CBD vs THC: Health Benefits, Dosage, Side-Effects, Legal Status and More

CBD vs THC: Health Benefits, Dosage, Side-Effects, Legal Status and More | EDO CBD

MEDICAL DISCLAIMER: All content in this article was created for informational purposes only. The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition.


By Dr. Victor Chou

From nearly 70 cannabinoids isolated to date, cannabidiol (CBD) and tetrahydrocannabinol (THC) are the two most popular and most well-researched.

Currently, several other cannabinoids are being researched, including cannabigerol (CBG) and tetrahydrocannabivarin (THCV).

Aside from these active ingredients, it is estimated that cannabis possesses over 120 active compounds, serving as a powerful combination for treating various conditions. [1]

Also known as phytocannabinoids, THC and CBD are two naturally occurring compounds in the cannabis plant that possess various differences and similarities. There is an ongoing debate about which component offers greater healing powers, so we will try to provide a through answer to cover this topic of discussion.

However, as we are entering the scientific world of these two cannabinoids, it will becomes more and more clear that there is no CBD vs. THC in the true sense of the word, but two components with different healing properties, each unique on their own.

Let’s take a look at their chemical structure, psychoactive components, health benefits, legal status, interaction with the endocannabinoid system, entourage effect, side-effects, benefits for chronic pain, and more.

Chemical Structure

Cannabidiol (CBD) and tetrahydrocannabinol (THC) are the two major components present naturally in the hemp plant. These two phytocannabinoids interact directly or indirectly with specific cannabinoid receptors found in the body — mainly in the brain — causing various effects in the human body. [2]

These two components are fundamentally different because of the manifestation of their distinctive psychological effects. While THC classifies as a psychotropic drug, CBD is the compound that doesn’t elicit a “high” but has gained ground thanks to the growing list of medicinal benefits it offers. [3]

The most well-known cannabinoid, THC (the full scientific name is delta-9-tetrahydrocannabinol) is the principal, mind-altering proactive molecule in cannabis sativa that reduces nausea, relieves pain, and suppresses muscle spasm, among others health benefits.

The isolation of this psychoactive ingredient was achieved in the 1960s and 1970s, whilst CBD was first isolated in 1940. The understanding of THC’s intoxicating properties came to light in 1965, when the Israeli scientist Raphael Mechoulam synthesized the molecule.  

CBD and THC have lots of similarities. They both share the exact same molecular formula C21H30O2, are compounds from a family of around 113 bi – and tri – cyclic cannabinoid compounds found in cannabis, contain 21 atoms of carbon, 30 atoms of hydrogen and 2 of oxygen.

Besides, THC and CBD have a nearly identical molecular mass with 314.469 g/mol and 314.464 g/mol, respectively.

Also, both components are chemically similar to the endocannabinoids present in the body, which is why CBD and THC can interact with the cannabinoid receptors and release neurotransmitters in the brain. The neurotransmitters relay messages between cells in the human body.

In addition, the biosynthesis of these two components follows a similar pathway, with one important difference. In the part where THC contains a cyclic ring, CBD has a hydroxyl group. This seemingly small difference in the molecular structure brings the entirely different pharmacological properties.

And although the exact mechanism of both components is not fully understood, the analgesic, anticonvulsant, muscle relaxant, anxiolytic, neuroprotective, antioxidant, and antipsychotic activity of CBD is likely due to the component’s complex pharmacological mechanisms. [4]

Another study found that CBD might be useful as a protective agent against external stresses such as ultraviolet irradiation and oxidative stressors, due to its effects on melanogenesis. [5]

Cannabinoids and the Endocannabinoid System

Patients across the US use cannabis as an open door to treating a growing number of medical conditions.

For example, in Colorado, the medical card qualifies nine different conditions addressed by cannabis, including cancer, glaucoma, persistent muscle spasms, seizures, nausea, severe pain, PTSD, HIV or AIDS and cachexia.

A vital question many people ask when looking at this list of conditions, is how cannabis interact with the body to address all of these and many more conditions in an effective way?

The answer to that complex question lays in the even more complex system found in the human body, the endocannabinoid system.

The Endocannabinoid System Maintains Homeostasis

Each year, scientist dive into the partly unknown mechanisms of the endocannabinoid system to discover more about this important part of the human body.

The endocannabinoid system is responsible for maintaining homeostasis in the body.

As Encyclopedia Britannica defines it, homeostasis is, “any self-regulating process by which biological systems tend to maintain stability while adjusting to conditions that are optimal for survival. If homeostasis is successful, life continues; if unsuccessful, disaster or death ensues.”

The first part of the endocannabinoid system is the endocannabinoid receptor. These receptors are found throughout the body, on the surface of cells in the brain, organs, tissues, and glands. Embedded in cell membranes, endocannabinoid receptors provide different reactions when stimulated by cannabinoids.

There are two cannabinoid receptors discovered by researchers, the CB1 and CB2 receptors. The CB1 receptors are found in the brain and the peripheral nervous system and are the receptors that THC interacts with, producing a high in the user.

CB2 receptors can be found in the immune system and the gastrointestinal system and are responsible for regulating inflammatory responses in the bowels, cardiovascular activity, appetite, mood, memory, and pain. CB2 receptors are a large part of the endocannabinoid system and are also found in the brain.

The role of the CB1 receptor in the human body. First discovered in 1990, the CB1 receptor can be found in the brain, the central nervous system, connective tissue, and other glands. By activating the CB1 receptor with medical marijuana or hemp, the user gets the following benefits:

  • Relieved symptoms of depression [6]
  • Increased formation of myelin formation [7]
  • Decreased intestinal permeability (Leaky Gut Syndrome) [8]
  • Lowered blood pressure [9]
  • Reduced GPR55 signaling [10] [11]
  • Reduced anxiety [12]
  • Reduced paranoia [13]
  • Lowered prolactin [14]
  • Increased BDNF levels [15] [16]
  • Increased PPARy expression [17] [18]

There are some risks included with the activation of the CB1 receptor from an agonist such as THC, including lowered thyroid hormones, [19] decreased cognitive function, [20] constipation, [21] increased anxiety, [22] and others.

The role of the CB2 receptor in the human body. First discovered in 1993, the CB2 receptor is mostly found in the spleen, tonsils, thymus, and immune cells, with only a small number found in the brain. This receptor plays a role in any type of human disease from cardiovascular and gastrointestinal, to neurodegenerative, psychiatric and even autoimmune. It has a role in regulating liver and kidney function, bone and skin health, and pain. [23]

The second part of the endocannabinoid system is the endocannabinoid, naturally present in the body. The two primary endocannabinoids are anandamide (AEA) and 2-arachidonoylglycerol (2-AG). THC and CBD are cannabinoids that come from another place, the cannabis plant, and are known as phytocannabinoids.

Anandamide is a high-affinity, partial agonist of the CB1 receptor, and almost inactive at the CB2 receptor. 2-AG acts as a full agonist at both CBRs with moderate-to-low affinity. [24]

The third part of the endocannabinoid system is the metabolic enzyme. Enzymes destroy the endocannabinoids once used, ensuring the interaction only happens when needed.

