A Positive THC Urine Test: “But I’m only taking CBD!!”


More and more commonly, people with a positive urine test for THC are insisting they only used cannabidiol (CBD). Someone ingesting only CBD should not have a positive urine sample for THC.

Individuals often assume they are taking only CBD because the product label says “CBD”. However, they may be taking hemp oil, which can contain up to 0.3% THC, by law. When someone ingests hemp oil, they may have a positive urine test for THC, even though they only ingested a small amount of THC, because urine tests are designed to detect and measure very small amounts of THC. Every time an unreliable company mis-labels its products as “CBD”, when it contains other products, including THC, that company puts unsuspecting individuals at risk for having a positive THC urine test.

Some scientists have a theory that under an unusual and specific circumstance, it may be possible for a person ingesting only CBD to produce a positive THC urine test, but this possibility is not yet proven. To understand the possible positive urine test, it is necessary to review THC urine testing.

Urine is not tested for Delta9-THC, the form of THC that makes people high. Urine is tested for a metabolite of THC, 11-nor-delta9-THC, because this metabolite stays in the body at detectable levels for much longer than Delta9-THC. After someone ingests Delta9-THC, it is metabolized in the liver to 11-nor-delta9-THC. A “positive THC urine test” means the test found levels of 11-nor-delta9-THC. However, for simplicity, we always say we are testing for THC and this convention will be used for the remainder of this paper.

There are two types of tests that are used to assess cannabis use: 1) Immunoassay test and 2) GC-MS test. The immunoassay is used as a screening test because it is easy and cheap. For example, dipsticks are a form of immunoassay. However, immunoassays for THC produce a high rate of false positives (the test is positive even when THC has not been used) but not many false negatives (the test is negative even when THC has been used). Every time the immunoassay is positive, it should be followed up with GC-MS as a confirmatory test. The confirmatory GC-MS test is extremely specific and produces almost no false positives. However, the GC-MS is both time consuming and expensive. Almost all law enforcement and major companies use immunoassay for screening and follow-up with GC-MS confirmatory testing.

Generally, CBD is not converted into THC in the human body. However, there is scientific debate as to whether CBD can be converted to THC in the stomach.1-5 This discussion started when a study using simulated gastric juice found that synthetic CBD could be converted to delta9-THC and other cannabinoids.1 In contrast, studies in humans have not found any delta-9 THC in the blood stream nor any clinical evidence of any form of THC.2-4

However, one of these studies did find a slight increase in nor-11-delta9-THC three hours after ingestion of high doses of CBD (>600mg).2 It is unlikely that such low blood levels of nor-11-delta9-THC would produce enough 11-nor-delta9-THC in urine to return a positive urine test. The only situation where a positive result might exist would be when very sensitive urine testing limits (10 nanograms/ml) were used, the urine was obtained at a very specific time after ingestion, the urine was very concentrated, and the individual was orally ingesting very high quantities of CBD (>600mg/day).5 Ingestion of CBD via any other means than oral have never been found to be converted to THC or any of its metabolites.

To definitively answer this debate a study examining the relationship between urine THC testing and CBD ingestion would need to be performed. Such a study has never been reported in the literature.

Bottom Line:

Positive screening tests for THC can occur in individuals that are consuming CBD because false positives are common with the immunoassay screening kits. However, a confirmatory test using GC-MS should not be positive. When it does occur, most of the time, the individual will be consuming a product that contains some amount of THC, either knowingly or unknowingly. There is a rare theoretical possibility that an individual who is taking very large amounts of CBD orally (>600mg/day) may have a positive THC urine test. However, such a case has never been documented.
If someone desires to consume CBD and wants to avoid a positive urine THC, they need to obtain their CBD from a reliable source that tests its products for the presence (or absence, in this case) of THC. CBD American Shaman produces a THC-free CBD products specifically for this purpose. They test each product in their lab for the absence of TCH before it is released. Other companies may produce THC-free CBD products that can also be used, but I am not familiar with their internal processes for manufacturing and testing to be able to recommend them at this time. At this point, there have been no confirmed reports of positive THC urine tests from individuals that are using CBD American Shaman THC-free products only.



