Full Report

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.

Eczema (Atopic Dermatitis)

The Disease

Atopic Dermatitis (AD), commonly called “eczema, is a disease of the skin characterized by dry skin, severe itching, inflammation, abnormal skin barrier function, and secondary infection.  Often familial, most patients with severe AD have at least one abnormal gene for filaggrin, essential for maintaining skin hydration.  AD usually onsets in childhood and its severity usually decreases with age, however, it may persist into adulthood and be very debilitating.  Typically, the lesions will come and go, usually in the same areas of the skin.  The lesions are inflammatory, and scratching causes the inflammation to worsen and often leads to secondary infection.  Scratching is uncontrollable in most individuals but even those who can control the scratching while awake, scratch during the night.  The itch in AD is does not appear to be caused by one factor, however, recent research has shown that mast cells in the skin in AD patients release compounds that: 1) stimulate nerves in the skin causing the itch sensation and 2) trigger inflammatory reactions in the skin.  This scratching of the skin causes these mast cells to release more of these compounds causing the scratching and inflammation to increase leading to the development of the typical lesions seen in AD flare-ups.   Recent evidence suggests prevention of the itch (and subsequent scratching) may eliminate all the signs and symptoms of the disease.  This seems to be true even though the abnormalities in skin barrier function remain active.  Typical anti-itch medications, including antihistamines, may provide some temporary relief but do not eliminate the itch and scratching completely.  Creams and topical steroids have been shown to be helpful in treating and preventing AD, but relapses are common, and the side effects of chronic steroid use can great significant health problems. 


The itching and subsequent scratching worsens the dermatitis in AD and causes the level of IgE (allergy antibodies) to increase, causing the skin to be more sensitive and react more violently to anything that person may be allergic to.1,2 Scratching causes mast cell activation which causes the release of inflammatory compounds and the opening of Transient Receptor Protein channels on the sensory nerves.  When sensory nerve TRP channels open, the nerve does 2 things:  1) it sends the “itch” message to the spinal cord, 2) it releases compounds that cause inflammation, and 3) it causes the nerve to make more TRP channels.3-6 The increase in TRP channels causes more itching and inflammation, further increasing the severity of the disease.   The reason that histamine doesn’t work well in AD patients is that activation of the TRP channels is what causes the majority of and the persistent itching in AD rather than histamine.7,8  Many of the TRP channels on the nerves are associated with and controlled by cannabinoid receptors.9,10  As severity of the disease increases, the TRP channels and their associated cannabinoid receptors increase together. 11   When cannabinoids bind to these receptors, they can modify the TRP channels making it harder for the nerve to be stimulated, which effectively controls the “itch” sensation.12,13 Studies have shown that CB1 receptor synthetic stimulators decrease the mast cell activation and CB2 receptor synthetic antagonists suppress the itch. 12,13 In addition to the effects of cannabinoid binding to CB1-2 receptors, CBD-like compounds that bind to G-protein coupled orphan receptors GRP55 and GRP119 inhibit itching in patients with chronic itching diseases.14   CBD has other anti-inflammatory effects which may help control the inflammation found in AD.15  


Bottom Line

Recent research has found that the itching in AD is caused by compounds that stimulate receptors in the “itch” nerves of the skin and that cannabinoids can suppress this itch.  This suggests that cannabinoids may have the potential to reduce the signs and symptoms of the atopic dermatitis. 