Psychoactive Components

As we’ve established so far, CBD is a non-psychoactive component, while THC produces a high. This is one of the main reasons why CBD is the common, main ingredient in many dietary and natural supplements.

CB1 is a G protein-coupled cannabinoid receptor that is activated by the endogenous transmitters anandamide and 2-arachidonoylglycerol. THC is a potential partial agonist of CB1, stimulating the receptor to cause psychotropic effects experienced when consuming marijuana.

CBD is a negative allosteric modulator of CB1, which means that it effectively alters the shape of the receptor. [25] In addition, CBD’s effect makes it difficult for THC to stimulate the receptor, which is the reason why it doesn’t produce the psychotropic effects associated with THC.

THC and the Endocannabinoid System

How does THC work and why does it produce high

THC produces the euphoric effect of marijuana because it is an agonist or an activator that binds well with CB1 receptors. The CB1 receptors are present in very high levels in the brain and lower amounts throughout the entire body.

Although the exact mechanisms of how the process happens are not entirely clear, it is believed that the CB1 receptor is the critical target in the brain the produces a state of intoxication. To support those claims, a study conducted in people who have had their CB1 receptor blocked by a different antagonist drug, showed no results to cannabis, simply it didn’t get them high. [26]

Also, during brain imaging, the prefrontal cortex region of the brain showed increased blood flow during THC intoxication. [27] The prefrontal cortex region in the brain is responsible for attention, decision-making, and executive functions, including motor skills, all affected by THC intoxication to a certain degree. A well-known fact is that cannabis also activates the reward pathway in the human brain, which makes the intoxicated individual feel good and euphoric. [28]

THC is also known to partially mimic the effects of anandamide, aka the ‘bliss molecule,’ a naturally occurring endocannabinoid. The resemblance to anandamide means that during activation of CB1 receptors, THC helps to produce the blissful feeling experienced when consuming weed.

CBD and the Endocannabinoid System

How does CBD work and why it doesn’t produce high

CBD, on the other hand, does not bind directly to the CB1 or CB2 receptors but works to inhibit the Fatty Acid Amide Hydrolase (FAAH enzyme) that breaks down anandamide, making anandamide available for longer periods of time in the body.

Anandamide is also known as the “bliss molecule,” and for its role in the neural generation of pleasure and motivation. Anandamide also affects the immune system, eating and sleeping patterns, anxiety and nervous thought patterns, as well as pain. [29]

CBD also activates the Transient Receptor Potential Vanilloid 1 (TRPV1) receptors, involved in regulating pain, body temperature, and inflammation. [30]

Working as an antagonist of CB1 receptors, CBD suppresses the CB1-activating qualities of THC. So, when working together, CBD goes against the effects of THC, and instead of feeling “high,” the person is less stressed, anxious, and doesn’t experience the common negative feelings, like when taking pure THC.

While THC affects the CB1 receptor, CBD is a negative allosteric modulator of the CB1 receptor. This means that although the CBD molecule is almost identical to the THC molecule, CBD counteracts the effects of THC. [31] The psychoactive effects are reduced, and person has much lower chances of experiencing paranoia, as when using only THC. [32]

For example, if combined, CBD and THC work great for treating chronic pain. If THC alleviates the pain, CBD reduces the psychotic effects. They both work towards reducing symptoms of depression, anxiety, arthritis, migraines, and other chronic non-cancer pain. [33]

Although THC is the main component in marijuana, and alters the mood and perception, it shows strong anti-inflammatory [34] and analgesic properties, [35] successfully relieving pain caused by arthritis and cancer. It also helps reduce symptoms and pain in participants with treatment-resistant spasticity in multiple sclerosis. [36]

In conclusion, choosing between these two components shouldn’t be a question. According to research, both compounds work in synergy and interact with each other in the best way possible, creating a balance in the body. It is important to remember that THC still causes mind alterations and should be consumed under certain circumstances, medical and legal, which brings us to the next point.

Legality of CBD vs. THC in the United States

In the United States, all forms of cannabis are prohibited under federal law, but, are legal for medicinal use in 20 states. In addition, nine states plus Washington, D.C., have legalized the use of marijuana with high levels of THC for recreational purposes.

In the states where marijuana is legal for both medical or recreational purposes, it is possible for a person to buy CBD legally. Some states have passed laws to make CBD for medical purposes legal. It is important to be aware of the state’s laws [37] before buying CBD products because you might face legal penalties if buying in a state where it isn’t legalized.

In 2014, Uruguay legalized weed for recreational use and become the first country in the world, followed by Canada in 2018. CBD is also a subject to the same Schedule I Drug classification, but it is legal for medicinal use in 46 states, only if it comes from industrial hemp. The industrial hemp must have a THC level below 0.3%.

A progress has been made in the US with the 2014 Farm Bill that semi-legalized hemp production for academic and research purposes.

As of June 25th, 2018, FDA approved the use of an epilepsy medication called Epidolex. [38] The drug is a CBD oral solution for the treatment of seizures associated with two rare and severe forms of epilepsy, Dravet and Lennox-Gastaut syndrome. Epidiolex is the first FDA approved drug that can be used for children two years of age and older.

Medical Benefits of THC and CBD


A 2013 study found that low-dose vaporized cannabis significantly improves neuropathic pain. Thirty-nine patients with central and peripheral neuropathic pain who were experiencing the pain despite traditional treatment underwent a procedure of inhaling a medium and low dose of delta-9-tetrahydrocannabinol (THC). The results showed that the analgesia obtained from a low dose of THC (1.29%) was as an effective pain reliever as the medium dose (3.53%), showing 30% reduction in pain intensity compared to placebo. [39]

Another study showed the efficacy of medical marijuana for treating chronic non-cancer pain. The study concluded that using low-dose medical marijuana (THC) in refractory neuropathic pain together with traditional analgesics showed significant pain relief with non-serious side effects. [40]


Multiple studies show promising results of using THC to treat MS-related symptoms in patients. Even the minimum THC dose of 5 mg reduced pain and muscle stiffness throughout 15 weeks. [41] Also, studies found suggestive evidence for treatment effects of THC on some aspects of disability of patients with MS, improving the overall quality of life. [42] [43]


Minnesota NORML, a medical marijuana activist group point to the many benefits of medical treatments for arguing why Marijuana should not be considered a schedule 1 narcotic. Executive director Michael Ford recently quoted the  National Cancer Institute in early 2017 stating “the potential benefits of medicinal Cannabis for people living with cancer include antiemetic effects, appetite stimulation, pain relief, and improved sleep.”[101]

The first clinical study that assessed cannabinoid antitumoral action in nine patients with recurrent glioblastoma multiforme, a deadly and hard to treat form of brain cancer, showed that THC inhibited tumor cell proliferation and increased the median life expectancy by 24 weeks. The study’s primary endpoint was to determine the safety of intracranial THC administration in patients with glioblastoma multiforme that had previously failed standard surgery and radiotherapy and still showed evidence of tumor progression. [44]

In addition, the combination of THC and CBD in treating this type of brain tumor shows promising results. Results suggest that CBD may improve the overall effectiveness of THC in the treatment in cancer patients. [45]

There are three well-known things about THC in cancer prevention. First, THC blocks a tumor from forming blood vessels, which starves the cancer cell because it’s left without food and oxygen supply.

