THE PURE CRAFT JOURNAL

CBD Oil for Alcohol-Disrupted Sleep: Science and Recovery Guide

October 13, 2026

By PureCraft Editorial Team | PureCraft CBD | Updated October 2026

The nightcap is one of the oldest sleep remedies in human history — and one of the most counterproductive. Alcohol does reliably reduce sleep onset latency, which is why millions of people reach for a glass of wine or a beer to "wind down" before bed. But the sedation alcohol produces is not sleep. It's a neurological suppression that actively dismantles the sleep architecture your brain and body depend on — with consequences that ripple from the moment you close your eyes to how you feel, think, and perform the following day.

Understanding exactly how alcohol corrupts sleep helps explain why so many people feel exhausted after drinking even a moderate amount, why anxiety spikes at 3 AM after an evening drink, and why those in alcohol recovery often identify sleep as their hardest ongoing challenge. This guide covers the sleep science, the specific mechanisms through which CBD oil may help, and the practical considerations for using CBD oil to support sleep in the context of alcohol — whether you drink occasionally, frequently, or are in recovery.

How Alcohol Actually Affects Sleep Architecture

The core paradox of alcohol and sleep is this: alcohol is a CNS depressant that accelerates sleep onset, yet substantially worsens sleep quality. To understand why, you need to understand what happens to sleep architecture across the night.

The First Half of the Night: Artificially Suppressed

In the first 1–4 hours after alcohol consumption, GABA-A receptor activation produces CNS sedation that suppresses REM sleep almost entirely. Alcohol at recreational doses typically eliminates or drastically reduces the first REM period, which normally occurs 70–90 minutes into sleep. Simultaneously, slow-wave sleep (SWS, N3) in the first half of the night increases above baseline — a rebound effect driven by adenosine accumulation. The first four hours after drinking may actually show elevated SWS as a compensatory response, which can feel deceptively restorative.

The Second Half of the Night: Rebound Disruption

As blood alcohol concentration falls — typically in the second half of the night — the neurological picture reverses dramatically. The CNS, which was suppressed by alcohol, rebounds into a hyperactivated state. This "rebound hyperarousal" produces:

REM rebound: Intense, vivid, often disturbing dreams as the brain compensates for the suppressed first-half REM deficit
Fragmented sleep: Multiple awakenings as the hyperactivated nervous system breaks through sleep maintenance
Sympathetic surge: Elevated heart rate, sweating, anxiety — the physiological signature of acute alcohol withdrawal, even in moderate drinkers
Cortisol elevation: HPA axis activation driving cortisol to peak in the early morning hours rather than the normal gradual rise after dawn
Alpha-wave intrusion: Waking-state alpha waves entering NREM sleep, producing the subjective feeling of "half-awake" sleeping

The 3 AM wake-up after an evening drink is one of the most consistently reported sleep disruption patterns. It is not coincidental — it is the pharmacological fingerprint of alcohol's CNS rebound at the point of metabolic clearance.

Alcohol's Effect on Sleep Architecture by Dose

Dose	First-Half Effects	Second-Half Effects	Net Sleep Impact
Low (1 drink)	Mild sleep onset reduction; modest REM suppression	Mild rebound; slight fragmentation	Modest negative; often unnoticed
Moderate (2–3 drinks)	Faster onset; significant REM suppression first half	3 AM awakening common; vivid dreams; sweating	Significant negative; reduced efficiency
High (4+ drinks)	Rapid sedation; near-total REM elimination first half	Severe fragmentation; anxiety; palpitations; early waking	Severely degraded; next-day impairment
Chronic heavy use	Tolerance to sedating effect; poor sleep even when drinking	Severe insomnia; REM suppression even abstaining	Severely disrupted; persists weeks into abstinence

The Cascading Consequences of Alcohol-Disrupted Sleep

The sleep architecture damage from alcohol is not merely uncomfortable — it has measurable downstream consequences on nearly every biological system.