1. Merrick J, etal. Identification of psychoactive degradants of cannabidiol in simulated gastric and physiological fluid, Cannabis and Cannabinoid Research 1:1:102–112.
2. Consroe P, etal. Assay of plasma cannabidiol by capillary gas chromatography/ion trap mass spectroscopy following high-dose repeated daily oral administration in humans. Pharmacol Biochem Behav. 1991 Nov;40(3):517-22.
3. Martin-Santos R, etal. Acute effects of a single, oral dose of d9-tetrahydrocannabinol (THC) and cannabidiol (CBD) administration in healthy volunteers. Curr Pharm Des. 2012;18(32):4966-79.
4. Grotenhermen F, etal. Even high doses of oral cannabidiol do not cause THC-like effects in humans: Comment on Merrick et al. Cannabis and Cannabinoid Research 2016;1(1):102-112; DOI:10.1089/can.2015.004
5. Bonn-Miller M, etal. Conversion of cannabidiol following oral administration: Authors’ response to Grotenhermen et al. DOI: 10.1090/can.20160036. Cann Canna Res 2017;2(1):5-7.

Sublingual versus Oral CBD—Which is best?

Many so called “experts” insist that holding CBD-rich hemp oil via the oro-mucosal route (holding it under the tongue or in the mouth) causes higher blood levels and increases bioavailability of CBD as compared to taking it orally (swallowing it). The theory is that when taken orally, CBD was being metabolized by the liver before it could get distributed to the rest of the body and this didn’t happen when it was taken via the oro-mucosal routes. This occurred because of the unique circulation of the gut. Blood comes from the heart and goes to the stomach and intestines where it absorbs nutrients and material. After leaving the intestines, the blood then passes through the liver which takes up certain nutrients and materials and metabolizes them prior to returning them to the blood stream for circulation to the rest of the body. CBD is metabolized in the liver and its metabolites are not as active as the original CBD. This makes sense and older studies showed that the oral route was not as good as the oro-mucosal routes. However, this is where research can actually provide wrong answers
The older studies on which this “truth was based used the two armed study concept. One arm consisted of group of individuals taking hemp oil orally and another arm consisted of a different group of individuals taking it sublingually. Because there is tremendous variation in the absorption and metabolism of cannabinoids from one individual to another1, this is a terribly inaccurate method for comparing PK values and yielded results that we now know are untrue. Two newer studies using the same individuals in each arm of the study found that there are no differences in maximum blood levels or bioavailability between oral and sublingual administration of regular CBD hemp oil.2,3
Several years ago, nano-emulsification technology was first introduced into hemp products by CBD American Shaman. Hemp oil naturally forms into large droplets when mixed with water and water is abundant in the mouth and stomach. Nano-emulsification technology breaks the oil up into small droplets that are less than 100 nanometers in diameter with the droplets being coated with an emulsifier that keeps the droplets small when exposed to water (rather than coalescing into a large droplet). Two different studies have found that the maximum blood levels of oral “nano-emulsified” CBD was 1.7 to 4 times that of sublingual and the bioavailability was similarly increased 134% to 220%.4-6 This increase in oral absorption over sublingual absorption may be due to one or more of the following:

  1. Increased CBD absorption into the blood stream because of increased surface area of droplets contacting the gut surface.7
  2. Immediate protein binding of the CBD (because of its small size) after absorption into the blood stream (this inhibits the liver cells from taking up the CBD as it passes through the liver).1
  3. Absorption of so much CBD so fast directly from the stomach that it overcomes the ability of the liver cells to remove it all and a large amount of CBD passes stays in the blood stream as it passes through the liver.
  4. Direct absorption of the CBD into the cells of the gut and transportation to the rest of the body via the lymphatics which allows the CBD to bypass the liver and be distributed throughout the body.8
  5. Phagocytosis of the nano-CBD particles by macrophages which shield the CBD from being taken up by the liver.9
  6. Continued absorption as the CBD passes throughout the gut.7

Whatever, the reason, “nano-emulsification” of CBD hemp oil improves both the maximum blood levels and the bioavailability of CBD when taken orally over “untreated” CBD hemp oil taken sublingually.
Clinically in my and other physician practices, we have found that patients taking CBD American Shaman oral “nano-emusified” products require much less (about 4 times less) CBD than “non-nano” sublingual products. No “nano-emulsified” products for oromucosal use have not yet every been tested, although I expect this will occur soon. What the absorption characteristics of such a product might be is unknown at this time, theoretically they could be better in some aspects and worse in others. Only appropriate experimentation will be able to answer these questions.

