36 Years of CBD Research

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Welcome to our CBD research page that lists, in chronological order, the rise and breadth of CBD studies over the last 36 years.

It’s by no way comprehensive, there’s plenty more where these came from, but the list is a great study resource and shows how the medical science around CBD is evolving. Enjoy!

1980

Chronic administration of cannabidiol to healthy volunteers and epileptic patients.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=42&

All patients and volunteers tolerated CBD very well and no signs of toxicity or serious side effects were detected on examination. 4 of the 8 CBD subjects remained almost free of convulsive crises throughout the experiment and 3 other patients demonstrated partial improvement in their clinical condition.

 

1981

The cannabinoids as potential antiepileptics.

http://www.ncbi.nlm.nih.gov/pubmed/6975285

The anticonvulsant nature of cannabidiol suggests that it has a therapeutic potential in at least three of the four major types of epilepsy: grand mal, cortical focal, and complex partial seizures.

 

1984

Treatment of Meige’s syndrome with cannabidiol.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=114&

CBD was initiated at 100 mg/day, in divided doses, and slowly increased over several weeks to 400 mg/day. Other drugs were kept the same. Spasm frequency, counted twice daily by a relative while the patient was either talking or driving, gradually decreased from 20 to 30 per min before CBD to 7 or 15 per min at a dosage of 400 mg/day. Examinations at weekly intervals using a standard rating scale confirmed at least 50 % improvement in spasm severity and frequency.

 

1985

Beneficial and adverse effects of cannabidiol in a Parkinson patient with sinemet-induced dystonic dyskinesia.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=142&

Trihexyphenidyl and bromocriptine each produced only slight improvement. To stable optimal dosages of the three drugs, CBD was added, starting with 100 mg/d and increasing by 100 mg weekly. At 100 to 200 mg/d, there was a decrease in clinical fluctuations and in dyskinesia scores (by 30%) without a significant worsening of the parkinsonism.

 

1986

Open label evaluation of cannabidiol in dystonic movement disorders.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=14&

Cannabidiol (CBD), a nonpsychoactive cannabinoid of Cannabis, was given to 5 patients with dystonic movement disorders in a preliminary open pilot study. Oral doses of CBD rising from 100 to 600 mg/day over a 6 week period were administered along with standard medication. Dose-related improvement in dystonia was observed in all patients and ranged from 20 to 50%.

 

Cannabidiol in dystonic movement disorders.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=139&

CBD (200 mg, orally) produced an amelioration of his symptoms (especially of his more severely affected right leg) within two hours of administration. Following CBD administration, he was able to walk without support, an effect that lasted about 24 hours. In both cases, CBD produced no adverse effects.

 

1991

Controlled clinical trial of cannabidiol in Huntington’s disease.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=97&

“Correspondingly, plasma levels of CBD were assayed by GC/MS, and the weekly levels (mean range of 5.9 to 11.2 ng/ml) did not differ significantly over the 6 weeks of CBD administration. In summary, CBD, at an average daily dose of about 700 mg/day for 6 weeks, was neither symptomatically effective nor toxic, relative to placebo, in neuroleptic-free patients with HD.”

These findings were later countered by This CBD research and This CBD research both from 2011, and This CBD research from 2012 which all show promise and ask desperately for more research to be funded and conducted on cannabinoid-based HD treatments.

 

2003

A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=36&

Cannabis medicinal extracts can improve neurogenic symptoms unresponsive to standard treatments. Unwanted effects are predictable and generally well tolerated. Larger scale studies are warranted to confirm these findings.

 

Therapeutic potential of cannabinoids in CNS disease.

http://www.ncbi.nlm.nih.gov/pubmed/12617697

“Evidence suggests that cannabinoids may prove useful in Parkinson’s disease by inhibiting the excitotoxic neurotransmitter glutamate and counteracting oxidative damage to dopaminergic neurons. The inhibitory effect of cannabinoids on reactive oxygen species, glutamate and tumour necrosis factor suggests that they may be potent neuroprotective agents.”