Second, cannabis compounds are likely to stop cancer cells from metastasizing, and third, cannabinoids are likely to act as potent immunosuppressive and anti-inflammatory agents that also mediate apoptotic mechanisms (cell death) of immunosuppression on different immune cell populations.

In conclusion, the activation of CB2 provides a “novel therapeutic modality against inflammatory and autoimmune diseases as well as malignancies of the immune system, without exerting the untoward psychotropic effects”. [46] [47]

A bit controversial evidence on the topic of THC’s healing properties of breast cancer. One study found that treatment of breast cancer in mice with low doses of THC (.5 mg a day) showed significant anti-tumor properties. The results showed that THC reduced tumor growth, number and amount/severity of lung metastases. [48] However, another study found that THC is likely not beneficial in breast cancer types that don’t harbor cannabinoid receptors, resulting in enhanced breast cancer growth and metastasis by suppressing antitumor immune response. [49]


The connection between THC and atherosclerosis lies in foam cells and the CB2 receptors. Namely, patients developing hardening of arteries show increased levels of foam cells that lead to deposition of cholesterol and fatty plaque. On the other hand, foam cells carry CB2 receptors on their surface, which are activated by THC (even low levels) causing anti-inflammatory effects that reduce platelet accumulation and promote immune functions that inhibit atherosclerosis. [50] [51] [52]

THC’s Therapeutic Effects on Alzheimer’s Disease

Studies strongly suggest that low doses of THC can be a potential treatment option for Alzheimer’s through multiple functions and pathways. [53] [54]

THC and Deep Sleep

A study found that THC treatment in patients with Obstructive Sleep Apnea is safe and well-tolerated at doses of 2.5mg -10mg daily and significantly reduces the Apnea-Hypopnea Index in the short term. [55] Another study found that THC significantly decreases the time it takes to fall asleep in physically healthy insomniacs. [56]

THC and Seizure Prevention

Currently, CBD is known for its anticonvulsant properties, but THC also has its share in this area. Although used only in a rat model, THC use showed anticonvulsant activity, making the component a modulator of seizure termination and duration through activation of the CB1 receptor. [57]

THC Increases Insulin Sensitivity

A study that included two groups, the first one has been using marijuana in the past and the second one consisted of current marijuana users. The results indicated that current marijuana use was associated with 16% lower fasting insulin levels and smaller waist circumference. [58]

Various studies show that CBD offers proven benefits in treating different conditions, including chronic pain, epilepsy, multiple sclerosis, Parkinson’s, schizophrenia and much more.

CBD Relieves Chronic Pain

People with chronic pain rely on opioids for relief and although CBD products are not FDA approved for chronic pain,a  lot of people find CBD oils, gummies, and pills a great option for treating different conditions, such as chronic back and neck pain, arthritis, and osteoarthritis. Studies support CBD findings of its efficacy in treating chronic pain. One study found that CBD is effective in overall pain management without showing adverse side effects. [59]

Another study used CBD in rats with arthritis and after four days of treatment, researchers noted reduced inflammation and pain in the affected joins, again without side effects. [60] Although more human studies are needed, CBD is showing promising results in treating both cancer and chronic non-cancer pain.

Speaking of, the National Cancer Institute (NCI) stated that CBD is a possible option for relieving symptoms in patients undergoing chemotherapy. [61]

CBD Effectively Treats Epilepsy Patients

Epidiolex is the first FDA approved, CBD-rich medicine for treating Dravet Syndrome and Lennox-Gastaut Syndrome, two rare, difficult-to-control forms of epilepsy. [62] The breakthrough medicine is a life-saving treatment for children suffering from these forms of epilepsy, since traditional treatment of specialized diets and brain surgery shows mixed success rates.

The story of the young girl named Charlotte that took an ingestible oil derived from the CBD strain known as Charlotte’s Web and experienced a drastic fall in seizure attacks [63] from 1,200 to about three per month, gave hope to parents looking for a promising treatment that will alleviate the symptoms of these conditions for their children.

A study concerning this exact issue showed that the adjunctive use of CBD improves seizure control in patients with specific epilepsy syndromes. Studies found that CBD has been shown as superior to placebo in reducing the frequency of convulsive seizures and atonic seizures in patients with Dravet syndrome and Lennox-Gastaut syndrome, respectively. [64] [65]

CBD Helps Patients with Multiple Sclerosis (MS)

Both CBD and THC are known to help alleviate pain and muscle spasms in patients with MS, even when traditional treatment is not as effective. What is interesting is, that CBD has shown as an even better alternative than THC in treating multiple sclerosis. Various studies have shown that cannabis strains containing CBD levels equal or higher than THC positively affect muscle spasticity and pain in patients with MS. [66] [67] The positive effects of cannabis plant on spasticity and pain, as well as its safety in patients has been emphasized by the American Academy of Neurology. [68]

CBD and Amyotrophic Lateral Sclerosis (ALS)

A study that was focused on the alleviation of ALS-related symptoms, not the control of disease progression, states that the cannabinoid system seems to be involved in the pathogenesis of ALS. Furthermore, an observational study of patients with ALS revealed that cannabis use showed moderate relief of symptoms such as appetite loss, depression, pain, and drooling. Also, the mixture of THC (2.7 mg) and CBD (2.5 mg) in approximately 1:1 ratio, was found to be effective in delaying ALS progression in the early stages of disease in animals. The mixture is commercially known as Sativex, recently approved cannabinoid-based drug for clinical use in Europe. [69]

CBD and Parkinson’s Disease

Clinical studies show that cannabinoids may improve certain motor and nonmotor symptoms associated with Parkinson’s disease. A small, open-label study showed improvement in tremor, rigidity, pain, sleep, and bradykinesia in patients, after smoking cannabis. Another small, 4-week, open-label study of CBD for non-motor symptoms, psychosis in Parkinson’s Disease, showed improvement on the Brief Psychiatric Rating Scale and Parkinson Psychosis Questionnaire. [70]

According to a review, cannabinoids may constitute a novel window of opportunity to treat inflammatory and autoimmune disorders. Furthermore, the review suggests that cannabinoids have been tested in several experimental models such as MS, colitis, hepatitis, and rheumatoid arthritis and have shown to protect the host from the pathogenesis through induction of multiple anti-inflammatory pathways. Also, cannabinoids show as beneficial in chronic-inflammation triggered types of cancers. During such a situation, both THC and CBD, either directly inhibit tumor growth or suppress inflammation. [71]