Bottom Line:

Oral “nano-emulsified” CBD hemp oil is absorbed more completely and has better bioavailability than sublingual administration of “non-nano” treated CBD hemp oil.


  1. Huestis, M. Human Cannabinoid Pharmacokinetics. Chem Biodivers 4(8):1770-1804.
  2. Guy GW, Robson P. A phase I, open label, four-way crossover study to compare the pharmacokinetic profiles of a single dose of 20 mg of a cannabis based medicine extract (CBME) administered on 3 difference areas of the buccal mucosa and to investigate the pharmacokinetics of CBME per oral in healthy male and female volunteers. J Cannabis Ther. 2003; 3:79–120.
  3. Karschner EL, etal. Plasma cannabinoid pharmacokinetics following controlled oral delta9-tetrahydrocannabinoil and oromucosal cannabis extract administration. Clin Chem 2011;57(1):66-75
  4. Atsmon J, etal. PTL401, a New Formulation Based on Pro-Nano Dispersion Technology, Improves Oral Cannabinoids Bioavailability in Healthy Volunteers. J Pharm Sci. 2018 May;107(5):1423-1429.
  5. Atsmon J, etal. Single-Dose Pharmacokinetics of Oral Cannabidiol Following Administration of PTL101: A New Formulation Based on Gelatin Matrix Pellets Technology. Clin Pharmacol Drug Dev. 2018
  6. Cherniakov I, etal. Piperine-pro-nanolipospheres as a novel oral delivery system of cannabinoids: Pharmacokinetic evaluation in healthy volunteers in comparison to buccal spray administration. J Control Release. 2017 Nov 28;266:1-7.
  7. Xie X, etal. PLGA nanoparticles improve the oral bioavailability of curcumin in rats: characterizations and mechanisms. J Agric Food Chem. 2011 Sep 14;59(17):9280-9.
  8. Zgair A, etal. Oral administration of cannabis with lipids leads to high levels of cannabinoids in the intestinal lymphatic system and prominent immunomodulation. Sci Rep 7(1):14542.
  9. Oh N, Park J. Endocytosis and exocytosis of nanoparticles in mammalian cells. Int J Nonomed 9 Suppl 1:51-63.

Can I take hemp oil (CBD) safely while on other drugs?

The Research

The major cannabinoid in hemp oil is cannabidiol (CBD) which is metabolized in the liver via hydroxylation by the CYP450 enzymes CYP2C9, CYP2C19, and CYP3A4.1  In animals, CBD has been shown to affect the metabolism of drugs that are metabolized by these and other CYP450 enzymes.1-6  This effect on other enzymes may not be a direct effect of CBD but of the covalent binding of a CBD metabolite to a hepatic microsomal P450.7   Even though there is significant risk of DDI’s with CBD, the clinical incidence and significance is much less than would be expected given this extensive range of metabolic interference.7,8  The answer to this dilemma can be found in the amount of CBD required to produce a DDI. 

Most of the data on DDI interactions has been performed in animals and, when extrapolated to humans, 90% absorption of an oral dose of over 5mg/kg of CBD would be needed to effect the concentration of a drug metabolized via the CYP2B6 pathway, the pathway which is affected by the lowest CBD intake.Much higher doses oral doses are reguired to effect the other CYP enzymatic pathways.9   At 30% absorption, a much more realistic oral absorption rate than 90%, 50 mg/kg would be necessary to affect any CYP pathway metabolism of a drug.  It is important to note that all of the above effects are changes in drug concentrations, which may not result in any clinically significant DDI’s.

These animal extrapolations and are similar to what has been found in humans that take Epidiolex, a CBD enriched hemp oil product approved by the FDA for treatment of some childhood epilepsies.   Dosages greater than 5mg/kg (2.27mg/pound) are needed to cause a change in the blood levels of some drugs metabolized via the CYP system and the severity of the effect increase with increasing dosages of CBD.10  This means a 150 pound person would need to take a minimum of 340mg/day of CBD to have a change in blood levels of another drug.   However, in this study10, all of the changes in blood levels were minimal and not outside the therapeutic range, except for Clobazam and Desmethylclobazam whose levels fell below the normal therapeutic range, however, there was no apparent worsening in epileptic activity.  This means that although there is a statistical finding of interaction, there was no adverse clinical significance of the interaction.  All patients in this study had increasing amount of CBD being given and all ended at a maximum dose of 50mg/kg (~24mg/lb. or 3400mg/day for a 150# person).  Even at this high dose, no adverse clinical reactions were reported.  This is not unexpected as no serious side effects have been reported in normal patients receiving up to 6000/day.11  Similar findings with CBD and Clobazam in low and high doses have been reported in other studies. 12-14  In as study of CBD artisan use (patients using CBD on their own) in patients with epilepsy, no adverse clinical DDI were found.15