 

2004

Effect of Delta-9-tetrahydrocannabinol and cannabidiol on nocturnal sleep and early-morning behavior in young adults.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=223&

15 mg CBD appears to have alerting properties as it increased awake activity during sleep and counteracted the residual sedative activity of 15 mg THC.

 

Effects of cannabidiol (CBD) on regional cerebral blood flow.

http://www.ncbi.nlm.nih.gov/pubmed/14583744

These results suggest that CBD has anxiolytic properties, and that these effects are mediated by an action on limbic and paralimbic brain areas.

 

Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines.

http://www.ncbi.nlm.nih.gov/pubmed/14617682

In conclusion, the nonpsychoactive CBD was able to produce a significant antitumor activity both in vitro and in vivo, thus suggesting a possible application of CBD as an antineoplastic agent.

 

Neuroprotective effect of cannabidiol, a non-psychoactive component from Cannabis sativa, on beta-amyloid-induced toxicity in PC12 cells.

http://www.ncbi.nlm.nih.gov/pubmed/15030397

Our results indicate that cannabidiol exerts a combination of neuroprotective, anti-oxidative and anti-apoptotic effects against beta-amyloid peptide toxicity, and that inhibition of caspase 3 appearance from its inactive precursor, pro-caspase 3, by cannabidiol is involved in the signalling pathway for this neuroprotection.

 

2005

Enhancing cannabinoid neurotransmission augments the extinction of conditioned fear.

http://www.ncbi.nlm.nih.gov/pubmed/15637635

These results demonstrate that the eCB system can be modulated to enhance emotional learning, and suggest that eCB modulators may be therapeutically useful as adjuncts for exposure-based psychotherapies such as those used to treat Post-Traumatic Stress Disorder and other anxiety disorders.

 

Cannabis use in sickle cell disease: a questionnaire study.

http://www.ncbi.nlm.nih.gov/pubmed/16173972

Cannabinoids are increasingly being considered for the management of various painful conditions, and could be considered as an option for treating acute pain in sickle cell disease (SCD)…We conclude that research in the use of cannabinoids for pain relief in SCD would be both important and acceptable to adult patients.

 

2006

Cannabidiol monotherapy for treatment-resistant schizophrenia.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=182&

One patient showed mild improvement, but two patients didn’t show any improvement during CBD monotherapy. All patients tolerated CBD very well and no side effects were reported.”

This study was later contradicted in CBD research from 2012 which is also listed below.

 

Treatment with CBD in oily solution of drug-resistant paediatric epilepsies.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=173&

So far obtained results in our open study appear encouraging for various reasons: 1) no side effects of such a severity were observed as to require CBD discontinuation; 2) in most of the treated children an improvement of the crises was obtained equal to, or higher than, 25% in spite of the low CBD doses administered; 3) in all CBD- treated children a clear improvement of consciousness and spasticity (whenever present) was observed.

 

Topical cannabinoid agonists. An effective new possibility for treating chronic pruritus.

http://www.ncbi.nlm.nih.gov/pubmed/16874533

Topical cannabinoid agonists represent an new effective and well-tolerated therapy for refractory itching of various origins. Creams with a higher concentration may be even more effective with broader indications.

 

Endocannabinoids and the gastrointestinal tract.

http://www.ncbi.nlm.nih.gov/pubmed/16751708

Under pathophysiological conditions, the endocannabinoid system conveys protection to the GI tract, eg from inflammation and abnormally high gastric and enteric secretion. For such protective activities, the endocannabinoid system may represent a new promising therapeutic target against different GI disorders, including frankly inflammatory bowel diseases (eg, Crohn’s disease), functional bowel diseases (eg, irritable bowel syndrome), and secretion- and motility-related disorders.

 

2007

Cannabidiol as a novel inhibitor of Id-1 gene expression in aggressive breast cancer cells.

http://www.ncbi.nlm.nih.gov/pubmed/18025276

These effects seemed to occur as the result of an inhibition of the Id-1 gene at the promoter level. Importantly, CBD did not inhibit invasiveness in cells that ectopically expressed Id-1. In conclusion, CBD represents the first nontoxic exogenous agent that can significantly decrease Id-1 expression in metastatic breast cancer cells leading to the down-regulation of tumor aggressiveness.