  1. Mihara K. et al. Vital role of the itch-scratch response in development of spontaneous dermatitis in NC/Nga mice. Br J Dermatol 2004 Aug;151(2):335-45.
  2. Hashimoto Y, et al. Itch-associated scratching contributes to the development of dermatitis and hyperimmunoglobulinaemia E in NC/Nga mice.  Exp Dermatol. 2011 Oct;20(10):820-5.
  3. Wilson S, et al. TRPA1 is required for histamine-independent, Mas-related G protein-coupled receptor-mediated itch. Nat Neurosci 2011 May; 14(5): 595-602.
  4. Lui B, etal. TRPA1 controls inflammation and pruritogen responses in allergic contact dermatitis.  FASEB J. 2013 Sep; 27(9): 3549–3563.
  5. Feng J, etal. Sensory TRP channels contribute differentially to skin inflammation and persistent itch.  Nature Comm 2017;8:980.
  6. Sugimoto M, et al. Putative mechanism of the itch-scratch circle: repeated scratching decreases the cutaneous level of prostaglandin D2, a mediator that inhibits itching. Prostaglandins Leukot Essent Fatty Acids. 2007 Feb;76(2):93-101.
  7. Wilson S, et al. The Ion Channel TRPA1 Is Required for Chronic Itch. J Neurosci 2013 May; 33(22): 9283-9294
  8. Oh MH, et al. TRPA1-Dependent Pruruitus in IL-13-induced Chronic Atopic Dermatitis. J Immunol 2013 Dec 1; 191(11): 5371-5382.
  9. Ankopian AN, etal Role of ionotropic cannabinoid receptors in peripheral antinociception and antihyperalgesia. Trends Pharmacol Sci 2009; 30(2):79-84.
  10. Ru F, et al. Mechanisms of pruritogen-induced activation of itch nerves in isolated mouse skin.  J Physiol 2017; 595(11):3651-3666.
  11. Ueda Y, et al. Involvement of cannabinoid CB2 receptors in the IgE-mediated triphasic cutaneous reaction in mice. Life Sci. 2007 Jan 9;80(5):414-9.
  12. Nam G, et al. Selective Cannabinoid Receptor-1 Agonists Regulate Mast Cell Activation in an Oxazolone-Induced Atopic Dermatitis Model. Ann Dermatol 2016: 28(1): 22-29.
  13. Maekawa T, et al. The cannabinoid CB2 receptor inverse agonist JTE-907 suppresses spontaneous itch-associated responses of NC mice, a model of atopic dermatitis. Eur J Pharmacol. 2006 Aug 7;542(1-3):179-83. Petrosino S, et al. Anti-inflammatory Properties of Cannabidiol, a Nonpsychotropic Cannabinoid, in Experimental Allergic Contact Dermatitis. J Pharmacol Exp Ther. 2018 Jun;365(3):652-663.
  14. Ständer S, et al. Topical cannabinoid agonists. An effective new possibility for treating chronic pruritus. 2006 Sep;57(9):801-7.
  15. Biro T, et al. The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities. Trends Pharmacol Sci 2009 Aug; 30(8): 411-420.

Pain: Nociceptive Pain

The Disease

Nociceptive pain is pain that originates because of stimulation of nerves located in the tissues in our body.  Let’s assume we cut some skin off our finger.  When this happens, receptors at the ends of the nerves in the skin of our finger are stimulated; this causes an “action potential” in the nerve which transfers the information along that nerve; that nerve will transfer the information to another nerve or nerves until it gets to the spinal cord; the spinal cord transfers this information up to our brain stem; the brain stem distributes this information to many different parts of the brain; each part “reports their analysis of this information” back to the brain stem;  the brain stem sends a “report” to the pain center in our brain, and our pain center analyzes this information and decides whether or not to let you know if your finger hurts.  I am sure many of you have cut your finger at some point and didn’t feel pain until you saw that you had cut your finger.  Until you saw the cut, your brain had decided that the information being sent to it from your nerves was false information.  When you saw the cut, your brain got more information from a different source, added this information the report, the pain center re-analyzed the situation and “changed its mind” and told you “your finger hurts”; and told you exactly where it hurt.  

As you can see from the above, lots of different kinds of nerves are involved in nociceptive pain, but it always starts by stimulation of receptors on the ends of the nerves.   Nociceptive pain can be caused by: mechanical forces (pinching, cutting, stretching, etc.), heat and cold, chemical irritation, and inflammation.  In all cases, the of these receptors are located on the ends of nerves and are stimulated via transient receptor potential (TRP) channels that sense and detect and damage occurring in the tissue.

