Cannabidiol, or CBD, is a natural compound that has gained popularity in recent years, thanks in part to a growing body of research into its potential health benefits, which may include treating depression. The initial results of some studies into CBD and depression look promising.

CBD is one of over 100 compounds called cannabinoids, which are found in the plant Cannabis sativa.

While CBD is similar to tetrahydrocannabinol (THC), the two compounds act differently in the body. THC is responsible for the feelings of euphoria, or the “high,” that a person experiences while using cannabis.

CBD does not have these effects on the body — it does not cause a high or feelings of euphoria.

In this article, learn about the potential for CBD to help relieve the symptoms of depression. CBD may not be right for everyone, and there are some other things to consider before using CBD treatment for any condition.

CBD for depression


CBD could be useful in treating depression, as it appears to have a positive interaction with serotonin receptors in the brain.

Depression and anxiety disorders are common mental health conditions that can have lasting effects on a person’s health, social life, ability to work, and overall well-being.

A doctor may prescribe pharmaceutical drugs to help a person treat or manage depression. Many of these drugs have difficult side effects, such as mood swings, sleeplessness, and sexual dysfunction.

CBD has shown promise in initial studies as a treatment for both depression and anxiety, and it may cause fewer side effects in some people.

The findings of research from 2014 may help explain why CBD could be useful in treating depression. They indicate that, in most studies, CBD appears to have a positive interaction with serotonin receptors in the brain.

Serotonin impacts a range of functions in the body, including a person’s emotional state and feelings of well-being or happiness. Keeping serotonin levels balanced is often a key therapy for people with depression.

What the research says

Testing in animal models has provided some evidence for the use of CBD to help treat depression.

According to the authors of the 2014 review, results from a variety of studies indicate that CBD appears to act as an antidepressant and antianxiety compound in animal models of depression.

Authors of a review from 2018 also noted that many studies have shown the anti-stress and antidepressant activity of CBD in animal models.

The compound exhibits a clear anti-stress effect after short- or long-term use. In certain tests, CBD acted as an antidepressant.

The authors also found that the compound worked without activating the brain’s endocannabinoid receptors directly, which may indicate that there is less risk of CBD becoming habit-forming, or addictive.

This is important because many people are concerned about the habit-forming potential of antidepressants and cannabis compounds.

In a study from 2018, researchers indicated that CBD has promise as a fast-acting antidepressant.

Most researchers conducting animal studies of CBD call for more direct research in humans, but their initial results are an essential step toward establishing how CBD works in the body.


CBD for panic and anxiety


Taking CBD may be helpful for people with anxiety or panic disorder.

Some studies in humans show that CBD may be useful for other issues commonly associated with depression, such as anxiety or panic disorder.

A 2017 review of the potential benefits of CBD for panic disorder found some positive results.

According to the authors, panic disorder affects approximately 5 percent of the worldwide population and causes unexpected and recurring panic attacks.

In human models, a single dose of 300 milligrams (mg) of CBD caused a notable decrease in anxiety levels after a simulated public speaking test, according to one study in the review.

Another found that 600 mg of CBD caused a significant reduction of anxiety measures in people with social anxiety disorder.


Side effects

Taking CBD orally, inhaling it, or using it topically usually does not appear to cause side effects.

However, if someone is sensitive to the compounds in CBD, they may experience:

  • changes in appetite or weight
  • fatigue
  • diarrhea

CBD can also interact with a range of medications. Anyone considering using CBD should speak to a doctor about their existing medications to check for any interactions.


How to use it


People can take CBD using various tinctures, capsules, and oils.

Many people choose to take CBD orally, using various tinctures, capsules, and oils.

CBD may be most effective when a person uses it regularly.

There does not appear to be a risk of developing an addiction to CBD, so long-term use may be safe for most people.

The Food and Drug Administration (FDA) does not regulate natural supplements such as CBD, so it is crucial to buy only reputable products.

Also, it is a good idea to check for third-party lab results that indicate the levels of CBD in any given product.



CBD is a potent compound that is gaining popularity as an alternative medicine.

While there is some promising evidence for the future use of CBD as an antidepressant, more research in humans is necessary to determine whether it is safe or effective.

Anyone interested in using CBD for depression or anxiety should speak to a doctor about how to use it and the risk of interactions with other medications.


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The endocannabinoid system and digestive imbalance play major roles in Parkinson’s disease. Research on CBD, THC, and THCV has demonstrated that cannabis medicine may help to manage PD symptoms.
  • The endocannabinoid system plays a major role in Parkinson’s Disease (PD).
  • PD is associated with impairment of motor control after the loss of 60-80% of dopamine-producing neurons in a critical brain region.
  • Digestive imbalance may play a role in the advancement of PD & the severity of symptoms.
  • Cannabinoids have neuroprotectant, anti-oxidant and anti-inflammatory properties which can be beneficial for managing PD.
  • Various combinations of CBD, THC, and THCV may provide relief for Parkinson’s symptoms.
How cannabinoid therpay may help Parkinson's disease
Photo credit: pixabay

Scientists at the University of Louisville School of Medicine in Kentucky have identified a previously unknown molecular target of cannabidiol (CBD), which may have significant therapeutic implications for Parkinson’s Disease (PD).

A poster by Zhao-Hui Song and Alyssa S. Laun at the 2017 meeting of the International Cannabinoid Research Society in Montreal disclosed that CBD activates a G-coupled protein receptor called “GPR6” that is highly expressed in the basal ganglia region of the brain. GPR6 is considered an “orphan receptor” because researchers have yet to find the primary endogenous compound that binds to this receptor.(1)

It has been shown that a depletion of GPR6causes an increase of dopamine, a critical neurotransmitter, in the brain. This finding suggests GPR6 could have a role in the treatment of Parkinson’s, a chronic, neurodegenerative disease that entails the progressive loss of dopaminergic (dopamine-producing) neurons and consequent impairment of motor control. By acting as an “inverse agonist” at the GPR6 receptor, CBD boosts dopamine levels in preclinical studies.

Parkinson’s affects an estimated 10 million people worldwide, including one million Americans. It is the second most common neurological disorder (after Alzheimer’s Disease). Over 96 percent of those diagnosed with PD are over 50 years old with men being one-and-a-half times more likely to have PD than women. Uncontrolled PD significantly reduces the patient’s quality of life and can render a person unable to care for themselves, trapped in a body they cannot control.

Dopamine depletion

Parkinson’s Disease is most associated with compromised motor function after the loss of 60-80% of dopamine-producing neurons. As dopaminergic neurons become damaged or die and the brain is less able to produce adequate amounts of dopamine, patients may experience any one or combination of these classic PD motor symptoms: tremor of the hands, arms, legs or jaw; muscle rigidity or stiffness of the limbs and trunk; slowness of movement (bradykinesia); and /or impaired balance and coordination (postural instability).