CBD Successfully Treats Acne

Among the variety of physiological processes regulated by the endocannabinoid system are cutaneous cell growth and differentiation. Researchers found evidence that due to CBD’s lipostatic, antiproliferative, and anti-inflammatory effects, it is a promising therapeutic agent for treating patients with acne vulgaris. [72]

Dyskinesia, Tics, and Dystonia

Clinical research showed a clear role for cannabis products in symptom management for dyskinesia, tics and possibly dystonia. Movement disorders are worsened in anxious patients, but cannabis is shown to have a direct effect in various formulations in these diseases, and a promising role in their therapy. [73]

CBD Helps with Psoriasis

Researchers investigated the effects of CBD and THC for their ability to inhibit the proliferation of a hyper-proliferating human keratinocyte cell line and overall involvement of cannabinoid receptors. The results indicated that “cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis.” [74]

Depression and Anxiety

Multiple studies show a large-spectrum therapeutic potential of cannabidiol in psychiatric disorders, including anxiety, psychosis, and depression. It is clear that more than one mechanism is involved, and that CBD showed anxiolytic, anti-compulsive, antidepressant or antipsychotic-like therapeutic effects. [75] A study showed that CBD exhibited anti-anxiety and antidepressant effects in animals. [76] Preclinical evidence shows CBD’s efficacy in reducing anxiety symptoms, also relevant to other disorders, such as post-traumatic stress disorder (PTSD), obsessive-compulsive disorder (OCD), generalized anxiety disorder (GAD), personality disorders (PD), and seasonal affective disorder (SAD), with a notable lack of anxiogenic effects. [77]

SchizophreniaIt is known that CBD is not only very well tolerated by patients, but it counteracts several effects of THC, including anxiety, euphoria and psychosis. Cannabidiol also attenuates THC-induced memory impairment. Furthermore, preclinical animal studies have shown that CBD normalized psychotic-like behaviors induced in mice. Five clinical studies have examined the antipsychotic effects of CBD in humans, with the largest one showing that CBD treatment significantly increased the anandamide levels, which caused improvement in symptoms. Also, the group experienced significantly fewer side effects than with THC. [78]

The list of CBD benefits goes on and on, including conditions like mad cow disease, [79] diabetes, [80] ADHD, [81] nausea, [82] substance abuse/withdrawal, [83] heart disease, [84] bacterial infections, [85] irritable bowel syndrome, [86] broken bones, [87] and more.


Do CBD and THC work better together?

The answer is yes. Research has found that all compounds present in the marijuana plant — cannabinoids, flavonoids, and terpenoids — work the best for medical purposes, if combined. [88]

This system of working towards healing together is known as the entourage effect, where marijuana’s components create positive effects in the body together, which are impossible to achieve if consumed separately. [89] All of the cannabis compounds interact with each other to produce physical benefits.

For example, 50mg of isolated CBD may be substantially less effective at pain relief than a 50mg of a whole-plant CBD-rich cannabis extract. A great, study-proven example of the entourage effect — that we’ve mentioned several times in this article — is the THC’s effective treatment for pain or cancer, while CBD mitigates the psychotic symptoms.

For example, 50mg of isolated CBD may be substantially less effective at pain relief than a 50mg of a whole-plant CBD-rich cannabis extract. A great, study-proven example of the entourage effect — that we’ve mentioned several times in this article — is the THC’s effective treatment for pain or cancer, while CBD mitigates the psychotic symptoms.

Side Effects: CBD vs. THC

It is interesting how the side effects of CBD tend to be minimal to non-existent in people consuming CBD products on a day-to-day basis. Some side effects include dry mouth, low blood pressure, and drowsiness, but nothing serious.

According to research, the side-effects that occur in the body with CBD intake are likely a result of interactions between CBD and other medications the user is taking. [90]

The problem lays in the inability of the liver to break down most of the pharmaceuticals because of a CBD inhibition.

This makes taking medicine for conditions such as arrhythmia or high blood pressure ineffective, causing complications in the body. And makes a strong reason to talk to your doctor before using a CBD product.

While CBD is known for its mild side effects, THC causes an entire list of temporary side effects, including:

  • Reduced cognitive functions
  • Slower reaction times
  • Coordination problems
  • Increased heart rate
  • Dry mouth
  • Red eyes
  • Memory loss

Although nothing fatal, high THC is likely to cause long-term psychiatric effects. According to a 2017 study, cannabis abuse in adolescence is associated with an increased risk of psychotic disorders, like schizophrenia. [91]

How THC Works for Chronic Pain

As research suggests, THC is likely to help patients with spasticity and cramp-related pain, more effectively than CBD. [92] High doses of THC should be avoided because they can exacerbate the symptoms. [93]

THC resembles the two cannabinoid chemicals naturally occurring in the body, so when consumed, it stimulates the cannabinoid receptors of the brain (CB1 and CB2).

The CB2 receptor is associated with lymphoid and immune tissues, serving as an important mediator for surprising pain and inflammatory processes.

Additionally, THC activates the brain’s reward system, stimulating neurons to release dopamine at high levels. [94]

Also, it interferes with the glutamatergic system which is, “integral to development and maintenance of neuropathic pain, and is responsible for generating secondary and tertiary hyperalgesia in migraine and fibromyalgia via NMDA mechanisms.” [95]

THC inhibits glutamate release, producing 30%-40% glutamate reduction in NMDA responses. In addition to THC being a neuroprotective antioxidant, it reduces pain sensitivity via calcitonin gene-related peptide.

Also, THC blocks capsaicin-induced hyperalgesia at sub-psychoactive doses in animals. THC also stimulates beta-endorphin production, which prevents development of tolerance to and withdrawal from opiates.

How CBD Works for Chronic Pain

Cannabidiol shares neuroprotective effects with THC, also inhibits glutamate neurotoxicity and displays antioxidant activity greater that vitamin C or vitamin E.

But, “while THC has no activity at vanilloid receptors, CBD, like AEA, is a TRPV1 (vanilloid receptor) agonist that inhibits fatty acid amidohydrolase (FAAH), AEA’s hydrolytic enzyme, and also weakly inhibits AEA reuptake”.

The continuous activation of TRPV1 receptor causes analgesia, which has made this receptor a viable drug target for clinical use in management of pain. [96]

Together with endorphin and inflammatory, the vanilloid/transient receptor potential are some of the major endogenous pain control systems which also interact with the endocannabinoid system.

This means that CBD is an endocannabinoid modulator, additionally affecting THC’s function and reducing associated intoxication, panic, anxiety, and tachycardia.

The two most prominent cannabinoids are produced by both marijuana and hemp, with a major difference. Namely, marijuana has a higher concentration of THC, while hemp has a higher concentration of CBD, which makes hemp ideal for CBD oil production.