 

Meta-analysis of cannabis based treatments for neuropathic and multiple sclerosis-related pain.

http://www.ncbi.nlm.nih.gov/pubmed/17257464

Cannabinoids including the cannabidiol/THC buccal spray are effective in treating neuropathic pain in MS.

 

2008

Endocannabinoids in endocrine and related tumours.

http://www.ncbi.nlm.nih.gov/pubmed/18508995

The endocannabinoid system is involved in a broad range of functions and in a growing number of physiopathological conditions. Indeed, recent evidence indicates that endocannabinoids influence the intracellular events controlling the proliferation of numerous types of endocrine and related cancer cells, thereby leading to both in vitro and in vivo anti tumor effects. In particular, they are able to inhibit cell growth, invasion and metastasis of thyroid, breast and prostate tumors.”

 

The nonpsychoactive Cannabis constituent cannabidiol is a wake-inducing agent.

http://www.ncbi.nlm.nih.gov/pubmed/19045957

These findings suggest that this cannabinoid is a wake-inducing compound that presumably activates neurons in LH and DRN.

Regulation of endocannabinoid signaling by stress: implications for stress-related affective disorders.

http://www.ncbi.nlm.nih.gov/pubmed/18433869

Therapeutically, these data suggest that the endocannabinoid system could be dysregulated in affective disorders, such as depression, which are characterized by maladaptive stress coping. In this review, we discuss the evidence demonstrating that the endocannabinoid system is affected by and can oppose the effects of prolonged stress and, as such, represents a potential target for the development of novel antidepressant agents.

 

The endocannabinoid system and liver diseases.

http://www.ncbi.nlm.nih.gov/pubmed/18426499

Thus, molecules targeting the CB(1) and CB(2) receptors may represent potential therapeutic agents for the treatment of liver diseases. At present, the CB(1) antagonists represent the most attractive pharmaceutical tool to resolve fat accumulation in patients with non-alcoholic fatty liver disease and to treat patients with cirrhosis, as they may slow the progression of fibrosis and attenuate the cardiovascular alterations associated with the advanced stage of the disease.

 

2009

Cannabidiol: a promising drug for neurodegenerative disorders?

http://www.ncbi.nlm.nih.gov/pubmed/19228180

Among Cannabis compounds, cannabidiol (CBD), which lacks any unwanted psychotropic effect, may represent a very promising agent with the highest prospect for therapeutic use.

 

The endocannabinoid system and the treatment of mood and anxiety disorders.

http://www.ncbi.nlm.nih.gov/pubmed/19839936

A growing body of evidence unequivocally demonstrates that deficits in endocannabinoid signalling may result in depressive and anxiogenic behavioral responses, while pharmacological augmentation of endocannabinoid signalling can produce both antidepressive and anxiolytic behavioral responses…Collectively, both clinical and preclinical data argue that cannabinoid receptor signalling may be a realistic target in the development of a novel class of agent for the pharmacotherapy of mood and anxiety disorders.

The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities.

http://www.ncbi.nlm.nih.gov/pubmed/19608284

It seems that the main physiological function of the cutaneous ECS is to constitutively control the proper and well-balanced proliferation, differentiation and survival, as well as immune competence and/or tolerance, of skin cells. The disruption of this delicate balance might facilitate the development of multiple pathological conditions and diseases of the skin (e.g. acne, seborrhea, allergic dermatitis, itch and pain, psoriasis, hair growth disorders, systemic sclerosis and cancer).

 

2010

The endocannabinoid system and migraine.

http://www.ncbi.nlm.nih.gov/pubmed/20353780

Although the exact ECS-dependent mechanisms underlying migraine are not fully understood, the available results strongly suggest that activation of ECS could represent a promising therapeutical tool for reducing both the physiological and inflammatory components of pain that are likely involved in migraine attacks.

 

Motion sickness, stress and the endocannabinoid system.

http://www.ncbi.nlm.nih.gov/pubmed/20505775

These findings demonstrate that stress and motion sickness in humans are associated with impaired endocannabinoid activity. Enhancing ECS signaling may represent an alternative therapeutic strategy for motion sickness in individuals who do not respond to currently available treatments.