Research Findings

As stated above, nociceptive pain occurs because of stimulation of transient receptor potential (TRP) channels on the ends nerves that lie in the tissues of our body.1  Only three of the six TRP sub-families, TRPV, TRPA, and TRPM, have been have been identified as being responsible for nociceptive pain.1 In each of these subfamilies only six specific channels (TRPV1,TRPV2,TRPV3, TRPV4, TRPA1 and TRPM8) are found to in nociceptive nerves.2,3  Activation of these nociceptive TRP channels by specific noxious and/or pain-producing stimuli serves as the principal mode of detection/transduction of pain under physiological and pathophysiological conditions.1  Some nerves will have only one specific TRP channel which allows them only to respond to the stimuli that activate that specific channel, i.e. certain nerves have only TRPM8 allowing them to respond only to pressure and shearing pain.1  However, most nerves have multiple TRPV channels allowing that nerve to respond to multiple types of pain.1  TRPV1 and TPRA1 are often found together on nerves and both activated in many noxious situations including inflammatory pain, visceral pain, migraines, etc.1    Nociceptive TRP channels are membrane proteins, and most are found in the neuronal/cell membrane.4 However, a significant number are present in intracellular organelle membranes of the nerves and these channels will migrate to the cell membrane when the cell undergoes significant and/or persistent injury or inflammation, increasing the intensity of the “felt pain” and leading to hyperalgesia (see neuropathic pain).1,5-9  Often inflammation in the tissue begins after the inciting stimulus.  This causes the release of various chemicals which cause vasodilation (the source of the redness and swelling associated with inflammation) and sensitization of the TRP channels leading to hyperalgesia (minor touching of the damaged area that normally doesn’t cause pain but now does).1,5-8,10  All of these changes result in constant activation and mobilization of the TRP’s which is responsible for the feeling of constant and increasing pain, even though the initial stimulus that caused the pain is no longer present.

CBD desensitizes TRPV1-4 and TRPA1 receptors such that they are unable to generate an action potential, causing the nerves to be unable to send “pain” messages to the spinal cord.11,12  In addition, CBD inhibits TRPM8 receptors which does the same thing.13 However, other cannabinoids including cannabinol (CBN), cannabichromene (CBC), cannabigerol (CBG), and THC also desensitize these receptors and inhibit the nerves from depolarizing and sending “pain” messages to the spinal cord.11  Often TRP channels are linked with other known cannabinoid receptors, i.e., CB2, 5-HT1A, etc.11  Cannabinoids binding to these receptors interact with their associated TRP channels causing desensitization and prohibition of generating nerve impulses.11

Numerous studies have been performed using chemically produced blockers of TRP’s and several have found them to be somewhat effective in the relief of specific types of nociceptive pain, however, because they all have been specific blockers of only one type of TRP (example: blocks only TRPV1 and not any others) and, in most painful situations, multiple TRP’s are being stimulated, they have not been universally useful in nociceptive pain.  However, because of its ability to block all the TRP’s associated with nociceptive pain, CBD-enhanced full spectrum hemp oil should be more effective in preventing nociceptive pain than chemically produced TRP blockers.  In addition, because it contains many other cannabinoids known to also block TRP’s, CBD-enriched hemp oil should be better at controlling nociceptive pain than CBD alone.

Bottom Line

Nociceptive pain is the most common type of pain and is caused by physical damage or potential damage to the body.  CBD-enriched hemp oil containing multiple other cannabinoids has great potential in being able to block sensory nerves from generating nerve impulses resulting in the elimination of nociceptive pain.  No studies of CBD-enriched hemp oil in nociceptive pain have been reported and, at this time, the FDA does not approve the use of CBD products for nociceptive pain.