On average, a marijuana strain contains about 12 percent THC, while the CBD oil may contain small amounts of THC because the component is present in the hemp plant. [97]

High-CBD Cannabis Strains

Although CBD is the second most abundant cannabinoid in the cannabis plant, a strain may have a higher or lower THC vs. CBD ratio:

  • High THC, low CBD (e.g.,10-30% THC, trace amounts of CBD)
  • Balanced CBD/THC (e.g., 5-15% THC and CBD)
  • High CBD, low THC (e.g., 5-20% CBD, THC under 5%)

High-CBD strains are typically consumed by people who are extremely sensitive to the side effects of THC, such as anxiety, dizziness, and paranoia.

These strains tend to deliver clear-headed functional effects, without the euphoric high, also perfect for people that need to medicate through the day for chronic pain, or inflammation. The hemp oil is extracted from industrial hemp, from cannabis sativa, which primarily consist of CBD and very low amounts of THC.

Some high-CBD strains are:

  • ACDC
  • Harlequin OG
  • Suzzy Q

Balanced CBD/THC strains offer a more euphoric feeling than the CBD dominant, and are much less likely to induce anxiety or paranoia. These strains are effective for pain relief and can be consumed as CBD-infused edibles, oil capsules, lotions, and and tinctures. [98] On the other hand, high-THC strains are attractive to recreational users.

What is Pure CBD vs. Full Spectrum CBD

As the name suggests, a CBD isolate is pure, isolated CBD compound, existing all by itself without any other active compounds. Contrary to previous beliefs that the pure CBD was the “gold standard” of non-psychoactive cannabis therapy, the discovery of the entourage effect debunked each claim.

The first byproduct that manufacturers get from extracting oils from the hemp plant is a full spectrum CBD hemp oil. After getting the full-spectrum product with 20% actual CBD and 80% other elements, it is broken down until isolating other elements. The end byproduct is CBD isolate, 99% pure cannabidiol.

There are many benefits of CBD isolate, because you are getting a small, but effective dose that provides immediate relief. A CBD isolate can be used topically, orally, can be smoked, vaporized, and dabbed.

A full-spectrum oil contains other active cannabinoids, such as CBN, CBL, and CBCVA, THC, together with aromatic terpenes like limonene and pinene. The limonene can relieve stress and boost mood, while pinene increases alertness and memory.

Most CBD consumers find greater relief in full-spectrum CBD oil, rather than the isolate. One of the most important things in choosing between pure CBD and full spectrum CBD is finding a reliable supplier.

How to Dose CBD vs. THC (and vice versa) for Your Medical Issue

From the studies referred to in this article, it is safe to say that the therapeutic benefits of cannabis can be achieved at a lower dose than the one needed to produce euphoria.

It is important to remember the adage “start low, go slow,” regardless of the administration method used.

For example, the first couple of days, a 2.5 mg of only CBD or THC, once a day is a good start, and then continue to increase the dose itself, as well the number of times it is taken during the day.

A power combination, THC and CBD offer remarkable medicinal attributes. Although there is no single CBD:THC ratio that works universally, a 2.5 mg of CBD mixed with a small amount of THC can have a therapeutic effect.

THC dominant options (0:1) provide high degrees of psychoactivity and a variety of side-effects.

A 1:3 CBD:THC ratio also causes some psychoactivity, but minimizes the unwanted side effects caused by THC.

A 1:1 CBD to THC ratio is considered highly effective for pain relief, fibromyalgia, insomnia, nausea and spasticity.

A 2:1 or 3:1 now CBD vs THC ratio is great for autoimmune disorders, Crohn’s disease, arthritis, ideal for patients that want to avoid THC’s psychoactive effects.

Hemp based CBD and the ratio of 25:1 or 1:0 are most effective for anxiety, depression, seizures, PTSD, psychosis, and Parkinson’s, due to CBD’s strong anticonvulsant properties. [99]

A 2014 Review of Medical Cannabis Studies relating to Chemical Compositions and Dosages for Qualifying Medical Conditions by the Minnesota Department of Health, [100] summarizes clinical trials and prospective observational studies in humans in the following recommended doses for different diseases:

  • Cancer pain: most effective approach is a combination of THC and CBD rather than THC alone. If used doses of THC higher than 25mg during an entire day, substantial number of patients might poorly tolerate the drug.
  • Seizures: 200 to 300 mg CBD daily.
  • Crohn’s Disease: THC:CBD ratio 1:10 (5 mg THC and 50 mg CBD, twice daily) and CBD only (5 mg CBD in olive oil twice daily).
  • Tourette’s Syndrome: THC:CBD ratio of 1:1 (versus 2:1 or 3:1)
  • Muscle spasms: average doses of 20 to 25 mg of THC alone or in combination with CBD.
  • Glaucoma: 5 mg single dose of THC reduces symptoms for 4 to 5 hours.

If you want to know more about using cannabidiol for sleep or chronic pain, check out the following links:

The Ultimate Guide To CBD For Pain

CBD Tinctures Effects on Sleep: Everything You Should Know About Taking Cannabidiol for Sleep

CBD Gummies For Pain- Everything To Consider Before Buying

CBD Gummies With No THC | High Potency Cannabidiol Gummy Bears

What Should You Expect When Taking CBD for the First Time?


What is CBD vs THC?

Cannabidiol (CBD) and tetrahydrocannabinol (THC) are both naturally occurring compounds found in cannabis sativa L. CBD and THC are present in marijuana in different quantities, with CBD comprising up to 40% of the plant’s extract while THC only comprises roughly 3%. CBD has little to no psychoactive effects.

What is the difference between THC and CBD?

Although CBD and THC are both cannabinoids, they each affect the body in very different ways. While THC has psychoactive effects that can make users feel high or stoned, CBD doesn’t produce a similar reaction especially when isolated from THC  and effectively treat certain ailments. 

What’s better for pain CBD vs THC?

This way, CBD does not affect motor coordination or perception. It seems it can be used by patients who are taking other medications without issues. CBD increases alertness – although not nearly as much as THC.

What are the effects of CBD vs THC? 

They are similar in many ways, but CBD is non-intoxicating unlike THC which is intoxicating. CBD counteracts the psychoactive effect of THC due to its abundance within marijuana plants compared to that of THC. CBD also has a lot of healthy properties and doesn’t have any psychoactive effects like THC.