 

Cannabinoid receptors as target for treatment of osteoporosis: a tale of two therapies.

http://www.ncbi.nlm.nih.gov/pubmed/21358974

This review summarises in vitro and in vivo findings relating to the influence of cannabinoid ligands on bone metabolism and argues in favour of the exploitation of cannabinoid receptors as targets for both anabolic and anti-resorptive therapy for treatment of complex multifaceted bone diseases such as osteoporosis.

 

2011

Subjective and Physiological Effects After Controlled Sativex and Oral THC Administration.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=305&

Oral THC and Sativex [1:1 THc to CBd Product] produced similar, clinically insignificant increases in heart rate, anxiety, and “good drug effects” with no serious adverse events.

 

Cannabidiol Reduces the Anxiety Induced by Simulated Public Speaking in Treatment-Naïve Social Phobia Patients.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=306&

Pretreatment with CBD significantly reduced anxiety, cognitive impairment and discomfort in their speech performance, and significantly decreased alert in their anticipatory speech. The placebo group presented higher anxiety, cognitive impairment, discomfort, and alert levels when compared with the control group as assessed with the VAMS. The SSPS-N scores evidenced significant increases during the testing of placebo group that was almost abolished in the CBD group. No significant differences were observed between CBD and HC in SSPS-N scores or in the cognitive impairment, discomfort, and alert factors of VAMS. The increase in anxiety induced by the SPST on subjects with SAD was reduced with the use of CBD, resulting in a similar response as the HC.

 

Regulation of nausea and vomiting by cannabinoids.

http://www.ncbi.nlm.nih.gov/pubmed/21175589

Considerable evidence demonstrates that manipulation of the endocannabinoid system regulates nausea and vomiting in humans and other animals…Preclinical research indicates that cannabinioids, including CBD, may be effective clinically for treating both nausea and vomiting produced by chemotherapy or other therapeutic treatments.

 

Neural basis of anxiolytic effects of cannabidiol (CBD) in generalized social anxiety disorder: a preliminary report.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=315&

Within-subject between-condition rCBF comparisons were performed using statistical parametric mapping. Relative to placebo, CBD was associated with significantly decreased subjective anxiety, reduced ECD uptake in the left parahippocampal gyrus, hippocampus, and inferior temporal gyrus, and increased ECD uptake in the right posterior cingulate gyrus. These results suggest that CBD reduces anxiety in SAD and that this is related to its effects on activity in limbic and paralimbic brain areas.

 

2012

Cannabidiol in Humans—The Quest for Therapeutic Targets

http://www.mdpi.com/1424-8247/5/5/529

The aim of the present systematic review is to examine the randomized and crossover studies that administered CBD to healthy controls and to clinical patients. A systematic search was performed in the electronic databases PubMed and EMBASE using the key word “cannabidiol.”

A comprehensive look at 34 studies concerning CBD research within documented medical scientific literature concerning a wide array of applications.

 

Cannabidiol inhibits angiogenesis by multiple mechanisms.

http://www.ncbi.nlm.nih.gov/pubmed/22624859

This study reveals that CBD inhibits angiogenesis by multiple mechanisms. Its dual effect on both tumour and endothelial cells supports the hypothesis that CBD has potential as an effective agent in cancer therapy.

 

Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=171&

Moreover, cannabidiol treatment was accompanied by a significant increase in serum anandamide levels, which was significantly associated with clinical improvement. The results suggest that inhibition of anandamide deactivation may contribute to the antipsychotic effects of cannabidiol potentially representing a completely new mechanism in the treatment of schizophrenia.

 

Acute effects of a single, oral dose of d9-tetrahydrocannabinol (THC) and cannabidiol (CBD) administration in healthy volunteers.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=291&

There were no differences between CBD and placebo on any symptomatic, physiological variable. Conclusions: In healthy volunteers, THC has marked acute behavioural and physiological effects, whereas CBD has proven to be safe and well tolerated.