Two cases of cannabis DDI’s have been reported with warfarin, one was a patient smoking marijuana and the other was a patient taking CBD for epilepsy.16,17  The first case may have been a THC induced DDI, while the second was probably a CBD-induced DDI.  In the second case17, the dose of CBD the person was taken when the DDI started occurring was 15mg/kg (33mg/pound), a very high CBD dose.  

The administration of CBD alone versus CBD in hemp oil that contains other cannabinoids may be a significant factor in minimizing clinical DDI effects.  The entourage effect of the other cannabinoids and compounds in the hemp oil seem to minimize the effect of CBD on the CYP450 enzymes.8,18,19   The magnitude of this effect is not known at this time, but the entourage effect of hemp oil in increasing the effectiveness of CBD in other disease states is well known.

 However, not all CBD induced changes in drug concentrations may be due to CBD interfering with the liver’s CYP450 enzyme system. In the study referenced above10, the blood level of Rufinamide, a drug not metabolized by the CYP450 system, was decreased when CBD, however, the level stayed well within the therapeutic range.  Again, a statistical finding with no clinical significance.

Bottom Line

High levels of CBD (>340mg/day) can cause interactions with the metabolism of some drugs but few clinical significant DDI’s have been reported.20  Low dose CBD does not seem to cause any interactions with other drugs.   American Shaman Water Soluble Hemp oil (ASWSHO) is a nano-technology treated hemp oil which most people take in the amounts of 5mg to 15mg twice a day and report great results.21  Ingestion at these low amounts should not result in any drug-drug interactions.   However, I highly recommend that all doctors follow their patients closely and monitor for interactions, regardless of the dosage, until more information is available.   


Note:  The FDA has not approved CBD for the treatment of any diseases other than the approval of Epidiolex for the treatment of some specific pediatric epilepsies. 


1.        Zendulka O, etal.  Cannabinoids and Cytochrome P450 Interactions. Curr Drug Metab. 2016;17(3):206-26.
2.        Arellano AL, etal. Neuropsychiatric and General Interactions of Natural and Synthetic Cannabinoids with Drugs of Abuse and Medicines.  CNS Neurol Disord Drug Targets. 2017;16(5):554-566.
3.        Arnold WR, Weigle AT, Das A.  Cross-talk of cannabinoid and endocannabinoid metabolism is mediated via human cardiac CYP2J2.  J Inorg Biochem. 2018 Jul;184:88-99.
4.        Yamaori S, etal.  Biochem Pharmacol. Characterization of major phytocannabinoids, cannabidiol and cannabinol, as isoform-selective and potent inhibitors of human CYP1 enzymes.  2010 Jun 1;79(11):1691-8.
5.        Yamaori S. etal.  Cannabidiol, a major phytocannabinoid, as a potent atypical inhibitor for CYP2D6.   Drug Metab Dispos. 2011 Nov;39(11):2049-56.
6.        Yamaori, S., et al. Differential inhibition of human cytochrome P450 2A6 and 2B6 by major phytocannabinoids Forensic Toxicol 2011;29: 17.
7.        Kosel B, etal.  The effects of cannabinoids on th pharmacokinetics of indinavir and nelfinavir.  AIDS 2002;16(4):543-50.
8.        Bergamaschi MM, et al. (2011) Safety and side effects of cannabidiol, a Cannabis sativa constituent. Curr Drug Saf. 2011 Sep 1;6(4):237-49.
9.        Iffand K, Grotenhermen F. (2017) An update of the safety and side effects of cannabidiol: a review of clinical data and relevant animals studies.  Cannabis Cannabinoid Res 2017;2.1
10.     Gaston TE, etal. (2017)   Interactions between cannabidiol and commonly used antiepileptic drugs.  Epilepsia. 2017 Sep;58(9):1586-1592.
11.     Taylor L, etal.  A phase 1, randomized, double-blind, placebo-controlled, single ascending dose, multiple dose, and food effect trial of the safety, tolerability and pharmacokinetics of highly purified cannabidiol in healthy subjects.  CNS Drugs 2018;32:1053-67.
12.     Devinsky O, etal. Randomized, dose-ranging safety trial of cannabidiol in Dravet syndrome.  Neurology® 2018;90:e1204-e1211.
13.     Lattanzi S , etal.  Efficacy and Safety of Cannabidiol in Epilepsy: A Systematic Review and Meta-Analysis.  Drugs. 2018 Nov;78(17):1791-1804.
14.     Morrison G, etal.  A Phase 1, Open-Label, Pharmacokinetic Trial to Investigate Possible Drug-Drug Interactions Between Clobazam, Stiripentol, or Valproate and Cannabidiol in Healthy Subjects.  Clin Pharmacol Drug Dev. 2019 Feb 21.
15.     Porcari GS, etal.   Efficacy of artisanal preparations of cannabidiol for the treatment of epilepsy: Practical experiences in a tertiary medical center.   Epilepsy Behav. 2018 Mar;80:240-246.
16.     Damkier P, etal.   Interaction between warfarin and cannabis.   Basic Clin Pharmacol Toxicol. 2019 Jan;124(1):28-31.
17.     Grayson L, etal.  An interaction between warfarin and cannabidiol, a case report.  Epilepsy & Behav Case Reports 2017:9:10-11
18.     Stott CG, Ayerakwa L, Wright S, et al. (2007) Lack of human cytochrome P450 induction by Sativex. 17th Annual Symposium on the Canna- binoids. Saint-Sauveur, Quebec, Canada: International Cannabinoid Research Society. p 211.
19.     Stott CG, Guy GW, Wright S, et al. (2005) The effects of cannabis extracts Tetranabinex and Nabidiolex on human cytochrome P450-mediated metabolism. June 27 2005; Clearwater, FL. International Cannabinoid Research Association. p 163.
20.     Stout SM, Cimino NM. Exogenous cannabinoids as substrates, inhibitors, and inducers of human drug metabolizing enzymes: a systematic review.  Drug Metab Rev. 2014 Feb;46(1):86-95.
20. Kaufmann, R.  (unpublished observations). April 5, 2019.