  1. Mickle AD, etal. Nociceptive TRP channels: Sensory detectors and transducers in multiple pain pathologies. Pharmaceuticals 2016;9:72
  2. Marwaha L, etal. TRP channels: potential drug target for neuropathic pain.  2016 Dec;24(6):305-317.
  3. Sałat K, etal. Transient receptor potential channels – emerging novel drug targets for the treatment of pain.  Curr Med Chem. 2013;20(11):1409-36.
  4. Ferrandiz-Huertas C, etal. Trafficking of thermo-TRP channels. Membranes 2014;4:525–64.
  5. Mickle A.D, etal. Induction of thermal and mechanical hypersensitivity by parathyroid hormone-related peptide through upregulation of TRPV1 function and trafficking. Pain 2015;156:1620–36.
  6. Zhang X, etal. NGF rapidly increases membrane expression of TRPV1 heat-gated ion channels. EMBO J. 2005;24:4211–23.
  7. Schmidt M, etal. Nociceptive signals induce trafficking of TRPA1 to the plasma membrane. Neuron 2009;64:498–509.
  8. Meng J, etal. TNF alpha induces co-trafficking of TRPV1/TRPA1 in VAMP1-containing vesicles to the plasmalemma via Munc18-1/syntaxin1/SNAP-25 mediated fusion. Sci. Rep. 2016;6:21226.
  9. Bandell, M, etal. Noxious cold ion channel TRPA1 is activated by pungent compounds and bradykinin. Neuron 2004;41:849–57.
  10. Julius D. TRP channels and pain. Annu Rev Cell Dev Biol. 2013;29:355-84.
  11. Akopian AN, etal. Role of ionotropic cannabinoid receptors in peripheral antinociception and antihyperalgesia.  Trends Pharmacol Sci 2009;30(2):79-84.
  12. Iannotti FA, etal. Non-psychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability. ACS Chem Neurosci. 2014;5(11):1131-41.
  13. De Petrocellis L, etal. Plant-derived cannabinoids modulate the activity of transient receptor potential channels of ankyrin type-1 and melastatin type-8. J Pharmacol Exp Ther. 2008 Jun;325(3):1007-15.




Pain: Psychogenic

The Disease

Psychogenic pain (AKA, psychalgia) is pain that is caused, aggravated, or prolonged by emotional, mental, or behavioral factors.  Headache, stomach ache, heart ache, and other emotion-related pains are one type of psychogenic pain.  However, any pain from any cause can have a component of psychogenic pain, as pain often produces emotions that can magnify one’s perception of the pain.

Pain is not a disease but a perception to a real or perceived noxious stimulus.  The final determinate to whether something is painful or not is made in the brain.  In nociceptive pain, receptors on our peripheral nerves are stimulated (i.e., we cut our finger), they transfer this information through our peripheral nerves to the spinal cord, the spinal cord transfers this information up to our brain stem, the information is then distributed to many different parts of the brain who “report their analysis of this information” to the pain center in our brain which then “decides whether or not our finger hurts”.  As you can see, the final determination of “hurt or not hurt” is made in the brain.  In psychogenic pain, the brain decides that something hurts, not because that part of our body is sending messages to the brain but because our emotions, mental state, or behavior has made the brain “decide” to make us feel pain in that area.

Although it may magnify idiopathic pain (pain where the cause is unknown), psychogenic pain is different in that the cause is usually unown, i.e., stomach ache in emotionally upset children, heart ache after the loss of a loved one, etc.  Psychogenic pain is different from neuropathic pain (pain caused by damage to the nerves) and from allodynia (pain felt due to the stimulation of non-painful peripheral nerves) in that in psychogenic pain the nerves are normal and the stimulation of the pain originates in the brain rather than in the periphery.  We “feel” the pain in the periphery (in our stomach, chest, abdomen, etc.) but the pain is not originating there.  For many cases, psychogenic pain doesn’t last for relatively short time and resolves when the emotional stimulus has been removed.  However, for some the stimulus causing the pain is not readily removable or is continuously or frequently remembered and they may suffer from psychogenic pain for a long time.  This constant stimulus of pain can become ingrained in their brain and cause them to continue to have pain, even after the stimulus that originally caused the pain has been removed.

The Research

Little to no direct research has been reported using cannabinoids to treat psychogenic pain, however, lots of research has been done examining the effect of cannabinoids on the perception of pain and the “remembering” of experiences associated with emotional pain (i.e., PTSD, etc.).  A portion of our brain’s frontal lobe called the Anterior Cingulate Cortex (ACC) link the feeling of pain with the emotional experience of the pain.1,2  In both animals and humans, the nerves in the ACC help us to identify situations that cause pain and to avoid those situations and damage to the ACC can prevent one from learning that a particular stimulus produces pain.3-6  Therefore, psychogenic pain may be caused by emotions stimulating the ACC and subsequently causing us to “feel” pain somewhere in our body.  It is known that injecting CBD into the ACC in rats that were experiencing nociceptive pain caused the rats not to exhibit any fear of the stimulus causing the pain.6  Neuroimaging studies in humans have found evidence for a critical modulatory role of the ACC in the effects of CBD.7  Therefore, it appears that CBD tends to disassociate emotions from pain through its actions on the ACC.  This ability of CBD to disassociate emotions from memory recall via the ACC has been shown to be extremely beneficial in PTSD patients (see Diseases/Post Traumatic Stress Disorder in this website for more details) and it may be that similar disassociation may be helpful in persistent psychogenic pain.