Additional symptoms include decreased facial expressions, dementia or confusion, fatigue, sleep disturbances, depression, constipation, cognitive changes, fear, anxiety, and urinary problems. Pesticide exposure and traumatic brain injury are linked to increased risk for PD. Paraquat, an herbicide sprayed by the DEA in anti-marijuana defoliant operations in the United States and other countries, resembles a toxicant MPTP [methyl-phenyl-tetrahydropyridien], which is used to simulate animal models of Parkinson’s for research purposes.(2)

Within the PD brain there are an inordinate number of Lewy bodies – intracellular aggregates of difficult to break down protein clusters – that cause dysfunction and demise of neurons.(3) This pathological process results in difficulties with thinking, movement, mood and behavior. The excessive presence of Lewy bodies, coupled with the deterioration of dopaminergic neurons, are considered to be hallmarks of Parkinson’s. But mounting evidence suggests that these aberrations are actually advanced-stage manifestations of a slowly evolving pathology.

It appears that non-motor symptoms occur for years before the disease progresses to the brain, and that PDis actually a multi-system disorder, not just a neurological ailment, which develops over a long period of time. According to the National Parkinson’s Foundation, motor symptoms of PD only begin to manifest when most of the brain’s dopamine-producing cells are already damaged.

Patients whose PD is diagnosed at an early stage have a better chance of slowing disease progression. The most common approach to treating PD is with oral intake of L-dopa, the chemical precursor to dopamine. But in some patients, long-term use of L-dopa will exacerbate PD symptoms. Unfortunately, there is no cure – yet.


Gut-brain axis

What causes Parkinson’s? One theory that is gaining favor among medical scientists traces the earliest signs of PD to the enteric nervous system (the gut), the medulla (the brainstem), and the olfactory bulb in the brain, which controls one’s sense of smell. New research shows that the quality of bacteria in the gut – the microbiome – is strongly implicated in the advancement of Parkinson’s, the severity of symptoms, and related mitochondrial dysfunction.

Defined as “the collection of all the microorganisms living in association with the human body,” the microbiome consists of “a variety of microorganisms including eukaryotes, archaea, bacteria and viruses.” Bacteria, both good and bad, influence mood, gut motility, and brain health. There is a strong connection between the microbiome and the endocannabinoid system: Gut microbiota modulate intestinal endocannabinoid tone, and endocannabinoid signaling mediates communication between the central and the enteric nervous systems, which comprise the gut-brain axis.

Viewed as “the second brain,” the enteric nervous system consists of a mesh-like web of neurons that covers the lining of the digestive tract – from mouth to anus and everything in between. The enteric nervous system generates neurotransmitters and nutrients, sends signals to the brain, and regulates gastrointestinal activity. It also plays a major role in inflammation.

The mix of microorganisms that inhabit the gut and the integrity of the gut lining are fundamental to overall health and the ability of the gut-brain axis to function properly. If the lining of the gut is weak or unhealthy, it becomes more permeable and allows things to get into the blood supply that should not be there, negatively impacting the immune system. This is referred to as “leaky gut.” Factor in an overgrowth of harmful bacteria and a paucity of beneficial bacteria and you have a recipe for a health disaster.

The importance of a beneficial bacteria in the gut and a well-balanced microbiome cannot be overstated. Bacterial overgrowth in the small intestine, for example, has been associated with worsening PD motor function. In a 2017 article in the European Journal of Pharmacology, titled “The gut-brain axis in Parkinson’s disease: Possibilities for food-based therapies,” Peres-Pardo et al examine the interplay between gut dysbiosis and Parkinson’s. The authors note that “PD pathogenesis may be caused or exacerbated by dysbiotic microbiota-induced inflammatory responses … in the intestine and the brain.”(4)

Mitochondria, microbiota and marijuana

The microbiome also plays an important role in the health of our mitochondria, which are present in every cell in the brain and body (except red blood cells). Mitochondria function not only as the cell’s power plant; they also are involved in regulating cell repair and cell death. Dysfunction of the mitochondria, resulting in high levels of oxidative stress, is intrinsic to PD neurodegeneration. Microbes produce inflammatory chemicals in the gut that seep into the bloodstream and damage mitochondria, contributing to disease pathogenesis not only in PD but many neurological and metabolic disorders, including obesity, type-2 diabetes, and Alzheimer’s.

The evidence that gut dysbiosis can foster the development of PD raises the possibility that those with the disease could benefit by manipulating their intestinal bacteria and improving their microbiome. Enhancing one’s diet with fermented foods and probiotic supplements may improve gut health and relieve constipation, while also reducing anxiety, depression and memory problems that afflict PD patients.

Cannabis therapeutics may also help to manage PD symptoms and slow the progression of the disease. Acclaimed neurologist Sir William Gowers was the first to mention cannabis as a treatment for tremors in 1888. In his Manual of Diseases of the Nervous System, Grower noted that oral consumption of an “Indian hemp” extract quieted tremors temporarily, and after a year of chronic use the patient’s tremors nearly ceased.

Modern scientific research supports the notion that cannabis could be beneficial in reducing inflammation and assuaging symptoms of PD, as well as mitigating disease progression to a degree. Federally-funded preclinical probes have documented the robust antioxidant and neuroprotective properties of CBD and THCwith “particular application … in the treatment of neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease and HIV dementia.” Published in 1998, these findings formed the basis of a U.S.government patent on cannabinoids as antioxidants and neuroprotectants.

Pot for Parkinson’s

Although clinical studies focusing specifically on the use of plant cannabinoids to treat PD are limited (because of marijuana prohibition) and convey conflicting results, in aggregate they provide insight into how cannabis may aid those with Parkinson’s. Cannabidiol, THC, and especially THCV all showed sufficient therapeutic promise for PD in preclinical studies to warrant further investigation. Additional research might shed light on which plant cannabinoids, or combination thereof, is most appropriate for different stages of Parkinson’s.

Anecdotal accounts from PD patients using artisanal cannabis preparations indicate that cannabinoid acids (present in unheated whole plant cannabis products) may reduce PD tremor and other motor symptoms. Raw cannabinoid acids (such as CBDA and THCA) are the chemical precursors to neutral, “activated” cannabinoids (CBD, THC). Cannabinoid acids become neutral cannabinoid compounds through a process called decarboxylation, where they lose their carboxyl group through aging or heat. Minimal research has focused on cannabinoid acids, but the evidence thus far suggests that THCA and CBDA have powerful therapeutic attributes, including anti-inflammatory, anti-nausea, anti-cancer, and anti-seizure properties. In a 2004 survey of cannabis use among patients at the Prague Movement Disorder Centre in the Czech Republic, 45 percent of respondents reported improvement in PD motor symptoms.