Works Cited

[1] ElSohly, Mahmoud A., and Desmond Slade. “Chemical constituents of marijuana: The complex mixture of natural cannabinoids.” Life Sciences (2005): 539-548. https://www.sciencedirect.com/science/article/abs/pii/S002432050500891X

[2] Pacher, Pal, et al. “The Endocannabinoid System as an Emerging Target of Pharmacotherapy.” Pharmacological Reviews (2006): 389–462. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2241751/

[3] Kogan, Natalya M. “Cannabinoids in health and disease.” Dialogues in CLinical Neuroscience (2007): 413–430. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3202504/

[4] National Center for Biotechnology Information. Cannabidiol. n.d. 19 Nov 2018. https://pubchem.ncbi.nlm.nih.gov/compound/cannabidiol#section=Top

[5] Hwang, Young Sun, et al. “Cannabidiol upregulates melanogenesis through CB1 dependent pathway by activating p38 MAPK and p42/44 MAPK.” Chemico-Biological Interactions (2017): 107-114. https://www.ncbi.nlm.nih.gov/pubmed/28601556

[6] Valverde, O. and M. Torrens. “CB1 receptor-deficient mice as a model for depression.” Neuroscience (2012): 193-206. https://www.ncbi.nlm.nih.gov/pubmed/21964469

[7] Gomez, O., et al. “Cannabinoid receptor agonists modulate oligodendrocyte differentiation by activating PI3K/Akt and the mammalian target of rapamycin (mTOR) pathways.” British Journal of Pharmacology (2011): 1520–1532. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165960/

[8] Alhamoruni, A., et al. “Pharmacological Effects of Cannabinoids on the Caco-2 Cell Culture Model of Intestinal Permeability.” Journal of Pharmacology and Experimental Therapeutics (2010): 92-102. http://jpet.aspetjournals.org/content/335/1/92.full

[9] Godlewski, Grzegorz, et al. “Presynaptic cannabinoid CB1 receptors are involved in the inhibition of the neurogenic vasopressor response during septic shock in pithed rats.” British Journal of Pharmacology (2004): 701–708. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1575049/

[10] Contributors, Wikipedia. GPR55. n.d. 19 Nov 2018. https://en.wikipedia.org/wiki/GPR55

[11] Idris, Aymen I. and Stuart H. Ralston. “Role of cannabinoids in the regulation of bone remodeling.” Frontiers in Endocrinology (2012). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499879/

[12],[13] [16] [22] Hill, Matthew N., and Sachin Patel. “Translational evidence for the involvement of the endocannabinoid system in stress-related psychiatric illnesses.” Biology of Mood & Anxiety Disorders (2013). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3817535/

[14] Ho, Begonia Y., et al. “Cannabinoid CB1 receptor-mediated inhibition of prolactin release and         signaling mechanisms in GH4C1 cells.” Endocrinology (2000): 1675–1685. https://www.ncbi.nlm.nih.gov/pubmed/10803576

[15] Contributors, Wikipedia. Brain-derived neurotrophic factor. n.d. 19 Nov. 2018. https://en.wikipedia.org/wiki/Brain-derived_neurotrophic_factor

[17] Contributors, Wikipedia. Peroxisome proliferator-activated receptor. n.d. 19 Nov. 2018. https://en.wikipedia.org/wiki/Peroxisome_proliferator-activated_receptor

[18] Du, Huizhi, et al. “Inhibition of COX-2 expression by endocannabinoid 2-arachidonoylglycerol is mediated via PPAR-γ.” British Journal of Pharmacology (2011): 1533-1549. https://www.ncbi.nlm.nih.gov/pubmed/21501147

[19] da Veiga, Marco Aurelio, et al. “Acute effects of endocannabinoid anandamide and CB1 receptor antagonist, AM251 in the regulation of thyrotropin secretion.” The Journal of Endocrinology (2008): 235-242. https://www.ncbi.nlm.nih.gov/pubmed/18755884

[20] Bilkei-Gorzo, A., et al. “Early age-related cognitive impairment in mice lacking cannabinoid CB1 receptors.” Proceedings of the National Academy of Sciences of the United States of America (2005): 15670-15675. http://www.pnas.org/content/102/43/15670#ref-20

[21] Wright, K L., et al. “Cannabinoid CB2 receptors in the gastrointestinal tract: a regulatory system in states of inflammation.” British Journal of Pharmacology (2008): 263–270. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219529/

[23] Basu, Sreemanti and Bonnie N. Dittel. “Unraveling the Complexities of Cannabinoid Receptor 2 (CB2) Immune Regulation in Health and Disease.” Immunologic Research (2011): 26–38. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4624216/

[24] Pertwee, R G., et al. “International Union of Basic and Clinical Pharmacology. LXXIX. Cannabinoid Receptors and Their Ligands: Beyond CB1 and CB2.” Pharmacological Reviews (2010): 588–631. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2993256/

[25], [31] Laprairie, R B., et al. “Cannabidiol is a negative allosteric modulator of the cannabinoid CB1 receptor.” British Journal of Pharmacology (2015). https://bpspubs.onlinelibrary.wiley.com/doi/full/10.1111/bph.13250

[26] Huestis, Marilyn A., et al. “Blockade of effects of smoked marijuana by the CB1-selective cannabinoid receptor antagonist SR141716.” Archives of General Psychiatry (2001): 322-328. https://www.ncbi.nlm.nih.gov/pubmed/11296091

[27] Martin-Santos, R., et al. “Neuroimaging in cannabis use: a systematic review of the literature.” Psychological Medicine (2010): 383-398. https://www.ncbi.nlm.nih.gov/pubmed/19627647

[28] Lupica, Carl R., et al. “Marijuana and cannabinoid regulation of brain reward circuits.” British Journal of Pharmacology (2004): 227–234. https://www.ncbi.nlm.nih.gov/pubmed/15313883

[29] Rettori E., et al. “Anti-inflammatory effect of the endocannabinoid anandamide in experimental periodontitis and stress in the rat.” Neuroimmunomodulation (2012): 293-303. https://www.ncbi.nlm.nih.gov/pubmed/22777139

[30] Tsuji, Fumio and Hiroyuki Aono. “Role of Transient Receptor Potential Vanilloid 1 in Inflammation and Autoimmune Diseases.” Pharmaceuticals (2012): 837–852. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3763671/

[32] Englund, Amir, et al. “Cannabidiol inhibits THC-elicited paranoid symptoms and hippocampal-dependent memory impairment.” Journal of Psychopharmacology (Oxford, England) (2013): 19-27. https://www.ncbi.nlm.nih.gov/pubmed/23042808

[33] Russo, Ethan, and Geoffrey W. Guy. “A tale of two cannabinoids: The therapeutic rationale for combining tetrahydrocannabinol and cannabidiol.” Medical Hypotheses (2006): 234-246. https://www.sciencedirect.com/science/article/pii/S0306987705004317

[34] Naftali, T., et al. “Treatment of Crohn’s Disease with Cannabis: An Observational Study.” Israel Medical Association Journal (2011). https://www.ima.org.il/MedicineIMAJ/viewarticle.aspx?aid=375

[35] Institute of Medicine (US). “4The Medical Value of Marijuana and Related Substances.” 1999. https://www.ncbi.nlm.nih.gov/books/NBK230711/

[36] Corey-Bloom, Jody, et al. “Smoked cannabis for spasticity in multiple sclerosis: a randomized, placebo-controlled trial.” The Canadian Medical Association Journal (2012 ): 1143-1150. http://www.cmaj.ca/content/184/10/1143.short

[37] State Laws. n.d. 19 Nov. 2018. https://norml.org/laws

[38] [62] U.S. Food & Drug Administration. FDA approves first drug comprised of an active ingredient derived from marijuana to treat rare, severe forms of epilepsy. n.d. 19 Nov. 2018. https://www.fda.gov/newsevents/newsroom/pressannouncements/ucm611046.htm