REM Suppression and Emotional Processing

REM sleep is the primary stage for emotional memory consolidation and stress regulation. The brain processes aversive emotional experiences during REM — essentially "filing" them in a lower emotional register, so that memories remain informative without remaining acutely distressing. REM suppression by alcohol prevents this processing. The result: emotional experiences from the preceding day retain their raw intensity rather than being metabolically tamed. This is one mechanistic explanation for why heavy drinkers report heightened anxiety, emotional reactivity, and mood instability — the REM-dependent emotional buffer is perpetually underfilled.

For individuals using alcohol as a tool to manage anxiety, this creates a vicious cycle: alcohol temporarily dulls anxiety before sleep, then REM suppression ensures that anxiety is worse the following day, increasing the drive to drink the next evening. The anxiety-sleep connection becomes circular and self-reinforcing.

Suppressed Growth Hormone and Physical Recovery

Even modest alcohol doses suppress the SWS-linked growth hormone pulse that drives tissue repair, muscle protein synthesis, and immune function. A 2012 study in the Journal of Clinical Investigation found that alcohol significantly reduced GH secretion independent of total sleep duration. For physically active people — athletes, manual laborers, anyone using exercise as stress management — drinking after training actively undermines the recovery process the training was meant to produce.

Circadian Rhythm Disruption

Alcohol disrupts circadian clock gene expression in peripheral tissues — particularly in the liver, which is the primary site of alcohol metabolism. This peripheral clock desynchronization produces a jet-lag-like state without the time zone change: organ systems that normally operate in coordinated circadian patterns lose synchrony, contributing to the metabolic dysregulation, GI disturbance, and hormonal irregularity of heavy alcohol use. For people already dealing with circadian disruption from travel or shift work, alcohol compounds the misalignment significantly.

Dehydration and Adenosine Disruption

Alcohol is a diuretic — it suppresses antidiuretic hormone (ADH), leading to increased urinary output and dehydration. Dehydration during sleep disrupts sleep continuity independently of alcohol's neurological effects, and the resulting thirst and dry mouth are among the most common causes of middle-of-the-night awakening after drinking. Alcohol also interferes with adenosine metabolism: while alcohol initially increases adenosine (contributing to the sedating effect), the subsequent metabolic rebound reduces adenosine signaling in the second half of the night, reducing sleep pressure at the time when it's needed to maintain sleep continuity.

Sleep in Alcohol Recovery: A Separate and Critical Issue

For individuals in recovery from alcohol use disorder, sleep disruption is one of the most significant barriers to sustained sobriety. This is distinct from the occasional-drinker picture and deserves specific attention.

Chronic alcohol use produces lasting changes in GABA-A receptor expression and function — the primary inhibitory system in the brain. Alcohol's sedating effects are mediated largely by GABA-A potentiation, and the brain adapts to chronic alcohol exposure by downregulating GABA-A receptor sensitivity. When alcohol is removed, this downregulation is exposed: the brain is left in a state of GABA-A deficiency, producing hyperexcitability, anxiety, insomnia, and in severe cases, seizures (alcohol withdrawal syndrome).

Even after the acute withdrawal phase resolves, sleep architecture remains abnormal for weeks to months in abstinent heavy drinkers. Research using polysomnography shows that abstinent alcohol-dependent individuals demonstrate:

Persistently suppressed SWS for up to 1–2 years in some studies, even after full abstinence
REM sleep abnormalities including altered REM distribution and increased REM density
Prolonged sleep onset latency (difficulty falling asleep without the sedating "crutch")
Increased awakenings and reduced sleep efficiency compared to age-matched non-drinkers
Heightened sleep-related anxiety and hyperarousal, particularly in the first weeks of abstinence
Relapse risk correlation: Insomnia during early recovery is one of the strongest predictors of relapse in the first 90 days, with poor sleep quality increasing relapse odds by up to 2–3× in prospective studies

Note for Individuals in Alcohol Recovery

If you are in recovery from alcohol use disorder, please discuss CBD oil use with your treatment team, sponsor, or physician before starting. While CBD is non-intoxicating and non-addictive, recovery programs vary in their guidance on supplement use, and your medical provider should be aware of any new supplements, particularly given CBD's interactions with certain liver-metabolized medications. The information in this article is educational and does not substitute for individualized recovery support.