Cannabis clinicians are finding that dosage regimens for medical marijuana patients with PDdon’t conform to a one-size-fits-all approach. In her book Cannabis Revealed (2016), Dr. Bonni Goldstein discussed how varied a PD patient’s response to cannabis and cannabis therapeutics can be:

“A number of my patients with PD have reported the benefits of using different methods of delivery and different cannabinoid profiles. Some patients have found relief of tremors with inhaled THC and other have not. A few patients have found relief with high doses of CBD-rich cannabis taken sublingually. Some patients are using a combination of CBD and THC … Trial and error is needed to find what cannabinoid profile and method will work best. Starting a low-dose and titrating up is recommended, particularly with THC-rich cannabis. Unfortunately, THCV-rich varieties are not readily available.”

Juan Sanchez-Ramos M.D., PhD, a leader in the field of movement disorders and the Medical Director for the Parkinson Research Foundation, told Project CBD that he encourages his patients to begin with a 1:1 THC:CBD ratio product if they can get it. In a book chapter on “Cannabinoids for the Treatment of Movement Disorders,” he and coauthor Briony Catlow, PhD, describe the dosage protocol used for various research studies that provided statistically positive results and a dosing baseline for PD. This data was included in a summary of dosing regimens from various studies compiled by Dr. Ethan Russo:

  • 300 mg/day of CBD significantly improved quality of life but had no positive effect on the Unified Parkinson Disease Rating Scale. (Lotan I, 2014)
  • 0.5 g of smoked cannabis resulted in significant improvement in tremor and bradykinesia as well as sleep. (Venderová K, 2004)
  • 150 mg of CBD oil titrated up over four weeks resulted in decreased psychotic symptoms. (Chagas MH, 2014)
  • 75-300 mg of oral CBD improved REM-behavior sleep disorder. (Zuardi AW, 2009)

A threshold dose

Of course, each patient is different, and cannabis therapeutics is personalized medicine. Generally speaking, an optimal therapeutic combination will include a synergistic mix of varying amounts of CBD and THC – although PD patients with sleep disturbances may benefit from a higher THC ratio at night.

Dr. Russo offers cogent advice for patients with PD and other chronic conditions who are considering cannabis therapy. “In general,” he suggests, “2.5 mg of THC is a threshold dose for most patients without prior tolerance to its effects, while 5 mg is a dose that may be clinically effective at a single administration and is generally acceptable, and 10 mg is a prominent dose, that may be too high for naïve and even some experienced subjects. These figures may be revised upward slightly if the preparation contains significant CBD content … It is always advisable to start at a very low dose and titrate upwards slowly.”

For information about nutritional supplementation to help manage PD, visit the Life Extension Foundation Parkinson’s page.

Lifestyle Modifications for PD Patients

It is important to treat the patient as a whole – mind, body and soul. The following are a few lifestyle modifications that may provide relief from PD symptoms and improve quality of life.

  • Do cardio aerobic exercise: This benefits the body in so many ways, including stimulating the production of one’s endocannabinoids, increasing oxygen in the blood supply, mitigating the negative impact of oxidative stress, and boosting the production of BDNF, a brain-protecting chemical found to be low in PD patients.
  • Eat more fruits and vegetables: The old saying “garbage in, garbage out” is so true. The majority of PDpatients suffer from chronic constipation. A high fiber diet can be helpful in improving gut motility and facilitating daily bowel movements.
  • Get restful sleep: Not getting good sleep can undermine one’s immune function, cognition and quality of life. The importance of adequate restful sleep cannot be over emphasized.
  • Reduce protein intake – This may help reduce the accumulation of protein bodies that result in Lewy bodies that appear in the enteric nervous system and the central nervous system and increase the uptake of L-dopa.
  • Practice meditation, yoga or Tai Chi: The focus on the integration of movement and breath not only improve mobility but it also improves cognition and immunity. One study showed an increase in grey matter density in the areas of the brain associated with PD. Another showed that yoga improved balance, flexibility, posture and gait in PD patients. Research shows that tai chi can improve balance, gait, functional mobility, and overall well being.
  • Consume probiotic food and supplements: Probiotic foods — raw garlic, raw onions, bananas, asparagus, yams, sauerkraut, etc.— are a great source for the good bacteria in your large intestine. Augmenting your diet with probiotic supplements, especially after taking antibiotics, can support the immune system by helping to repopulate the upper digestive tract with beneficial bacteria. Consult your doctor regarding a recommendation for a quality probiotic.
  • Drink coffee: The risk of PD is considerably lower for men who consume coffee daily.

Nishi Whiteley, a Project CBD research associate and contributing writer, is the author of Chronic Relief: A Guide to Cannabis for the Terminally and Chronically Ill (2016). Special thanks to Juan Sanchez-Ramos for reviewing this article, Ethan B. Russo, M.D. for providing a summary of Parkinson’s research for inclusion in this article, and to Adrian Devitt-Lee for his research support.

Copyright, Project CBD. May not be reprinted without permission.