Can CBD cause Low Platelets?

The Research

In a study of pediatric patients with Dravet’s syndrome epilepsy, high doses of a hemp-derived compound with a ratio of CBD:THC of 50:1 caused a  mild, transient thrombocytopenia (decreased platelet levels).1  However, this only occurred if the child was also on Valproate (a form of valproic acid used as an anticonvulsant).  The amount of CBD/THC being and the length of the transient thrombocytopenia was not specified but all patients platelet counts returned to normal while in the study and on the therapy.  The severity of the thrombocytopenia was mild and caused no symptoms in the patients.  The amounts of CBD being given during this study were high, starting at 2mg/kg and increasing weekly to 16mg/kg.  This is a very high dose of CBD to be giving to a child.   For example, a 44 pound child would start at 20mg twice a day and go up to 320mg twice a day. 

 The cause of the transient thrombocytopenia is unknown.  However, high doses of high CBD/low THC compounds can cause Drug-Drug Interactions (DDI) by interferring with the metabolism of other drugs that are metabolized by the CYP450 enzyme systems in the liver.2  Valproic acid (VA) is metabolized via the CYP450 system, however, only about 10% of is metabolized via this this route with the majority metabolized via glucouronidation and oxidation in the mitochondria, which is not known to be affected by CBD or THC.3 VA is known to cause immune thrombocytopenia and the risk of developing it is increased as the blood level of VA increases and when it is administered with other drugs.4,5   In addition, VA is known to elevate liver enzymes, an indicator of liver damage. (Gaston 2017) Therefore, the mechanism for the transient thrombocytopenia in the above study was very likely the combination of High CBD and VA levels and their concomitant  effects.   However, synthetic THC has been reported to cause immune thrombocytopenia, so effect of THC in this situation cannot be dismissed completely at this time.5,6

(For more info on DDI See upcoming blog: “Can CBD cause liver abnormalities?”)

 Clinical Significance

The incidence of the thrombocytopenia was small and limited to a specific set of patients—all the patients were pediatric, had epilepsy, and were on Valproate.  In addition, the thrombocytopenia was transient and resolved and created no symptoms. Therefore, the clinical significance of this occurrence is only academic at this time.