CBD Oil Mechanisms Relevant to Alcohol-Disrupted Sleep

CBD oil interacts with several neurological systems that are directly implicated in alcohol's sleep disruption — through mechanisms that are distinct from, and complementary to, alcohol's CNS effects.

HPA Axis and Cortisol Normalization

The 3 AM anxiety-and-awakening pattern after drinking is driven by acute HPA axis activation — a cortisol spike at the point of alcohol's metabolic clearance. CBD interacts with CB1 receptors in the hypothalamus and limbic system to modulate HPA axis activity, attenuating cortisol overexpression. By normalizing this stress hormone cascade, CBD may reduce the magnitude of the rebound hyperarousal that fragments sleep in the second half of the night.

GABAergic System Support

CBD has complex interactions with the GABA-A receptor system — distinct from alcohol's direct potentiation, and from benzodiazepines' allosteric enhancement. CBD appears to modulate GABA-A receptor function through mechanisms that may help restore normal inhibitory tone, particularly relevant in the recovery context where GABA-A downregulation from chronic alcohol exposure leaves the CNS in a hyperexcitable state. Unlike benzodiazepines — which are frequently prescribed for alcohol withdrawal but carry their own dependence risk and SWS-suppressing properties — CBD does not suppress slow-wave sleep and lacks abuse potential.

5-HT1A Agonism: Addressing Alcohol-Rebound Anxiety

CBD's partial agonism at the 5-HT1A serotonin receptor produces anxiolytic effects that directly target the hyperarousal state driving both the 3 AM awakening and the sleep-onset anxiety that many moderate drinkers experience when attempting to sleep without alcohol. Research by Blessing et al. (2015) established CBD's anxiolytic properties through this mechanism at doses achievable with standard supplementation — relevant because anxiety management is one of the primary reasons people use alcohol as a sleep aid in the first place.

FAAH Inhibition and Endocannabinoid Restoration

Chronic alcohol use disrupts the endocannabinoid system (ECS) — reducing anandamide levels and altering CB1 receptor density in key brain regions. This ECS disruption is one mechanism through which alcohol produces tolerance to its sedating effects and may contribute to the dysphoria and anxiety of alcohol withdrawal. CBD inhibits FAAH, the enzyme that degrades anandamide, helping restore endocannabinoid tone. In the context of alcohol-related ECS disruption, this mechanism has particular relevance to sleep recovery — the endocannabinoid system plays a central role in sleep-wake regulation, and restoring its tone supports natural sleep architecture.

Neuroprotective Properties: Alcohol-Related Brain Changes

Chronic heavy alcohol use produces oxidative stress and neuroinflammation in brain regions involved in sleep regulation. CBD's antioxidant and anti-neuroinflammatory properties — documented in preclinical research — are relevant in the chronic-use and recovery context, where neurological repair is an ongoing process. While no human RCTs specifically establish CBD as neuroprotective in alcohol recovery, the preclinical evidence is mechanistically coherent with CBD's known anti-inflammatory properties.