[39] Wilsey, Barth, et al. “Low-dose vaporized cannabis significantly improves neuropathic pain.” The Journal of Pain: Official Journal of the American Pain Society (2013): 136-48. https://www.ncbi.nlm.nih.gov/pubmed/23237736

[40] Deshpande, Amol, et al. “Efficacy and adverse effects of medical marijuana for chronic noncancer pain: Systematic review of randomized controlled trials.” Cannadian Family Physician (2015): 372-81. https://www.ncbi.nlm.nih.gov/pubmed/26505059

[41] Zajicek, John, et al. “Cannabinoids for treatment of spasticity and other symptoms related to multiple sclerosis (CAMS study): multicentre randomised placebo-controlled trial.” Lancet (London, England) (2003): 1517-26. https://www.ncbi.nlm.nih.gov/pubmed/14615106

[42] Zajicek, John P., et al. “Cannabinoids in multiple sclerosis (CAMS) study: safety and efficacy data for 12 months follow up.” Journal of Neurology, Neurosurgery, and Psychiatry (2005): 1664-9. https://www.ncbi.nlm.nih.gov/pubmed/16291891

[43] Zajicek, John P., et al. “Multiple sclerosis and extract of cannabis: results of the MUSEC trial.” Journal of Neurology, Neurosurgery, and Psychiatry (2012): 1125-32. https://www.ncbi.nlm.nih.gov/pubmed/22791906

[44] Guzman, M., et al. “A pilot clinical study of Delta9-tetrahydrocannabinol in patients with recurrent glioblastoma multiforme.” British Journal of Cancer (2006): 197-203. https://www.ncbi.nlm.nih.gov/pubmed/16804518

[45] Marcu, Jahan P., et al. “Cannabidiol enhances the inhibitory effects of Δ9-tetrahydrocannabinol on human glioblastoma cell proliferation and survival.” Molecular Cancer Therapeutics (2011): 180–189. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806496/

[46] Solinas, M., et al. “Cannabidiol inhibits angiogenesis by multiple mechanisms.” British Journal of Pharmacology (2012): 1218–1231. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504989/

[47] Rieder, Sadiye A., et al. “Cannabinoid-induced apoptosis in immune cells as a pathway to immunosuppression.” Immunobiology (2010): 598–605. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3005548/

[48] Caffarel, Maria M., et al. “Cannabinoids reduce ErbB2-driven breast cancer progression through Akt inhibition.” Molecular Cancer (2010). https://www.ncbi.nlm.nih.gov/pubmed/20649976

[49] McKallip, Robert J., et al. “Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response.” Journal of Immunology (2005): 3281-9. https://www.ncbi.nlm.nih.gov/pubmed/15749859

[50] Chiurchiù, Valerio, et al. “Detailed characterization of the endocannabinoid system in human macrophages and foam cells, and anti-inflammatory role of type-2 cannabinoid receptor.” Atherosclerosis (2014 ): 55-63. https://www.ncbi.nlm.nih.gov/pubmed/24529123

[51] Dushkin, M. I. “Macrophage/foam cell is an attribute of inflammation: mechanisms of formation and functional role.” Biochemistry (2012): 327-38. https://www.ncbi.nlm.nih.gov/pubmed/22809150

[52] Mach, F. and S. Steffens. “The role of the endocannabinoid system in atherosclerosis.” Journal of Neuroendocrinology (2008): 53-7. https://www.ncbi.nlm.nih.gov/pubmed/18426500

[53] Chuanhai, Cao, et al. “The Potential Therapeutic Effects of THC on Alzheimer’s Disease.” Journal of Alzheimer’s Disease (2014): 973-984. https://content.iospress.com/articles/journal-of-alzheimers-disease/jad140093

[54] Currais, Antonio, et al. “Amyloid proteotoxicity initiates an inflammatory response blocked by cannabinoids.” Aging and Mechanisms of Disease (2016). https://www.nature.com/articles/npjamd201612#article-info

[55] Prasad, Bharati, et al. “Proof of concept trial of dronabinol in obstructive sleep apnea.” Frontiers in Psychiartry Sleep Disorders (2013). https://www.frontiersin.org/articles/10.3389/fpsyt.2013.00001/full

[56] Cousens, Kenneth and Alberto DiMascio. “(−)δ9 THC as an hypnotic.” Psychopharmacologia (1973): 355–364. https://link.springer.com/article/10.1007%2FBF00437513#page-1

[57] Wallace, Melisa J., et al. “The endogenous cannabinoid system regulates seizure frequency and duration in a model of temporal lobe epilepsy.” The Journal of Pharmacology and Experimental Therapeutics (2003): 129-37. https://www.ncbi.nlm.nih.gov/pubmed/12954810

[58] Penner, , Elizabeth A., et al. “The Impact of Marijuana Use on Glucose, Insulin, and Insulin Resistance among US Adults.” The American Journal of Medicine (2013): 583–589. https://www.amjmed.com/article/S0002-9343(13)00200-3/fulltext

[59] [95] Russo, Ethan B. “Cannabinoids in the management of difficult to treat pain.” Therapeutics and Clinical Risk Management (2008): 245–259. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2503660/

[60] Hammell, D. C., et al. “Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis.” European Journal of Pain (2016): 936–948. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4851925/

[61] Cannabis and Cannabinoids (PDQ®)–Patient Version. n.d. 19 Nov. 2018. https://www.cancer.gov/about-cancer/treatment/cam/patient/cannabis-pdq#link/_15

[63] Young, Saundra. Marijuana stops child’s severe seizures. n.d. https://edition.cnn.com/2013/08/07/health/charlotte-child-medical-marijuana/index.html

[64] Perucca, Emilio. “Cannabinoids in the Treatment of Epilepsy: Hard Evidence at Last?” Journal of Epilepsy Research (2017): 61–76. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5767492/

[65] Rosenberg, Evan C., et al. “Cannabinoids and Epilepsy.” Neurotherapeutics (2015): 747–768. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4604191/

[66] Rudroff, Thorsten and Justin M. Honce. “Cannabis and Multiple Sclerosis—The Way Forward.” Frontiers in Neurology (2017). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481305/#B4

[67] Rog, D. J., et al. “Randomized, controlled trial of cannabis-based medicine in central pain in multiple sclerosis.” Neurology (2005): 812-9. https://www.ncbi.nlm.nih.gov/pubmed/16186518

[68] Koppel, Barbara S., et al. “Systematic review: efficacy and safety of medical marijuana in selected neurologic disorders: report of the Guideline Development Subcommittee of the American Academy of Neurology.” Neurology (2014): 1556-63. https://www.ncbi.nlm.nih.gov/pubmed/24778283

[69] Giacoppo, Sabrina and Emanuela Mazzon. “Can cannabinoids be a potential therapeutic tool in amyotrophic lateral sclerosis?” Natural Regeneration Research (2016): 1896–1899. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5270417/