 Bottom Line

High doses of a high CBD/low THC compound may cause transient thrombocytopenia in pediatric patients with Dravet’s syndrome who are also on Valproate and is probably due to the combination of the effects of high CBD and VA levels.  There is no credible evidence of thrombocytopenia occurring in another situations with CBD isolate or with high CBD/low THC compounds given in high or low doses.     

  1. McCoy B, Wang L, et al.  A prospective open-label trial of a CBD/THC cannabis oil in dravet syndrome.  Ann Clin Trans Neurology 2018:5(9):1077-88.
  2. Gaston TE, etal.   Interactions between cannabidiol and commonly used antiepileptic drugs.  Epilepsia. 2017 Sep;58(9):1586-1592.
  3. Ghodke-Puranik Y, etal.  Valproic acid pathway: pharmacokinetics and pharmacodynamics.  Pharmacogenet Genomics. 2013 April ; 23(4): 236–241.
  4. Buoli M, etal.  The Risk of Thrombocytopenia During Valproic Acid Therapy: A Critical Summary of Available Clinical Data.   Drugs R D. 2018 Mar;18(1):1-5.
  5.  Ko CH, Kong CK, Tse PW.  Valproic acid and thrombocytopenia: cross-sectional study.   Hong Kong Med J. 2001 Mar;7(1):15-21.
  6.   Castaneira G, Rojas K, etal.  Idiopathic thrombocytopenia purpura induced by synthetic cannabinoid.  J Addict Med 2018:Nov 29.
  7. Öztürk E, etal.  Synthetic marijuana “K2” induced ITP.   Platelets. 2015;26(3):258-9.

Anxiety-Fear Disorders

The Disease:

Fear and anxiety are adaptive responses essential to coping with threats to survival. Yet excessive or persistent fear may be maladaptive, leading to disability. Symptoms arising from excessive fear and anxiety occur in a number of neuropsychiatric disorders, including generalized anxiety disorder (GAD), panic disorder (PD), post-traumatic stress disorder (PTSD), social anxiety disorder (SAD), and obsessive–compulsive disorder (OCD). Currently available pharmacological treatments include serotonin reuptake inhibitors, serotonin–norepinephrine reuptake inhibitors, benzodiazepines, monoamine oxidase inhibitors, tricyclic antidepressant drugs, and partial 5-hydroxytryptamine (5-HT)1A receptor agonists. These medications are associated with limited response rates and residual symptoms and adverse effects may also limit tolerability and adherence.


Animal Research:

Anxiety causes physiologic changes in the brain in areas associated with fear including the amygdala, hippocampus, hypothalamus and cingulate cortex.1,2  Animal models of anxiety and fear clearly show an anxiolytic effect of CBD.2,3 CBD is anxiolytic either when given systemically or when injected into specific areas of the brain.4  This effect appears to be due to the interaction of CBD with receptors known to regulate fear and anxiety-related behaviors,  including CB1, 5HT1A, TRPV1, GPR 55, and others.5   This complex interaction of CBD with multiple receptors in the brain result in decreased anxiety and normalize the physiology in the areas of the brain associated with anxiety.1 Repeated use of CBD prevents the long-lasting anxiogenic effects of fear.5 CBD blocks anxiety-induced REM sleep alterations.6

Human Research:

CBD reduces the anxiety of individuals with generalized social anxiety disorder.7 In human patients with panic and anxiety, structural differences have been described in the amygdala, hippocampus, hypothalamus and cingulate cortex.8 Functional MRI studies show that CBD changes how the brain reacts to fear stimuli in these areas.9,10 CBD decreases fear expression, disrupts memory reconsolidation, attenuates fear upon memory retrieval, and enhances extinction (the psychological process by which exposure therapy inhibits learned fear).11-13 In addition, CBD displays antipsychotic properties, can prevent the acquisition of emotionally irrelevant memories, decreases salience attribution, reduces fear related to specific cues, and reverses adrenaline neuronal sensitization, all of which are helpful in anxiety/fear patients.12,14,15 CBD is so potent in reconsolidation that even older fear memories are equally vulnerable to disruption induced by CBD through reconsolidation blockade.16 It is theorized that CBD will help with dreams in patients with PTSD given that dreams are characterized by emotions, sensory perceptions, and bizarre components which are all affected by CBD in the alert state.17 CBD has no effect on sleep in healthy people when given at anxiolytic doses, but it may have an effect in patients with PTSD.18 CBD is so effective in decreasing anxiety that a single dose of CBD (300 mg, p.o.) decreased anxiety after the simulated public speaking test in healthy volunteers. However, CBD has minimal behavioral and subjective effects in healthy volunteers even when presented with emotional stimuli (negative or positive).19

Bottom Line:

CBD has been shown to decrease anxiety in patients with generalized social anxiety disorder.   CBD has been shown to decrease anxiety in certain situations and appears to have the potential to be very beneficial as an adjuvant in treating anxiety and fear disorders.  At this time, the FDA does not recommend CBD for the treatment of anxiety and/or fear.