  • Abrams, D. (2010, Winter). Cannabis in Pain and Palliative Care. The Pain Practitioner, pp. 35-45.
  • AC Howlett, F. B. (2002). International Union of Pharmacology. XXVII. Classification of cannabionid receptros. Pharmacological Reviews, 161-202.
  • Aidan J. Hampson, J. A. (2003). USA Patent No. 6,630,507.
  • Barbara A. Pickut, W. V. (2013). Mindfulness based intervention in Parkinson’s disease leads to structural brain changes on MRI A randomized longitudinal study. Clinical Neurology and Neurosurgery, 2419-2425.
  • Birony Catlow, J. S.-R. (2015). Cannabinoids for the Treatment of Movement Disorders. Current Treatment Options in Neurology.
  • C Garcia, C. P.-G.-A.-R. (2011). Symptom-relieving and neuroprotective effects of the phytocannabinoid Δ9THCV in animal models of Parkinson’s disease. British Journal of Pharmacology, 1495-1506.
  • Chagas MH, Z. A.-P. (2014). Effects of cannabidiol in the treatment of patients with Parkinson’s disease: an exploratory double-blind trial. Journal of Phsychopharmacology, 1088-98.
  • David N. Hauser, T. G. (2013). Mitochondrial dysfunction and oxidative stress in Parkinson’s disease and monogenic parkinsonism. Neurobiology of Disease, 35-42.
  • David Perlmutter, M. (2015). Belly and Brain on Fire. In M. David Perlmutter, Brain Maker (pp. 49-70). New York: Little, Brown and Company.
  • Foundation, N. P. (2017, June 19). What is Parkinson’s. Retrieved from National Parkinson’s Foundation:
  • Foundation, P. D. (2017, 6 21). Parkinson’s Statistics. Retrieved from Parkinson’s Disease Foundation :
  • Goldstein, B. (2016). Parkinson’s Diseas. In B. Goldstein, Cannabis Revealed (pp. 206-208). Bonni Goldstein.
  • L. Klingelhoefer, H. R. (2017). Hypothesis of Ascension in Idiopathic Parkinson’s Disease. Neurology Intereatnional, E28-35.
  • Leonard L. Sokol, M. J. (2016). Letter to the Editor: Cautionary optimism: caffeine and Parkinson’s disease risk. Journal of Clinical Movement Disorders, pp. 3-7.
  • Lisa Klingelhoefer, H. R. (2015). Pahtogenesis of Parkinson disease—the gut-brain axis and environmental factors. Nature, 625-636.
  • Lotan I, T. T. (2014). Cannabis (medical marijuana) treatment for motor and non-motor symptoms of Parkinson disease:. Clin Neuropharmacol, 37(2)-41-4.
  • Madeleine E. Hackney1 and Gammon M. Earhart1, 2. (2008). Tai Chi Improves Balance and Mobility in People with Parkinson Disease. Gait and Posture, 456-460.
  • National Institute of Health. (2017). NIH Human Microbiome Project HOME Page. Retrieved from NIH Human Microbiome Project:
  • Pal Pacher, S. B. (2006). The Endocannabinoid System as an Emerging Target. Pharmacological Reviews, 389-462.
  • Parker, R. M. (2013). The Endocannabinoid System and the Brain. The annual Review of Psychology, 21-47.
  • Paula Perez-Pardo, T. K. (2017). The gut-brain axis in Parkinson’s disease: Possibilities for food -based therapies. European Journal of Pharmacology,
  • Perlmutter, D. (2015). Brain Maker. New York: Little, Brown and Company.
  • Russo, E. (2011). Taming THC: potential cannabis synergy and phytocannabinoid-terpenoid entourage effects. British Journal of Pharmacology, 1344-64.
  • Russo, E. B. (2015). Current status and future of cannabis research. Clinical Researcher, 58-63.
  • Russo, E. B. (2015, January). Introduction to the Endocannabinoid system. Retrieved from…
  • Russo, E. B. (2016). The Medical Use of Cannabis and Cannabinoids in Parkinson’s Disease. Retrieved from The Answer Page:
  • Schecter, G. L. (2010). The Endocannabniond system. In J. Holland, The Pot Book (pp. 52-62). Rochester, Vermont: Park Street Press.
  • Venderová K, R. E. (2004). Survey on cannabis use in Parkinson’s disease: subjective improvement of motor symptoms. Movement Disorder, 1102-6.
  • Yevonne Searls Carlgrove, N. S. (2012). Effect of Yoga on Motor Function in People with parkinosn’s Disease: A Randomized Controled Piolot Study. Yoga and Physical Therapy.
  • Yudowski, D. A. (2017). Cannabinoid Receptors in the Central Nervous System: Their Signaling and Roles in Disease. Frontiers in Cellular Nueroscience, article 294.
  • Zuardi AW, C. J. (2009). Cannabidiol for the treatment of psychosis in Parkinson’s disease. Journal of Phsychopharmacology, 979-83.

(1) An inverse agonist binds directly to a receptor and modifies it in a way that causes the receptor to have the opposite effects of activating it normally.

(2) MPTP was found in an underground meperidine (Demerol) synthesis that caused a small epidemic of Parkinson syndrome in i.v. drug abusers in the San Francisco area in the mid-1980s.

The presence of Lewy bodies (a-synuclein protein clusters) in other parts of the body could potentially serve as an early detection marker for PD, especially in the olfactory bulb and the enteric nervous system.

(4) Peres-Prado et al analyzed gut microbiota in PD patients compared to controls and found the following:

  • Prevotellaceae, a bacterium which supports the production of health-promoting short chain fatty acids (SCFA), biosynthesis of thiamine and folate, and is thought to be associated with increased gut permeability, was 78% lower in the feces of PD patients versus that of their sex-matched and age-matched controls.
  • Biopsies of colonic tissue retrieved from PD patients indicate high levels of tumor necrosis factor-alpha and other inflammatory agents.
  • A lower abundance of SCFA-producing and anti-inflammatory bacteria from the class of Blautia, Coprococcus, and Roseburia were found in fecal samples of PD patients. (Paula Perez-Pardo, 2017)
  • Gastric abnormalities may increase small intestinal bacterial overgrowth (SIBO). SIBO is prevalent in PD patients and correlates directly to worse motor dysfunction.
  • Gut-derived lipopolysaccharide (LPS – an inflammatory toxin produce by bacteria) promotes the disruption of the blood-brain barrier.
  • Impaired gherlin, a gut hormone known as the hunger hormone, is thought to be associated with maintenance and protection of dopamine function in the nigrostriatal pathway which is one of four major dopamine pathways and is particularly involved in movement. Impaired gherlin has been reported in PD patients.



At sufficient dosages, CBD will temporarily deactivate cytochrome P450 enzymes, thereby altering how we metabolize a wide range of compounds.
With cannabidiol (CBD) poised to become widely available in pharmaceutical, nutraceutical, and herbal preparations, medical scientists are taking a closer look at CBD-drug interactions.
CBD cannabis drug interactions
Photo credit: Scientific Images

Cannabidiol is a safe, non-intoxicating, and non-addictive cannabis compound with significant therapeutic attributes, but CBD-drug interactions may be problematic in some cases.

CBD and other plant cannabinoids can potentially interact with many pharmaceuticals by inhibiting the activity of cytochrome P450, a family of liver enzymes. This key enzyme group metabolizes most of the drugs we consume, including more than 60 percent of marketed meds.

At sufficient dosages, CBD will temporarily deactivate cytochrome P450 enzymes, thereby altering how we metabolize a wide range of compounds, including tetrahydrocannabinol (THC), which causes the high that cannabis is famous for.

Metabolizing THC

When THC or any other foreign compound enters the body, it is metabolized. This process is generally very complicated. Metabolizing something properly can involve multiple molecular pathways and various enzymes that enable the body to get rid of the compound (often done by adding something to the original compound). Or metabolism can entail breaking down a compound into a more basic molecule that the body then uses.

Products of a drug’s metabolism are called its metabolites. These metabolites can have very different properties than the initial drug. Ethanol, for example, owes some of its effects, including much of the hangover, to its two-step metabolism. The buildup of acetaldehyde in the liver—while ethanol is converted first to acetaldehyde and then to acetic acid—is a major reason for ethanol’s liver toxicity and the nausea and vomiting caused by excessive consumption.

THC metabolites contribute significantly to the effects of cannabis consumption. Eleven-hydroxy-THC (11-OHTHC), for example, is a THC metabolite that activates the CB1 cannabinoid receptor in the brain and induces a high more potently than THC itself. This means that the body’s metabolism of THC can make it more potent.

Cytochrome P450 enzymes contribute to the metabolism of drugs by oxidizing them, which generally means incorporating an oxygen atom into the drug’s molecular structure. Oxidation will usually make a compound more water soluble and therefore easier for the kidneys to filter out. Both steps in the metabolism of ethanol, mentioned above, and the conversion of THC into 11-OHTHC involve oxidation (though ethanol is not oxidized specifically by cytochrome P450).