CBD Oil vs. Alcohol as a Sleep Aid: Direct Comparison

Sleep Factor	Alcohol	CBD Oil
Sleep onset	Reduces latency (via CNS sedation)	May reduce latency (via anxiety reduction, HPA normalization)
SWS / Deep sleep	Artificially elevated first half; suppressed net quality	May support SWS restoration via GABAergic effects
REM sleep	Suppressed first half; rebound second half; net disrupted	Does not suppress REM; may indirectly support REM
Sleep continuity	Severely fragmented second half	May improve sleep maintenance
Next-day function	Cognitive impairment even with adequate hours	No next-day impairment at sleep doses
Anxiety the next day	Often worsened (REM deprivation + cortisol spike)	May be reduced (5-HT1A + HPA normalization)
Dependence risk	High; tolerance develops rapidly	Not established; WHO considers low abuse potential
Growth hormone secretion	Suppressed (undermines physical recovery)	Unimpaired; does not suppress SWS-linked GH pulse

PureCraft Products for Alcohol-Related Sleep Support

The pharmacokinetics of alcohol's sleep disruption — with the primary damage occurring 3–6 hours post-consumption during blood alcohol clearance — inform how to time CBD supplementation for best effect. PureCraft's nanoemulsion technology achieves 15–30 minute onset versus 60–120 minutes for standard CBD oils, which matters when working within a specific disruption window.

Nano-CBD Broad Spectrum Oil — Primary Intervention

Sublingual delivery with 15–30 min onset. For occasional drinkers: 25–35 mg taken at bedtime (same time as or shortly after the last drink) to support second-half sleep continuity. The rapid onset is an advantage when you didn't plan ahead. For those reducing alcohol use: 30–40 mg at consistent bedtime nightly to establish a non-alcohol sleep routine while managing withdrawal-adjacent anxiety.

Nano-CBD Water-Soluble Softgels — Consistent Nightly Dosing

For anyone building a consistent nightly CBD routine to replace the "nightcap" habit. Softgels require 45–60 minute lead time and work best when taken before social drinking occasions rather than after. Reliable, measured dosing without the dropper.

Nano-CBD + CBN + D9 Gummies with Melatonin — Deeper Sleep Support

For nights when sleep disruption is significant. CBN has emerging research specific to sleep maintenance, making it particularly relevant for the alcohol-rebound awakening pattern. The melatonin component supports circadian anchoring when alcohol's clock-gene disruption has shifted sleep timing. Take 60 minutes before target sleep time.

Nano-CBD Broad Spectrum Gummies — Portable, Social-Context Friendly

Easy to incorporate into social occasions as an alcohol alternative or complement. Taking a CBD gummy during a social event in place of a second or third drink reduces cumulative alcohol load — directly reducing sleep disruption — without the social friction of abstaining entirely.

Nano-CBD Full Spectrum Berry Gummies — Evening Wind-Down Ritual

For those using alcohol as a "wind-down ritual" rather than specifically as a sleep aid, the gummies provide a behaviorally equivalent replacement: something consumed in the evening as part of relaxation, with the anxiolytic effects of CBD replacing alcohol's sedating effect without the second-half sleep destruction. The ritual aspect of the replacement matters for habit formation.

Dosing Strategy by Context

Context	Dose	Timing	Goal
Occasional drinker (1–2 drinks)	20–30 mg	At bedtime	Reduce second-half fragmentation
Heavier evening drinking (3–4 drinks)	30–40 mg	At bedtime or last drink	HPA modulation; reduce rebound anxiety
Replacing nightcap habit	25–35 mg nightly	Consistent pre-sleep ritual time	Habit substitution + anxiety reduction
3 AM awakening pattern	15–20 mg oil at wake	Upon middle-of-night waking	Rapid re-sedation via sublingual
Early recovery (alcohol abstinence)	30–40 mg	45 min before bed; consistent nightly	GABA-A support; anxiety reduction; sleep architecture repair

Drug Interactions: CBD and Alcohol

Understanding the pharmacological interaction between CBD and alcohol is important for safety and effectiveness.

Direct combination (CBD + alcohol same evening): At standard CBD sleep doses, combining CBD with alcohol does not produce dangerous additive CNS depression in the way that benzodiazepines or opioids might. However, CBD may mildly potentiate alcohol's sedating effects, and some users report feeling alcohol's effects more intensely when CBD is also present. If combining, start with lower alcohol intake and monitor your response.