  1. Patel S, etal. The endocannabinoid system as a target for novel anxiolytic drugs.  Neurosci Biobehav Rev 2017; 76(A): 55-66.
  2. Schier AR, et al. Cannabidiol, a Cannabis sativa constituent, as an anxiolytic drug.  Rev Bras Psiquiatr. 2012 Jun;34 Suppl 1:S104-10.
  3. Soares V and Campos A. Evidences for the anti-panic actions of cannabidiol. Curr Neuropharm 2017; 15:291-299.
  4. Blessing E, etal. Cannabidiol as a potential treatment for anxiety disorders. Neurotherapeutics 2015; 12:825-836.
  5. Campos AC, etal. Cannabidiol blocks long-lasting behavioral consequences of predator threat stress: possible involvement of 5HT1A receptors. J Psychiatr Res. 2012 Nov;46(11):1501-10.
  6. Hsiao YT, Yi PL, Li CL, Chang FC. Effect of cannabidiol on sleep disruption induced by the repeated combination tests consisting of open field and elevated plus-maze in rats. Neuropharmacology 2012 Jan;62(1):373-84.
  7. Bergamaschi MM, et al. Cannabidiol reduces the anxiety induced by simulated public speaking in treatment-naïve social phobia patients. 2011 May;36(6):1219-26.
  8. 8. Pannekoek, JN, etal. Advances in the neuroimaging of panic disorder. Human Psychopharmacol Clin. Exper., 2013, 28(6), 608-611.
  9. Crippa JA, etal. Effects of cannabidiol (CBD) on regional cerebral blood flow.  2004 Feb;29(2):417-26.
  10. Fusar-Poli P, etal. Distinct effects of {delta}9-tetrahydrocannabinol and cannabidiolon neural activation during emotional processing.  Arch Gen Psychiatry. 2009 Jan;66(1):95-105.
  11. Stern CA, etal. Δ9-Tetrahydrocannabinol alone and combined with cannabidiol mitigate fear memory through reconsolidation disruption. Eur Neuropsychopharmacol. 2015 Jun;25(6):958-65.
  12. Jurkus R, et al. Cannabidiol Regulation of Learned Fear: Implications for Treating Anxiety-Related Disorders.  Front Pharmacol. 2016 Nov 24;7:454.
  13. Lee JLC, et al. Cannabidiol regulation of emotion and emotional memory processing: relevance for treating anxiety-related and substance abuse disorders. Br J Pharmacol. 2017 Oct;174(19):3242-3256
  14. Hudson R, etal. Phytocannabinoids modulate emotional memory processing through interactions with the ventral hippocampus and mesolimbic dopamine system: implications for neuropsychiatric pathology. Psychopharmacology (Berl). 2018 Feb;235(2):447-458.
  15. Renard J, etal. Cannabidiol counteracts amphetamine-induced neuronal and behavioral sensitization of the mesolimbic dopamine pathway through a novel mTOR/p70S5 kinase signaling pathway. J Neurosci 2016; 36(18):5160-5169.
  16. Stern C, etal. On disruption of fear memory by reconsolidation blockage: evidence from cannabidiol treatment. Neuropsychopharmacology 2012; 37:2132-2142.
  17. Murillo-Rodriguez E, etal. The Endocannabinoid System Modulating Levels of Consciousness, Emotions and Likely Dream Contents.   CNS Neurol Disord Drug Targets. 2017;16(4):370-379.
  18. Linares I, etal, No actue effects of cannabidiol on the sleep-wake cycle of healthy subjects: a randomized, double-blind, placebo-controlled, crossover study. Frontiers Pharm 2018; 9:1-8.
  19. Arndt D and Wit H. Cannabidiol does not dampen responses to emotional stimuli in healthy adults. Cannabis Cannabinoid Res 2017: 2:105-113.

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