Different routes of cannabinoid administration have different effects. Inhaled THC enters capillaries in the lungs, passes into general circulation through the pulmonary arteries, and quickly crosses the blood-brain barrier. When ingested orally, however, THC is absorbed in the small intestine and then carried to the liver, where it is metabolized by subclasses of cytochrome P450 (abbreviated CYP), specifically the CYP2C and CYP3A enzymes.

These liver enzymes also metabolize CBD, converting it into 7-OHCBD and 6-OHCBD. But there has been relatively little research into the properties of these CBD metabolites.

Metabolizing CBD

The way CBD interacts with cytochrome P450 is pivotal; in essence, they deactivate each other. Preclinical research shows that CBD is metabolized by cytochrome P450 enzymes while functioning as a “competitive inhibitor” of the same liver enzymes. By occupying the site of enzymatic activity, CBD displaces its chemical competitors and prevents cytochrome P450 from metabolizing other compounds.

The extent to which cannabidiol behaves as a competitive inhibitor of cytochrome P450 depends on how tightly CBD binds to the active site of the metabolic enzyme before and after oxidation. This can change greatly, depending on how—and how much—CBD is administered, the unique attributes of the individual taking this medication, and whether isolated CBD or a whole plant remedy is used.

If the dosage of cannabidiol is low enough, it will have no noticeable effect on CYP activity, but CBD may still exert other effects. There is no clearly established cut-off dose, below which CBD does not interact with other drugs. A 2013 report on a clinical trial using GW Pharmaceutical’s Sativex, a whole plant CBD-rich sublingual spray, found no interactions with CYP enzymes when approximately 40mg of CBD were administered. A subsequent clinical trial, however, found that 25mg of orally administered CBDsignificantly blocked the metabolism of an anti-epileptic drug.

How do CBD-generated changes in cytochrome P450 activity impact the metabolic breakdown of THC? Animal studies indicate that CBD pretreatment increases brain levels of THC. That’s because CBD, functioning as a competitive inhibitor of cytochrome P450, slows down the conversion of THC into its more potent metabolite, 11-OHTHC. Consequently, THC remains active for a longer duration, but the peak of the extended buzz is blunted somewhat under the influence of cannabidiol.

Other factors figure prominently in CBD’s ability to lessen or neutralize the THC high.

Grapefruit and Ganja

Lester Bornheim, a research pharmacologist at the University of California in San Francisco, was among the first scientists to study the metabolism of CBD. In 1987, he was awarded a NIDA grant to investigate the effects of phytocannabinoids on cytochrome P450 enzymes. THC and cannabinol (CBN) also inhibit CYPactivity, but CBD, of all the plant cannabinoids studied, is the strongest cytochrome P450 deactivator.

“It’s a very unusual enzyme. Almost all other enzymes are designed to fit a single substrate and carry out a single chemical process resulting in a single product,” Bornheim noted, whereas numerous drugs are substrates for cytochrome P450, which seems to function like a generic breakdown mechanism for a wide range of exogenous and endogenous substances.

In 1999, Bornheim addressed the annual gathering of the International Cannabinoid Research Society (ICRS) and drew attention to the possibility that CBD could interfere with the metabolism of many medications. A year earlier, a team of Canadian scientists identified certain compounds in grapefruit that inhibit the expression of some cytochrome P450 enzymes—which is why physicians often warn patients not to eat grapefruit before taking their meds. CBD, it turns out, is a more potent inhibitor of cytochrome P450 enzymes than the grapefruit compound Bergapten (the strongest of several grapefruit components that inhibit CYPs).

What does this mean in practical terms for a medical marijuana patient on a CBD-rich treatment regimen who takes a prescription blood-thinner like warfarin, for example? CBD reduces the enzymatic degradation of warfarin, thereby increasing its duration of action and effect. A person taking a CBD-rich product should pay close attention to changes in blood levels of warfarin, and adjust dosage accordingly as instructed by their doctor.

Cancer and Epilepsy

In cancer treatment, the precise dosing of chemotherapy is extremely important; doctors often struggle to find the maximum dose that will not be catastrophically toxic. Many chemotherapy agents are oxidized by CYPs before their inactivation or excretion. This means that for patients using CBD, the same dose of chemotherapy may produce higher blood concentrations. If CBD inhibits the cytochrome-mediated metabolism of the chemotherapy and dosage adjustments aren’t made, the chemotherapy agent could accumulate within the body to highly toxic levels.

By and large, however, there have been few reported adverse cannabinoid-drug interactions among the many cancer patients who use cannabis to cope with the wrenching side effects of chemotherapy. It is possible that whole plant cannabis, with its rich compensatory synergies, interacts differently than the isolated CBD that is administered in most research settings. As well, the cytoprotective effects of the cannabinoids may mitigate some of the chemotherapeutic toxicity.

Some epileptic patients have encountered issues with how CBD interacts with their anti-seizure medication. A small clinical study at Massachusetts General Hospital involving children with refractory epilepsy found that CBD elevated the plasma levels and increased the long-term blood concentrations of clobazam, an anticonvulsant, and norclobazam, an active metabolite of this medication. A majority of these children needed to have their dose of clobazam reduced due to side effects. Given that both clobazam and CBD are metabolized by cytochrome P450 enzymes, a drug-drug interaction is not surprising. Published in May 2015, the study concluded that “CBD is a safe and effective treatment of refractory epilepsy in patients receiving [clobazam].” But the report also emphasized the importance of monitoring blood levels for clobazam and norclobazam in patients using both CBD and clobazam.

Dr. Bonni Goldstein has observed cases in which small doses of high-CBD/low-THC cannabis oil concentrate seemed to aggravate seizure disorders rather than quell them. How could this happen, given CBD’s renown anti-epileptic properties?

A 1992 review by Lester Bornheim and his colleagues indicated that CBD inhibits some cytochrome P450enzymes at smaller doses than what is required for CBD to exert an anti-epileptic effect. This means that a certain dose of CBD could alter the processing of an anti-epileptic drug taken by the patient, but this amount of CBD might not be enough to provide any anti-epileptic relief itself. The advice some physicians offer in this situation may seem counterintuitive: Increase the dose of CBD—perhaps even add a little more THC (or THCA, the raw, unheated, non-psychoactive version of THC)—and this may be more effective for seizure control.

Enigmatic Enzymes

But why would preventing the breakdown of an anti-epileptic drug reduce its effect? There are a number of possible answers, depending on the drug in question. The active component of the drug (the chemical that exerts an anti-epileptic effect) may be a breakdown product of the actual drug taken. So, by slowing the metabolism of the original drug, CBD would make that drug less active.

Other explanations are conceivable. For example, if the activity of certain CYPs is slowed, the drug may be broken down by another metabolic pathway, the products of which could then interfere with the drug’s activity. Or perhaps the inhibition of CYPs is not the predominant way that CBD interacts with certain anti-epileptic medications.