 

Cannabidiol inhibits growth and induces programmed cell death in kaposi sarcoma-associated herpesvirusinfected endothelium.

http://www.ncbi.nlm.nih.gov/pubmed/23264851

While CBD did not affect the efficiency with which KSHV infected ECs, it reduced proliferation and induced apoptosis in those infected by the virus. CBD inhibited the expression of KSHV viral G protein-coupled receptor (vGPCR), its agonist, the chemokine growth-regulated protein α (GRO-α), vascular endothelial growth factor receptor 3 (VEGFR-3), and the VEGFR-3 ligand, vascular endothelial growth factor C (VEGF-C). This suggests a potential mechanism by which CBD exerts its effects on KSHV-infected endothelium and supports the further examination of CBD as a novel targeted agent for the treatment of Kaposi sarcoma.

 

The role of cannabinoids in inflammatory modulation of allergic respiratory disorders, inflammatory pain and ischemic stroke.

http://www.ncbi.nlm.nih.gov/pubmed/22420307

The presence of endocannabinoid machinery in the central nervous system, together with high levels of CB1 expression, suggests that the endocannabinoid system is an important modulator of neuroinflammation and a possible drug target. In selected conditions, the activation of CB1 receptors in cerebral blood vessels can have beneficial antiischemic effects.

 

Cannabidiol inhibits lung cancer cell invasion and metastasis via intercellular adhesion molecule-1.

http://www.ncbi.nlm.nih.gov/pubmed/22198381

Overall, our data indicate that cannabinoids induce ICAM-1, thereby conferring TIMP-1 induction and subsequent decreased cancer cell invasiveness.

 

The endocannabinoid system and plant-derived cannabinoids in diabetes and diabetic complications.

http://www.ncbi.nlm.nih.gov/pubmed/22155112

Oxidative stress and inflammation play critical roles in the development of diabetes and its complications. Recent studies provided compelling evidence that the newly discovered lipid signaling system (ie, the endocannabinoid system) may significantly influence reactive oxygen species production, inflammation, and subsequent tissue injury, in addition to its well-known metabolic effects and functions. The modulation of the activity of this system holds tremendous therapeutic potential in a wide range of diseases, ranging from cancer, pain, neurodegenerative, and cardiovascular diseases to obesity and metabolic syndrome, diabetes, and diabetic complications.

 

2013

A Last Updated Study of Sativex in the Treatment of Central Neuropathic Pain Due to Multiple Sclerosis.

https://clinicaltrials.gov/ct2/show/NCT01604265?term=cannabidiol&rank=56

Cannabis-based medicine is effective in reducing pain and sleep disturbance in patients with multiple sclerosis related central neuropathic pain and is mostly well tolerated.

 

Cannabidiol as potential anticancer drug.

http://www.ncbi.nlm.nih.gov/pubmed/22506672

Indeed, cannabinoids possess anti-proliferative and pro-apoptotic effects and they are known to interfere with tumour neovascularization, cancer cell migration, adhesion, invasion and metastasization.

 

Cannabidiol enhances consolidation of explicit fear extinction in humans.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=507&

These findings provide the first evidence that CBD can enhance consolidation of extinction learning in humans and suggest that CBD may have potential as an adjunct to extinction-based therapies for anxiety disorders.

 

Cannabidiol for the treatment of cannabis withdrawal syndrome: a case report.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=508&

Daily symptom assessments demonstrated the absence of significant withdrawal, anxiety and dissociative symptoms during the treatment. Conclusion: CBD can be effective for the treatment of cannabis withdrawal syndrome.

 

Cannabidiol in inflammatory bowel diseases: a brief overview.

http://www.ncbi.nlm.nih.gov/pubmed/22815234

CBD is a very promising compound since it shares the typical cannabinoid beneficial effects on gut lacking any psychotropic effects. For years, its activity has been enigmatic for gastroenterologists and pharmacologists, but now it is evident that this compound may interact at extra-cannabinoid system receptor sites, such as peroxisome proliferator-activated receptor-gamma. This strategic interaction makes CBD as a potential candidate for the development of a new class of anti-IBD drugs.

