. The CYP2D6 interaction between CBD and SSRIs is more clinically significant at the high SSRI doses used in OCD (fluoxetine 60–80mg, sertraline 150–200mg) than at standard antidepressant doses. CBD inhibiting the enzyme that metabolizes these SSRIs at high OCD doses means blood levels could increase meaningfully. This requires physician awareness — not avoidance of the combination, but monitoring for any increase in SSRI side effects. For clomipramine (the most effective but most side-effect-prone OCD medication), the interaction complexity is higher and specialist oversight is essential. Full details:CBD and Drug Interactions: The CYP450 Guide.

 

CBD vs prescribed OCD treatments — which is better?

For most people with OCD, ERP therapy and high-dose SSRIs have far more clinical evidence than CBD and should be the foundation of treatment. CBD's evidence for OCD is at the preclinical (animal model) stage for the most specific findings, with limited human evidence. The honest positioning: CBD is a supplement that may provide meaningful anxiolytic support alongside — not instead of — first-line OCD care. For people who have exhausted first-line options and are in a treatment-resistant category, CBD represents a low-risk adjunct worth trialing under physician supervision. For people who have not yet engaged with ERP therapy, connecting with a trained ERP therapist is the highest-value step available — higher than any supplement.

 

How long before CBD helps OCD symptoms?

The timeline has two phases. CBD's acute anxiolytic effect (through 5-HT1A activation) begins within 30–60 minutes of sublingual dosing — this is relevant for managing high-distress moments but, as noted above, should not be used reactively as a compulsion substitute. The cumulative effects — HPA axis recalibration, 5-HT1A receptor sensitization, and the modulation of the anxiety substrate that feeds the obsessive cycle — operate on a 4–8 week timeline with consistent daily morning dosing. Meaningful reduction in the urgency of compulsive responses is typically not noticed until week 4–6. Assess at 8 weeks with consistent morning dosing before concluding whether CBD is or isn't contributing.

 

Does CBD help Pure-O OCD?

Pure-O OCD (primarily obsessional — intrusive thoughts without visible external compulsions) shares the same serotonergic and anxiety substrate as other OCD subtypes, so CBD's 5-HT1A and HPA mechanisms are equally relevant mechanistically. The practical difference is that Pure-O's compulsions are mental (rumination, mental checking, internal reassurance) rather than behavioral — making it harder to identify whether CBD is reducing compulsive urgency vs reducing general anxiety. People with Pure-O who use CBD consistently report that the 'volume' of obsessional thoughts feels reduced — not eliminated, but less overwhelming — which is consistent with reduced anxiety amplitude rather than thought suppression. ERP for Pure-O requires a therapist familiar with mental compulsions specifically — standard ERP therapists who focus on behavioral compulsions may not address the mental compulsion pattern adequately.

 

The Bottom Line: CBD for OCD

OCD is one of the conditions where CBD's mechanistic case is specific and plausible but the clinical evidence remains in early stages. The 5-HT1A-dependent anti-compulsive effect demonstrated in animal models aligns directly with OCD's known serotonergic neurobiology. CBD's HPA modulation addresses the anxiety substrate that amplifies each obsessional cycle. The combination of reduced anxiety amplitude and reduced compulsive urgency represents a meaningful — if modest — potential contribution to OCD management.

 

What CBD is not: a cure, a replacement for ERP therapy, or an appropriate reactive tool during OCD spikes. Used that way, it risks becoming a chemical compulsion — temporary relief that reinforces the obsessive cycle rather than weakening it.

 

What CBD may be: a daily anxiety-substrate supplement that, used consistently over 6–8 weeks alongside ERP therapy and appropriate physician-directed care, reduces the urgency and distress amplitude of obsessional cycles enough to make the therapeutic work more sustainable.

 

The evidence-aligned protocol:PureCraft Nano CBD Oil 1000mg — 20–30mg sublingually each morning, consistently, before coffee.CBD+CBN Sleep Gummies — 1 gummy 30–45 minutes before bed for OCD-related sleep disruption. Zero THC, nano-optimized,batch-tested COA. Disclose to your prescribing physician and OCD therapist before starting.

 

Important Medical Notice |  This article is for informational and educational purposes only. OCD requires professional treatment — Exposure and Response Prevention (ERP) therapy is the gold standard. CBD is a supplement, not an OCD treatment, and has not been FDA-approved for OCD or any obsessive-compulsive spectrum condition. CBD inhibits CYP2D6 and CYP3A4 enzymes that metabolize many OCD medications — disclose CBD use to your prescribing physician before combining with SSRIs or other psychiatric medications. Do not discontinue prescribed OCD medications to use CBD without explicit physician guidance. PureCraft CBD products are not intended to diagnose, treat, cure, or prevent any disease. Individual results may vary.

 

Related Articles — Mental Health Cluster

 

Sources & Citations

 



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