To complicate matters even further, a presentation by Dr. Kazuhito Watanabe at the 2015 International Cannabinoid Research Society meeting in Nova Scotia disclosed preliminary evidence that cannabidiol may “induce”—meaning amplify the activity of—some cytochrome P450 enzymes. (Induction of a protein involves increasing the transcription of its corresponding mRNA, which leads to greater synthesis of the protein.) This suggests that CBD can either increase or decrease the breakdown of other drugs. Again, it depends on the drug in question and the dosages used.

Any pharmaceutical, nutraceutical or green rush scheme to exploit the therapeutic potential of CBD must reckon with the fact that cannabidiol can both inactivate and enhance various cytochrome P450 enzymes in the liver—and this can potentially impact a wide range of medications. Drug interactions are especially important to consider when using life-saving or sense-saving drugs, drugs with narrow therapeutic windows, or medications with major adverse side effects. In particular, those who utilize high doses of CBDconcentrates and isolates should keep this in mind when mixing remedies.

Adrian Devitt-Lee is a senior at Tufts University, studying mathematics and chemistry.

Learn More:

AED Potential Interactions with CBD

Copyright, Project CBD. May not be reprinted without permission.



Drug interactions can be both useful and dangerous. Learn how CBD and THC may inhibit or amplify the effects of pain meds, statins, blood thinners, insulin & more.
  • THC and CBD interact with many common pharmaceuticals. Cannabinoids can inhibit or potentiate the effects of various drugs
  • More than half of all pharmaceuticals – including THC and CBD – are metabolized by a family of enzymes called cytochrome P450
  • Interactions between cannabinoids and other drugs can be exploited to mitigate side effects while synergistically improving a patient’s quality of life
  • Cannabinoid-opioid interactions show great therapeutic potential. THC significantly enhances the painkilling effects of opiates, while CBD is most promising for reducing withdrawal and dependence
Cannabis samples being prepared at Sonoma Lab Works for analysis
Cannabis samples being prepared at Sonoma Lab Works

Interactions between medications are very common, especially in elderly populations that medicate for pain, diabetes and high cholesterol. The geriatric population is also the fastest-growing group of medical cannabis users. Cannabis has demonstrated efficacy in treating pain, and some phytocannabinoids have been suggested for various metabolic conditions. Thus it is important to understand how cannabinoids can interact with common pharmaceuticals, both to predict and prevent negative interactions, while taking advantage of situations where cannabis and pharmaceuticals act synergistically.

Drug interactions can be both useful and dangerous. A drug that potentiates an opiate, for example, may increase the painkilling effect, but could also increase the likelihood of overdose. Or a second analgesic could allow the dose of an opiate to be reduced, which would slow tolerance and decrease other side effects.

But understanding all the convergent biological pathways of two drugs is difficult. Examining the metabolic interactions between drugs is one way to generically predict drug interactions: since more than half of all pharmaceuticals are metabolized by a family of enzymes called cytochrome P450 (CYP), knowing how cannabinoids affect CYPs provides a good first approximation to phytocannabinoid-drug interactions. In general, inhibiting the CYPs that metabolize a pharmaceutical will increase its blood concentration, leading to an increase in both effects and toxicity. But for prodrugs—which are metabolized into the active compound—inhibition of metabolism will decrease both the desired and adverse effects. And the interaction can change from inhibition to activation with different drugs. Due to complications like these, it is much easier to predict whether drug interactions are likely than to predict their exact effect.

This review will describe potential cannabinoid-drug interactions in the context of treating pain (with opiates and non-steroidal anti-inflammatory drugs) and metabolic disorders (using insulin, warfarin and statins). Owing to the highly complicated role of cannabinoids in the cardiovascular system—with at least four cannabinoid-like receptors initiating changes in the vasculature, multiple phases to the effects, and opposing effects under normal, stressed and pathological conditions–cannabinoid interactions with drugs used to treat hypertension are beyond the scope of this article …

You can read the full article by downloading the PDF attached below, or by viewing it in the Fall Edition of Sonoma Medicine magazine where this article was originally published.

Endocanabinoid Deficiency Leads to Fibromyalgia. National Pain Foundation Survey

In 2014, a survey of more than 1,300 fibromyalgia patients by the National Pain Foundation and National Pain Report found medical marijuana is more effective than Lyrica, Cymbalta or Savella, the three drugs approved by the Food and Drug Administration to treat the disorder. (If you’re curious about the effectiveness of Lyrica, Cymbalta and Savella, then you might be interested in my post, “Why your fibro meds aren’t working.”)

There’s growing anecdotal evidence that marijuana relieves fibromyalgia pain, but actual research is still scant. Cannabis remains a schedule I controlled substance in the United States, making it difficult for researchers to study the plant’s pain-relieving properties. To date, there have been less than a handful of small studies using cannabis or its derivatives to treat fibromyalgia. Most of those have shown it to be beneficial, especially for pain relief.

But why does cannabis seem to work so well? Dr. Ethan Russo, medical director of PHYTECS, believes fibromyalgia’s multifaceted symptoms may be caused by a deficiency in the body’s endocannabinoid system (ECS), a condition he calls Clinical Endocannabinoid Deficiency (CED). Maybe the reason cannabis is so effective is because it’s simply supplementing what the body needs – similar to how people take a supplement to treat vitamin D or B12 deficiency.

Russo explores the evidence behind his hypothesis in a soon-to-be published review entitled, “Clinical Endocannabinoid Deficiency Reconsidered: Current Research Supports the Theory in Migraine, Fibromyalgia, Irritable Bowel and other Treatment-Resistant Syndromes.” While his idea is still theoretical, there is some early research indicating he may be onto something.

The ECS is made up of cannabinoid receptors within the brain, spinal cord, nerves, gut, organs and other locations in the body. It helps the body maintain homeostasis and is involved in a number of physiological processes, including pain sensation, mood, memory and appetite, among others. The body naturally makes endocannabinoids – the same kinds of endocannabinoids found in cannabis – that feed the ECS and keep it functioning.

Fibromyalgia causes symptoms throughout the body, with the primary ones being pain, fatigue, cognitive and sleep difficulties. Certain conditions, like irritable bowel syndrome (IBS) and migraine, are extremely common among those with fibromyalgia – so much so that Russo believes they may all be connected to an ECS deficiency.

His theory makes sense. The ECS plays a role in so many of the body’s major systems, so if it was indeed malfunctioning, that would account for why fibro sufferers have such varied symptoms. Supplementing the ECS with cannabinoids from the cannabis plant would, in theory, relieve symptoms because the deficiency is being treated.

Russo first posited that fibromyalgia, IBS and migraine may be caused by an ECS deficiency back in 2001. (Click here to read his first review on the subject.) His latest review gives an update on new research that supports ECS deficiency as a possible culprit for fibromyalgia, IBS and migraine.

“Additional studies have provided a firmer foundation for the theory,” he writes in the review, “while clinical data have also produced evidence for decreased pain, improved sleep and other benefits to cannabinoid treatment and adjunctive lifestyle approaches affecting the endocannabinoid system.”