Liver metabolism (CYP2E1 and CYP3A4): Alcohol is primarily metabolized by alcohol dehydrogenase and CYP2E1. CBD is metabolized by CYP3A4 and CYP2D6. These pathways have limited direct overlap, though heavy alcohol use induces CYP2E1 and may affect CYP3A4 expression. In moderate-drinking contexts, clinically significant CBD-alcohol metabolic interactions are not established. For heavy drinkers or individuals with known liver disease, physician guidance is warranted before CBD use.

Medications commonly used in alcohol recovery:

Medication	Use in Recovery	CBD Interaction	Guidance
Naltrexone (Vivitrol)	Craving reduction	No established pharmacokinetic interaction	Generally safe; inform prescriber
Acamprosate (Campral)	GABA/glutamate balance	Complementary GABAergic effects possible; additive not harmful	Inform prescriber
Benzodiazepines (detox phase)	Acute withdrawal management	Additive CNS depression; do not combine	Do not use CBD during benzo-managed detox
SSRIs/SNRIs (co-occurring depression)	Mood stabilization	CYP2D6/CYP3A4 overlap; varies by agent	Physician review required
Disulfiram (Antabuse)	Aversion therapy	Disulfiram inhibits CYP2E1/CYP3A4; may increase CBD levels	Physician guidance required

Beyond CBD: Evidence-Based Strategies for Alcohol-Related Sleep

CBD oil works best as one element of a broader strategy. These approaches have independent evidence for improving sleep quality in the context of alcohol use and recovery:

Alcohol cutoff timing: The most impactful behavioral change is moving alcohol consumption earlier in the evening. Finishing alcohol consumption 3–4 hours before bed allows blood alcohol to clear before sleep onset, dramatically reducing second-half disruption. One drink at 7 PM produces far less sleep disruption than one drink at 10 PM.

Hydration: Alcohol-induced diuresis is manageable with proactive hydration — 1–2 glasses of water for every alcoholic drink, and a full glass of water before bed. Hydration doesn't reverse alcohol's neurological sleep effects, but it eliminates the dehydration-related awakenings that compound the neurological disruption.

Cognitive Behavioral Therapy for Insomnia (CBT-I): For individuals with established chronic insomnia who have been using alcohol as self-medication, CBT-I is the evidence-based first-line treatment. CBT-I directly targets the cognitive patterns (catastrophizing about sleep, clock-watching) and behavioral patterns (compensatory napping, irregular sleep schedules) that perpetuate insomnia independently of alcohol. Studies show CBT-I is more effective than sleep medication long-term, and it specifically addresses the rebound insomnia that makes quitting the nightcap habit difficult.

Sleep schedule consistency: Fixed wake time — regardless of how poor the previous night's sleep was — is the single most powerful behavioral intervention for rebuilding sleep architecture. In the context of alcohol recovery, where sleep is disrupted for weeks to months, a consistent 7-day wake time anchors circadian rhythms and builds the sleep pressure (adenosine accumulation) that eventually drives more consolidated sleep.

Anxiety management during the day: Because alcohol-as-sleep-aid is frequently driven by anxiety rather than by sleep difficulty per se, daytime anxiety management — exercise, mindfulness, CBT, CBD oil at a sub-sedating daytime dose of 10–15 mg — reduces the anxious arousal that makes the evening drink feel necessary. Reducing the drive to drink is as important as managing the sleep disruption caused by drinking.

Frequently Asked Questions

Can I take CBD oil after drinking alcohol to improve my sleep?

Yes, CBD oil can be taken at bedtime after moderate alcohol consumption. At standard sleep doses (25–35 mg), CBD oil does not produce dangerous additive sedation with alcohol. It may help attenuate the HPA rebound and sympathetic hyperactivation that cause the characteristic 3 AM awakening pattern. PureCraft's nanoemulsion formulation provides 15–30 minute onset, making it practical to take just before bed even after an evening out. Be aware that some individuals find alcohol's effects slightly intensified when CBD is present, so if you're new to combining them, start with a drink less than usual.