 

Is the cardiovascular system a therapeutic target for cannabidiol?

http://www.ncbi.nlm.nih.gov/pubmed/22670794

In the heart, in vivo CBD treatment protects against ischaemia-reperfusion damage and against cardiomyopathy associated with diabetes. Similarly, in a different model of ischaemia-reperfusion, CBD has been shown to reduce infarct size and increase blood flow in animal models of stroke, sensitive to 5HT(1A) receptor antagonism. Although acute or chronic CBD treatment seems to have little effect on haemodynamics, CBD reduces the cardiovascular response to models of stress, applied either systemically or intracranially, inhibited by a 5HT(1A) receptor antagonist. In blood, CBD influences the survival and death of white blood cells, white blood cell migration and platelet aggregation.”

 

2014

A Randomized Study of Sativex on Cognitive Function and Mood: Multiple Sclerosis Patients.

https://clinicaltrials.gov/ct2/show/NCT01964547?term=cannabidiol&rank=59

Long-term treatment with THC:CBD spray is not associated with cognitive decline or significant changes in mood. Efficacy, assessed separately by the patient, physician and caregiver, is maintained in long-term treatment.”

See this news release from the Multiple Sclerosis Journal for the updated results of the CBD research from which that quote was taken.

 

Cannabinoids increase lung cancer cell lysis by lymphokine-activated killer cells via upregulation of ICAM-1.

http://www.ncbi.nlm.nih.gov/pubmed/25069049

“Altogether, our data demonstrate cannabinoid-induced upregulation of ICAM-1 on lung cancer cells to be responsible for increased cancer cell lysis by LAK cells. These findings provide proof for a novel antitumorigenic mechanism of cannabinoids.

 

Acute effects of smoked marijuana and oral delta9-tetrahydrocannabinol on specific airway conductance in asthmatic subjects.

http://www.cannabis-med.org/studies/ww_en_db_study_show.php?s_id=67&

These findings indicated that in the asthmatic subjects, both smoked marijuana and oral THC caused significant bronchodilation of at least 2 hours duration.

So airflow to the lungs is increased, but when a high-CBD strain is smoked then obviously the benefits for asthmatic patients are dramatically compounded.

 

What Studies Say about Hemp CBD.

http://www.nutritionaloutlook.com/womens-health/what-studies-say-about-hemp-cbd

A well-cited CBD research article covering in brief the effects of CBD on Anxiety, Sleep, and Schizophrenia specifically for women that also provides a smidgen of CBD market outlook data as well.

 

The role of the endocannabinoid system in eating disorders: neurochemical and behavioural preclinical evidence.

http://www.ncbi.nlm.nih.gov/pubmed/23829365

The endocannabinoid system has long been known as a modulator of several physiological functions, among which the homeostatic and hedonic aspects of eating. CB1 receptors are widely expressed in brain regions that control food intake, reward and energy balance. Animal and human studies indicate that CB1 receptor agonists possess orexigenic effects enhancing appetite and increasing the rewarding value of food. Conversely, CB1 antagonists have been shown to inhibit the intake of food.

 

Involvement of the endocannabinoid system in osteoarthritis pain.

http://www.ncbi.nlm.nih.gov/pubmed/24494687

This review summarizes the promising results that have been recently obtained in support of the therapeutic value of cannabinoids for osteoarthritis management.

 

2015

Cannabidiol for neurodegenerative disorders: important new clinical applications for this phytocannabinoid.

http://www.ncbi.nlm.nih.gov/pubmed/22625422

Within the endocannabinoid system, CBD has been shown to have an inhibitory effect on the inactivation of endocannabinoids (i.e. inhibition of FAAH enzyme), thereby enhancing the action of these endogenous molecules on cannabinoid receptors, which is also noted in certain pathological conditions. CBD acts not only through the endocannabinoid system, but also causes direct or indirect activation of metabotropic receptors for serotonin or adenosine, and can target nuclear receptors of the PPAR family and also ion channels.