CED is based on the premise that many brain disorders have been linked to neurotransmitter deficiencies. For example, dopamine has been implicated in Parkinson’s disease, and serotonin and norepinephrine have been associated with depression.

“If endocannabinoid function were decreased, it follows that a lowered pain threshold would be operative, along with derangements of digestion, mood and sleep among the almost universal physiological systems sub-served by the ECS,” Russo writes.

That’s a mouthful, but essentially it means if the ECS isn’t properly working, then it could account for the pain, sleep, digestive and other issues so common among fibromyalgia patients. Adding cannabinoids to the body through the use of cannabis may help to bring the ECS back into balance.

“It’s a key in a lock in your body that exists for a reason,” explains Dr. Jahan Marcu, chief scientist with Americans for Safe Access. “We send in cannabinoids to activate this system that’s supposed to be working. It’s a sort of care and feeding of the ECS so it can do its job.”

The best evidence for CED comes from an Italian migraine study, which found reduced levels of an endocannabinoid known as anandamide in patients with chronic migraines versus healthy controls.

“Reduced [anandamide] levels in the cerebrospinal fluid of chronic migraine patients support the hypothesis of the failure of this endogenous cannabinoid system in chronic migraine,” read the study.

Unfortunately, the Italian study will probably never be repeated in the United States because it required risky and invasive lumbar punctures.

In the gut, the ECS modulates the movement of food along the digestive tract, the release of digestive juices to break down food and inflammation.

Cannabis has long been used to treat digestive issues and was one of the first effective treatments for diarrhea caused by cholera in the 19th century.

“Unfortunately while many patient surveys have touted the benefit of cannabinoid treatment of IBS symptoms, and abundant anecdotal support is evident on the Internet, little actual clinical work has been accomplished,” Russo writes.

A few studies using marijuana for fibromyalgia have had positive results. Overall, marijuana has been found to decrease pain and anxiety, and improve sleep and general well-being.

“There is actually some evidence that the levels of at least one endocannabinoid (anandamide) increase in the circulation of patients with fibromyalgia,” says Prof. Roger G. Pertwee from the University of Aberdeen in Scotland. “There is also considerable evidence that anandamide is often released in a manner that reduces unwanted symptoms such as pain and spasticity in certain disorders. … It is generally accepted that THC, the main psychoactive constituent of cannabis, can relieve pain, including neuropathic pain for example, by directly activating cannabinoid receptors. … Some non-psychoactive constituents of cannabis have also been found to relieve signs of pain, at least in animal models.”

For anecdotal evidence, Russo cites the National Pain Foundation/National Pain Report survey in his review, saying, “The results of the survey strongly favor cannabis over the poorly effective prescription medicines. These results certainly support an urgent need for more definitive randomized controlled trials of a well-formulated and standardized cannabis-based medicine in fibromyalgia inasmuch as existing medicines with regulatory approval seem to fall quite short of the mark.”

More research needs to be done to either prove or disprove CED’s existence.

“What we really need is randomized controlled trials to look at this more carefully, and that’s the only kind of evidence that the [Food and Drug Administration] and most doctors are going to find acceptable in the end,” Russo says.

MRI and PET scans are not yet able to detect endocannabinoid levels in living patients, but as technology advances, that may become a possibility. The ability to actually test endocannabinoid levels in fibromyalgia patients and compare those against healthy controls would help to confirm Russo’s theory.

“We’re on the edge of having that capability,” Russo says. “It’s in my plans to look at this type of thing in the future.”



The Role of Neuron Creation in Anxiety Disorders
According to Aswin Suri, anxiety and stress disorders are among the major prevalent of PTSD. Separately, the clinical manifestations of these disorders provide a spectrum of alterations. To some extent, the present original trauma effects and when untreated, the disease can develop a significant impairment in functioning, reduced quality of life, and enormous economic burden. Recent studies have examined the underlying literature review on the neural mechanism when regulating impaired pattern present in anxiety.
According to the note submitted by Rene Hen, Ph.D., of Columbia’s Department of Psychiatry and the NY Psychiatric Institute, suggest that the production of the neuron or the in the brain have assisted in the treatment of anxiety that is associated with PTSD (Duval et al., 2015).
They further note that the thalamus is an implicated sensory integration. In effect, through activation, the thalamus is associated with high degree of anxiety and disgust in blood-injury-injection phobia, as well as automatic arousal in snake phobia. In the treatment with paroxetine reduces the activation of the thalamus, therefore, tend to reduce anxiety. Additionally, in the hippocampus, the dentate gyrus that is that separate is among the two areas of the brain where neurogenesis takes place. Among the possible improving patterns separation is the addition in the number of adult-generated neurons, so they are better able to process information. Besides, there is enough evidence that shows that reduced hippocampal can be achieved through functional neuroimaging.
Moreover, recent studies provide that in the current models of PTSD, hypoactivity in frontal regions suggests a reduced potential for top-down regulation of fear and fear extinction (Holzschneider & Mulert, 2011). The hippocampus provides information about the context of a situation, and the attenuated hippocampal response might be attributable to difficulties in identifying safe circumstances (Holzschneider & Mulert, 2011). Besides, the above mentioned functional modalities in the brain, including the hippocampus, amygdala, and medial prefrontal cortex, have shown possibilities in the patients with PTSD (Holzschneider & Mulert, 2011).
Therefore, the studies as mentioned earlier researchers emphasize on the using better use of technological advancement in imaging. Finally, research should be conducted on patient with impairments in pattern-separation tasks and decreased neurogenesis in the dentate gyrus.


Holzschneider, K., & Mulert, C. (2011). Neuroimaging in anxiety disorders. Dialogues in Clinical Neuroscience, 13(4), 453–461.

Duval, E. R., Javanbakht, A., & Liberzon, I. (2015). Neural circuits in anxiety and stress disorders: a focused review. Therapeutics and Clinical Risk Management, 11, 115–126.


Risk Factors
In the contemporary healthcare, anyone is susceptible to acquiring PTSD at any age. According to the research conducted by Otis, Marchand, and Courtois (2012) indicates the prevalence of PTSD persons are varying between 7 percent and 44 percent. The difference in the number is associated with the changes and variability observed in these studies. On the other hand, the above statistics are important in studying PTSD and the associated risk factors in different persons (Otis, Marchand, and Courtois, 2012). Furthermore, other research indicated that women are more likely to acquire PTSD than men, in the sense that gene and immune re the difference in both of them. Women are more likely to develop PTSD than men, and genes may make some people more likely to develop PTSD than others. Other risk factors that may be characterized by with PTSD include pre-traumatic factors that comprise of the characteristics of the individual that was present before the traumatic event.
Below are some of the factors that should be considered when it comes to the understanding of the risk factors for PTSD.

Why do some people develop PTSD and other people do not?