Why do I wake up at 3 AM after drinking, and can CBD oil help?

The 3 AM awakening after alcohol is one of the most predictable pharmacological effects of moderate-to-heavy drinking. As blood alcohol clears — typically 3–5 hours after your last drink — the CNS rebounds from alcohol's suppressive effects into a hyperactivated state: cortisol spikes, heart rate elevates, sympathetic nervous activity surges. This is the physiological signature of acute mini-withdrawal that occurs even in non-dependent drinkers. CBD oil taken at bedtime (before the 3 AM window) may reduce the magnitude of this cortisol rebound through HPA axis modulation. If you're already awake at 3 AM, sublingual CBD oil (15–20 mg) taken at that point can produce re-sedation within 15–30 minutes.

Is CBD oil safe to use during alcohol recovery?

CBD oil is non-intoxicating, non-addictive, and carries a favorable safety profile per the World Health Organization. These properties make it a conceptually appropriate supplement for people in alcohol recovery. However, individual recovery programs vary in their guidance on supplement use, and your treatment team should be informed of all supplements you're taking. The key contraindication is the acute medical detox phase when benzodiazepines are being used — do not add CBD during benzodiazepine-managed withdrawal without physician supervision. For individuals weeks or months into stable abstinence, CBD oil's anxiolytic and sleep-supporting properties are directly relevant to the sleep disruption and anxiety that drive relapse risk in early recovery.

How long does CBD oil take to work for alcohol-disrupted sleep?

PureCraft's nano-CBD oil produces onset in 15–30 minutes via sublingual delivery — significantly faster than standard CBD oils (60–120 minutes). For the specific 3 AM awakening pattern, this rapid onset is practically important. For the broader pattern of restoring sleep architecture after chronic alcohol disruption, consistent CBD use over 1–4 weeks produces progressive improvement as HPA axis recalibration and ECS tone restoration accumulate. Many people notice reduced sleep onset anxiety and fewer middle-of-night awakenings within the first week.

Can CBD oil replace alcohol as an evening wind-down tool?

For many people, yes. The evening drink serves two functions: pharmacological (CNS sedation, anxiety relief) and ritualistic (a behavioral cue that the workday is over, social lubrication). CBD oil's 5-HT1A agonism and HPA modulation address the pharmacological function — reducing anxiety and inducing a calm state — without alcohol's sleep-destructive second-half effects. CBD gummies or full-spectrum berry gummies can address the ritualistic function — something enjoyable consumed at a consistent evening time as part of a wind-down routine. The behavioral replacement is as important as the pharmacological one for habit formation.

Does CBD oil affect liver function, especially for heavy drinkers?

At very high doses (above 20 mg/kg/day — far beyond typical supplementation), CBD has shown hepatotoxic effects in animal studies, and this concern was flagged in the clinical development of Epidiolex (the pharmaceutical CBD product used at doses of 5–20 mg/kg/day for epilepsy). At standard sleep-support doses (25–50 mg for a 70 kg person — approximately 0.35–0.7 mg/kg/day), clinically significant liver effects are not established in human research. However, heavy alcohol use already stresses hepatic function significantly, and anyone with known liver disease, cirrhosis, or heavy alcohol use history should discuss CBD use with a hepatologist or their treating physician before starting.

Will CBD oil cause grogginess the morning after, like alcohol does?

No — this is one of the clearest advantages of CBD oil over alcohol as a sleep aid. Alcohol's next-day grogginess ("hangover brain fog") results from a combination of REM architecture disruption, dehydration, acetaldehyde toxicity, and electrolyte imbalance. CBD at standard sleep doses does not produce these effects. CBD's half-life is approximately 18–32 hours, but the active sedating effects at sleep-support doses dissipate during sleep, and next-day psychomotor impairment is not observed in studies at therapeutic doses. Many people report feeling more rested and clearer-headed than after a comparable alcohol-aided sleep night.