 

Safety and side effects of cannabidiol, a Cannabis sativa constituent.

http://www.ncbi.nlm.nih.gov/pubmed/22129319

Several studies suggest that CBD is non-toxic in non-transformed cells and does not induce changes on food intake, does not induce catalepsy, does not affect physiological parameters (heart rate, blood pressure and body temperature), does not affect gastrointestinal transit and does not alter psychomotor or psychological functions. Also, chronic use and high doses up to 1,500 mg/day of CBD are reportedly well tolerated in humans.”

 

Cannabidiol as a Treatment for Acne.

http://www.beyondthc.com/wp-content/uploads/2013/08/CBD-for-Acne.pdf

CBD had been shown by Audra Stinchcomb at the University of Kentucky College of Pharmacy to penetrate the skin readily through a transdermal patch…

we found that low concentrations of CBD were very effective in inhibiting lipid syn-thesis but did not affect the viability of cells. This was also in contrast to the effects of Vitamin A derivatives which inhibit the fat production of sebocytes by killing them.
Also talks about the possibility of using cannabinoid treatments to positively effect hair loss in humans, “In good accord with these data, a single animal study has shown that orally administered CB1 antagonists accelerated hair growth in mice.”

Cannabidiol exerts sebostatic and antiinflammatory effects on human sebocytes.

http://www.ncbi.nlm.nih.gov/pubmed/25061872

Collectively, our findings suggest that, due to the combined lipostatic, antiproliferative, and antiinflammatory effects, CBD has potential as a promising therapeutic agent for the treatment of acne vulgaris.

 

Cannabidiol and clozapine reverse MK-801-induced deficits in social interaction and hyperactivity in Sprague-Dawley rats.

http://www.ncbi.nlm.nih.gov/pubmed/22495620

Our findings reinforce several aspects of the validity of the MK-801-induced model of social withdrawal and hyperactivity and also support the use of this novel set-up for further investigations to assess the antipsychotic potential of novel compounds.

 

Cannabidiol, a Cannabis sativa constituent, as an anxiolytic drug.

http://www.ncbi.nlm.nih.gov/pubmed/22729452

Studies using animal models of anxiety and involving healthy volunteers clearly suggest an anxiolytic-like effect of CBD. Moreover, CBD was shown to reduce anxiety in patients with social anxiety disorder.

 

Cannabidiol reduces cigarette consumption in tobacco smokers: preliminary findings.

http://www.ncbi.nlm.nih.gov/pubmed/23685330

These preliminary data, combined with the strong preclinical rationale for use of this compound, suggest CBD to be a potential treatment for nicotine addiction that warrants further exploration.

 

Transdermal delivery of cannabidiol attenuates binge alcohol-induced neurodegeneration in a rodent model of an alcohol use disorder.

http://www.sciencedirect.com/science/article/pii/S0091305713002104

These results demonstrate the feasibility of using CBD transdermal delivery systems for the treatment of alcohol-induced neurodegeneration.

 

Cannabinoids for the Treatment of Agitation and Aggression in Alzheimer’s Disease.

http://www.ncbi.nlm.nih.gov/pubmed/26271310

Over the past few years, there has been a growing interest in the therapeutic potential of medications that target the endocannabinoid system (ECS). The behavioural effects of ECS medications, as well as their ability to modulate neuroinflammation and oxidative stress, make targeting this system potentially relevant in AD. This article summarizes the literature to date supporting this rationale and evaluates clinical studies investigating cannabinoids for agitation and aggression in AD.

 

The safety and efficacy of 3% Cannabis seeds extract cream for reduction of human cheek skin sebum and erythema content.

http://www.ncbi.nlm.nih.gov/pubmed/26142529

Base plus 3% Cannabis seeds extract showed safety. It was well tolerated for the reduction of skin sebum and erythema content. Its improved efficacy could be suggested for treatment of acne vulgaris, seborrhea, papules and pustules to get attractive facial appearance.

 

Endocannabinoid Signaling in Autism

http://link.springer.com/article/10.1007/s13311-015-0371-9

“It has been clearly documented that eCB signaling plays a key role in many human health and disease conditions of the central nervous system, thus opening the avenue to the therapeutic exploitation of eCB-oriented drugs for the treatment of psychiatric, neurodegenerative, and neuroinflammatory disorders.”

2016…