According to the emphasis relayed by Aswin Suri on the understanding of the PTSD, he posits that is significant to acknowledge that everyone can acquire PTSD regardless of the race, religion, or ethnicity. In this case, several risk factors might increase the rate at which a person might develop PTSD. Separately, scientific research indicates that other individuals cannot develop this mental disorder regardless of the nature of the risk factors.
Michael Membrino, President of Neuro-Endoceuticals, also notes that several factors play vital role when it comes to the development of PTSD. A comprehensive list below is summarized by Aswin Suri and his colleagues, to understand both various risk and reliance factors that are connected to PTSD.
Risk Factors and Resilience Factors for PTSD
When it comes to the development of PTSD, below are the risk factors:
· Disasters caused by human error
· Victims of rape or sexual assaults
· Living through dangerous events or traumas
· Those diagnosed with life-threatening illness
· Combat veterans
· Dealing with extra stress after events such as loss of the loved one’s ones, pain of injury or loss of job or mortgage
· Little or no social support that makes individual feel isolated
Some of the resilient factors that may reduce PTSD include:
· Getting social support from people and other family friend will create happiness.
· Participating in event such as traumatic events
· Understanding and practicing the effectiveness in feeling good.
· Having positive though bout people opinion and learning how to get along.
· The essence of managing fear, depression, and anxiety will help the situation
· Learning and adopting strategies of forgetting the bad events that might have led to trauma events.
Additionally, following the research conducted by Iversen et al. (2008) understanding the factors which increase and reduces the risk of PTSD is very important when it comes to its management. In their findings, they realized that the primary PTSD symptoms are associated with lower ranks in office, being un married, having less education in the military camp, and history of childhood adversity or victimizations (Iversen et al., 2008). Therefore, taking into considerations of these factors, it is suggested that possible solution towards PTSD will emerge in the near future.

Iversen, A. C., Fear, N. T., Ehlers, A., Hughes, J. H., Hull, L., Earnshaw, M., & Hotopf, M. (2008). Risk factors for Post-Traumatic Stress Disorder amongst United Kingdom Armed Forces personnel. Psychological Medicine, 38(4), 511–522.

Otis, C., Marchand, A., & Courtois, F. (2012). Risk Factors for Posttraumatic Stress Disorder in Persons With Spinal Cord Injury. Topics in Spinal Cord Injury Rehabilitation, 18(3), 253–263.



PTSD is s psychiatric disorder that results from the experience or witnessing of traumatic or life-threatening events.

An event becomes traumatic when it is very life-threatening. The disease involves the exposure to trauma from single events that may cause death or serious injury. These events that my case PTSD include crimes, natural disasters, accidents, sexual violence, domestic violence, and other threats to the life. PTSD has complex psychobiological affects, which can damage a person’s daily life and be life threatening. In light of current events a sharp rise in patients with PTSD diagnosis is expected in the next decade (Iribarren et al. 2005).

Signs and Symptoms.

The most symptoms of PTSD are the re-experiencing symptoms. This includes the flashbacks in which the person acts or feels as if the events are re-happening, nightmares, repetitive and distressing intrusive images. In children, signs of hyper-arousal include hypervigilance of the threat, exaggerated startle responses, and difficulty in concentration and change in sleeping habits. Further symptoms of PTSD can lead to a considerable distress and can significantly interfere with social, educational and occupational functioning.

During diagnosis, adult must have presented the following signs one-month earlier:


Aswin Suri posts that Multiple sclerosis (MS) is a neurodegenerative disorder that is characterized by repeated inflammatory episodes within the central nervous system. In additional to the relapsing-remitting neurological insults, resulting in the loss of function, a patient with MS always left the residue, troublesome with the symptoms and acute pain. Like most neurodegenerative disorders, MS gets worse with time as more neurons lose their sheaths and die. CB1 and CB2 receptors influence spasticity and tremors, two common symptoms of MS. Additionally, the contemporary advances in the cannabinoid biology are commencing to support these anecdotal observations. Following the recent clinical trials, cannabis sativa has the modalities of relieving pain, spasms, and spasticity of MS (Leussink, Verena et al., 2012).
The stimulation of the endocannabinoid with the patient with MS, either through the increase of the synthesis or inhibition of the endocannabinoids degradation offers the positive therapeutic potential of the cannabinoid system regulation of levels of the neurodegeneration that happens as a result of inflammatory insults. Further evidence is present in humans in which patient with active MS have a higher concentration of anandamide than those with silent from (Leussink, Verena et al., 2012). Additionally, in the regulation of MS, the combination of THC and CBD have been developed taking into consideration the synergistic and the reduction of the possible side effects. Double-blind, placebo-controlled attempts have indicated that THC and CBD therapeutically improve several aspects of MS, including pain, mobility factors, bladder problems, and spasticity (Leussink, Verena et al., 2012).
Leussink, V. I., Husseini, L., Warnke, C., Broussalis, E., Hartung, H.-P., & Kieseier, B. C. (2012). Symptomatic therapy in multiple sclerosis: the role of cannabinoids in treating spasticity. Therapeutic Advances in Neurological Disorders, 5(5), 255–266.


Up to modern times, Aswin Suri, Chairman of the Neuro-Endoceuticals, USA, notes that the inflammatory bowel disease is associated with several complications such as severe abdominal pain, malnutrition and other related consequences that often arises as a result of inflammatory. The disease is also characterized by relapsing and reemitting sequences of inflammation primary involving the gastrointestinal tract. Stintzing, Wissniowski, Lohwasser, Alinger, Neureiter, & Ocker (2011) argue that ECS is involved in many inflammatory disorders such as ulcerative colitis and Crohn’s disease. Indeed, the distribution and expression of the cannabinoids receptors when combined with inflammatory cytokines will assist in the regulation in most of the Crohn’s disease cases.
On the other hand, CB1 receptors are largely distributed across the gastrointestinal tract, together with endocannabinoids anandamide and 2-AG.
Besides, CB2 receptors are also present, including on macrophage white blood cells (that do not contain CB1 receptors). In this case, CB1 receptors have been found to be upregulated in the vascular endothelium and micro fibroblast that is located in the cirrhotic livers, while CB2 receptors have been identified in inflammatory cells, and they tend to regulate pathophysiology of the inflammatory bowel disease.
Additionally, it has been discovered that patients with severe and complex inflammatory bowel disease and represented in referral bias, shows that cannabis sativa can be used to relieve of diarrhea and that cannabis may have a role in mediating inflammation (Ahmed, & Katz, 2016). In conclusion, endocannabinoids temporary on a CB2 result in weakening of inflammatory feedback. Also, cannabinoids have proinflammatory effects in which their immunomodulatory effect is based on the incidence of cannabis sativa consumption, the dose directed, the particular type of cannabinoid used, and the cells on which they are acting on.


Ahmed, W., & Katz, S. (2016). Therapeutic Use of Cannabis in Inflammatory Bowel Disease. Gastroenterology & Hepatology, 12(11), 668–679.