[70] Bassi, Mario S., et al. “Cannabinoids in Parkinson’s Disease.” Cannabis and Cannbinoids Reasearch (2017): 21–29. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5436333/

[71] Nagarkatti, Prakash, et al. “Cannabinoids as novel anti-inflammatory drugs.” Future Medicinal Chemistry (2010): 1333–1349. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2828614/

[72] Olah, Attila, et al. “Cannabidiol exerts sebostatic and antiinflammatory effects on human sebocytes.” The Journal of Clinical Investigation (2014): 3713–3724. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4151231/

[73] Koppel, Barbara S. “Cannabis in the Treatment of Dystonia, Dyskinesias, and Tics.” Neurotherapeutics (2015): 788–792. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4604174/

[74] Wilkinson, Jonathan D., and Elizabeth M. Williamson. “Cannabinoids inhibit human keratinocyte proliferation through a non-CB1/CB2 mechanism and have a potential therapeutic value in the treatment of psoriasis.” Journal of Dermatological Science (2007): 87-92. https://www.ncbi.nlm.nih.gov/pubmed/17157480

[75] Campos, Alline C., et al. “Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders.” Philosophical Transactions of the Royal Society B: Biological Sciences (2012): 3364–3378. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3481531/

[76] de Mello Schier, Alexandre R., et al. “Antidepressant-like and anxiolytic-like effects of cannabidiol: a chemical compound of Cannabis sativa.” CNS & Neurological Disorders Drug Targets (2014): 953-60. https://www.ncbi.nlm.nih.gov/pubmed/24923339

[77] Blessing, Esther M., et al. “Cannabidiol as a Potential Treatment for Anxiety Disorders.” Neurotherapeutics (2015): 825–836. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4604171/

[78] Manseau, Marc W. and Donald C. Golf. “Cannabinoids and Schizophrenia: Risks and Therapeutic Potential.” Neurotherapeutics (2015): 816–824. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4604190/

[79] Dirikoc, Sevda, et al. “Nonpsychoactive cannabidiol prevents prion accumulation and protects neurons against prion toxicity.” The Journal of Neuroscience: the Official Journal of the Society of Neuroscience (2007): 9537-44. https://www.ncbi.nlm.nih.gov/pubmed/17804615

[80] Horváth, Bela, et al. “The Endocannabinoid System and Plant-Derived Cannabinoids in Diabetes and Diabetic Complications.” The American Journal of Pathology (2012): 432–442. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3349875/

[81] Cooper, R. E., et al. “Cannabinoids in attention-deficit/hyperactivity disorder: A randomised-controlled trial.” European Neuropsychopharmacology: The Journal of the European College of Neuropsychopharmacology (2017): 795-808. https://www.ncbi.nlm.nih.gov/pubmed/28576350

[82] Parker, Linda A., et al. “Regulation of nausea and vomiting by cannabinoids.” British Journal of Pharmacology (2011): 1411–1422. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165951/

[83] Prud’homme, Mélissa, et al. “Cannabidiol as an Intervention for Addictive Behaviors: A Systematic Review of the Evidence.” Substance Abuse: Research and Treatment (2015): 33–38. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4444130/

[84] Stanley, Christopher P., et al. “Is the cardiovascular system a therapeutic target for cannabidiol?” British Journal of Clinical Pharmacology (2013): 313-22. https://www.ncbi.nlm.nih.gov/pubmed/22670794

[85] Reiss, Carol S. “Cannabinoids and Viral Infections.” Pharmaceuticals (2010): 1873–1886. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2903762/

[86] Waseem, Ahmed and Seymour Katz. “Therapeutic Use of Cannabis in Inflammatory Bowel Disease.” Gastroenterology & Hepatology (2016): 668–679. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5193087/

[87] Kogan, Natalya M., et al. “Cannabidiol, a Major Non-Psychotropic Cannabis Constituent Enhances Fracture Healing and Stimulates Lysyl Hydroxylase Activity in Osteoblasts.” Journal of Bone and Mineral Research: The Oficial Journal of the American Society for Bone and MIneral Research (2015): 1905-13. https://www.ncbi.nlm.nih.gov/pubmed/25801536

[88] Russo, Ethan B. “Taming THC: potential cannabis synergy and phytocannabinoid-terpenoid entourage effects.” British Journal of Pharmacology (2011): 1344–1364. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3165946/

[89] Gallily, Ruth, et al. “Overcoming the Bell-Shaped Dose-Response of Cannabidiol by Using Cannabis Extract Enriched in Cannabidiol.” Pharmacology & Pharmacy (2015). https://file.scirp.org/Html/5-2500582_53912.htm

[90] CANNABIDIOL (CBD): Pre-Review Report. Geneva: World Health Organization, 2017. http://www.who.int/medicines/access/controlled-substances/5.2_CBD.pdf

[91] Segal-Gavish, Hadar, et al. “BDNF overexpression prevents cognitive deficit elicited by adolescent cannabis exposure and host susceptibility interaction.” Human Molecular Genetics (2017): 2462–2471. https://academic.oup.com/hmg/article/26/13/2462/3574683

[92] Malfitano, Anna Maria, et al. “Cannabinoids in the management of spasticity associated with multiple sclerosis.” Neuropsychiatric Disease and Treatment (2008): 847–853. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626929/

[93] Hill, Kevin P., et al. “Cannabis and Pain: A Clinical Review.” Cannabis and Cannabinoid Research (2017): 96–104. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5549367/

[94] How does marijuana produce its effects? n.d. 19 Nov. 2018. https://www.drugabuse.gov/publications/research-reports/marijuana/how-does-marijuana-produce-its-effects

[96] Jara-Oseguer, Andrea, at al. “TRPV1: On The Road To Pain Relief.” Current Molecular Pharmacology (2010): 255–269. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802457/

[97] ElSohly, Mahmood A., et al. “Changes in Cannabis Potency over the Last Two Decades (1995-2014) – Analysis of Current Data in the United States.” Biological Psychiatry (2017): 613–619. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4987131/

[98] Manzanares, J., et al. “Role of the Cannabinoid System in Pain Control and Therapeutic Implications for the Management of Acute and Chronic Pain Episodes.” Current Neuropharmacology (2006): 239–257. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430692/

[99] Viela, Luciano R., et al. “Anticonvulsant effect of cannabidiol in the pentylenetetrazole model: Pharmacological mechanisms, electroencephalographic profile, and brain cytokine levels.” Epilepsy & Behavior (2017): 29-35. https://www.ncbi.nlm.nih.gov/pubmed/28821005

[100] “A Review of Medical Cannabis Studies relating to Chemical Compositions and Dosages for Qualifying Medical Conditions.” 2014. http://www.health.state.mn.us/topics/cannabis/practitioners/dosage.pdf

[101] National Cancer Institute, “Cannabis and Cannabinoids (PDQ®)–Health Professional Version.” https://www.cancer.gov/about-cancer/treatment/cam/hp/cannabis-pdq

Leave a Reply

Your email address will not be published. Required fields are marked *