Can CBD oil help with alcohol cravings that disrupt sleep?

Emerging preclinical research — including animal studies using CBD in alcohol use disorder models — suggests CBD may reduce craving-related behaviors and anxiety, though human clinical trials are still in early phases. The mechanism proposed involves ECS restoration (alcohol disrupts endocannabinoid signaling, and CBD's FAAH inhibition may partially restore it) and the anxiolytic effect on the stress-induced craving that is most common in early recovery. CBD is not a treatment for alcohol use disorder, and craving management should involve your treatment team. However, CBD's sleep-supporting and anxiety-reducing properties are directly relevant to the craving context, since sleep deprivation and anxiety are the two strongest triggers for alcohol craving in early recovery.

Does CBD oil interact with the sleep medications sometimes used in early alcohol recovery?

This depends entirely on which medication. Benzodiazepines (diazepam, lorazepam, chlordiazepoxide) used in acute withdrawal management should not be combined with CBD — the additive CNS depression risk is significant. Trazodone, sometimes used for sleep in recovery, interacts with CYP2D6 and warrants physician review. Naltrexone and acamprosate, used for craving reduction, have no established harmful interactions with CBD. If you are in medically supervised recovery with prescribed medications, provide your prescriber with a complete list including CBD supplementation and ask specifically about each drug's CYP2D6 and CYP3A4 profile.

How much CBD oil should I take on a night when I've had more to drink than usual?

On nights of heavier drinking, 30–40 mg of CBD oil taken at bedtime is a reasonable target dose. More alcohol means more pronounced HPA rebound, more sympathetic hyperactivation, and greater circadian disruption — all of which CBD can partially attenuate at this dose range. Prioritize rehydration (a large glass of water before bed) alongside CBD. Be aware that heavier alcohol consumption may amplify CBD's effects somewhat, so avoid driving or operating machinery the following morning until you have assessed your alertness. If you regularly find yourself needing CBD to manage heavy drinking's sleep effects, that pattern is itself a signal worth reflecting on.

References

Blessing EM, et al. Cannabidiol as a Potential Treatment for Anxiety Disorders. Neurotherapeutics. 2015;12(4):825-836. PMID: 26341731
Shannon S, et al. Cannabidiol in Anxiety and Sleep: A Large Case Series. Perm J. 2019;23:18-041. PMID: 30624194
Russo EB. Clinical Endocannabinoid Deficiency Reconsidered. Cannabis Cannabinoid Res. 2016;1(1):154-165. PMID: 28861491
Crippa JA, et al. Neural basis of anxiolytic effects of cannabidiol (CBD) in generalized social anxiety disorder. J Psychopharmacol. 2011;25(1):121-130. PMID: 20829306
Corroon J, Phillips JA. A Cross-Sectional Study of Cannabidiol Users. Cannabis Cannabinoid Res. 2018;3(1):152-161. PMID: 30014049
Capano A, et al. Evaluation of the effects of CBD hemp extract on opioid use and quality of life indicators in chronic pain patients. Postgrad Med. 2020;132(1):56-61. PMID: 31711352

Medical Disclaimer

This article is for informational and educational purposes only and does not constitute medical advice, diagnosis, or treatment. CBD oil is not intended to diagnose, treat, cure, or prevent any disease or medical condition, including alcohol use disorder. If you or someone you know is struggling with alcohol dependence or alcohol use disorder, please seek support from a qualified healthcare provider, addiction specialist, or call SAMHSA's National Helpline at 1-800-662-4357 (free, confidential, 24/7). Information in this article is not a substitute for individualized medical guidance, particularly for individuals in recovery or taking prescription medications. CBD oil interactions with recovery medications should be discussed with your treating physician. PureCraft CBD products are not evaluated by the FDA.

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