In addition, many other hard to treat pain conditions that previously had unknown causes have been proposed to involve a deficiency of the endocannabinoid system.8 Treatment with CBD has been proposed as an alternative for these hard to treat pain conditions some of which were previously were thought to be psychogenic in nature.  A recent example of this is the pain caused by VGKC-complex autoimmunity. In this disease, the patient makes antibodies against their own nerves and these antibodies attach to voltage-gated potassium channels (VGKC).  When this happens, the nerve becomes hyperexcitable and starts sending “pain” signals to the brain.9 CBD inhibits VGKC-activation in neurons which would decrease the pain in these conditions.10   In psychogenic pain, it is thought that the neurons somewhere along the “pain pathway” from the sensory receptors in the periphery to the “pain deciding centers” in the brain have become hyperactive and are making the person feel pain.  If this is so, CBD may be able to eliminate this pain.

Bottom Line

Little to no direct research of the effect of CBD on psychogenic pain.  There is theoretical evidence that suggests it may be helpful for psychogenic pain by both its effects on separating emotional responses from memory and actions and by its inhibiting the pain associated with neuronal hyperexcitability.  At this time, the FDA has not approved CBD for the treatment of psychogenic pain.



  1. Lane RD, etal. Neural correlates of levels of emotional awareness. Evidence of an interaction between emotion and attention in the anterior cingulate cortex. J Cogn Neurosci 1998;10(4):525–35.
  2. Davis, KD., etal. “Functional MRI of pain- and attention-related activations in the human cingulate cortex”,  Neurophysiol.1997;77:3370–80.
  3. Qu C, etal. Lesion of the Rostral Anterior Cingulate Cortex Eliminates the Aversiveness of Spontaneous Neuropathic Pain FollowingPartial or Complete Axotomy. Pain 2001;152(7): 1641–1648.
  4. Hutchinson WD, etal. Pain-related neurons in the human cingulate cortex.  Nat Neurosci 1998;2:403-5.
  5. Koyama T, etal. Anterior cingulate activity during pain-avoidance and reward tasks in monkeys. Neurosci Res. 2001 Apr;39(4):421-30.
  6. Genaro K, etal. Cannabidiol is a potential therapeutic for the affective-motivational dimension of incision pain in prats.  Front Pharmacol 2017;8:391
  7. 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.
  8. Russo EB. Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions? Neuro Endocrinol Lett. 2008;29(2):192-200.
  9. Klein CJ, etal. Chronic pain as a manifestation of potassium channel-complex autoimmunity.  Neurology 2012 Sep 11;79(11):1136-44.
  10. Ghovanloo MR, etal. Inhibitory effects of cannabidiol on voltage-dependent sodium currents. J Biol Chem. 2018 Sep 14. pii: jbc.RA118.004929.


The Disease

Fibromyalgia patients have widespread pain, nonrestorative sleep, disturbed mood, and fatigue.1,2 The disease has no associated definitive histological or pathological findings associated with the symptoms.  The disease is characterized by hyperalgesia (increase sensitivity to pain), hyper-responsiveness of the autonomic nervous system and neuropathic pain.3,4 Based upon human research, a deficiency in the endocannabinoid system and low-grade inflammation in the CNS may be causative and/or associated with fibromyalgia and other diseases that were in the past thought to be neurological in nature.5-9  

Animal Studies

No animal studies of CBD and Fibromyalgia have been reported.

Human Studies

The hyperalgesia of fibromyalgia is associated with central endocannabinoid hypofunction in the spinal cord and endocannabinoids reduce this hyperalgesia.10,11 Natural and synthetic cannabis compounds improve the symptoms of fibromyalgia including the reduction of pain, feeling of well-being, sleep, and overall mental health.12-17  In fact, Cannabis has been rated the most effective therapy for fibromyalgia.18 

Bottom Line

Several studies have shown that cannabinoids have the potential to improve the symptoms associated with fibromyalgia.   However, at this time, the FDA does not recommend CBD for the treatment of anxiety and/or fear.

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