Cequa and Weed

{Fulldrug} and Weed

Authored by Pin Ng PhD

Edited by Hugh Soames

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Cequa and Weed


Most people who consume marijuana do so for its mood-altering and relaxing abilities. Weed gives people a high and allows them to relax. However, heavy consumption of weed can cause unwanted results. It can increase the anxiety and depression a person experiences, and it can interact with certain other drugs including Cequa. It is important to remember that interactions do occur with all types of drugs, to a great or lesser extent and this article details the interactions of mixing Cequa and Weed.


Mixing Cequa and Weed


Ciclosporin, also spelled cyclosporine and cyclosporin, is a calcineurin inhibitor, used as an immunosuppressant medication. It is taken orally or intravenously for rheumatoid arthritis, psoriasis, Crohn’s disease, nephrotic syndrome, and in organ transplants to prevent rejection. It is also used as eye drops for keratoconjunctivitis sicca (dry eyes).

Common side effects include high blood pressure, headache, kidney problems, increased hair growth, and vomiting. Other severe side effects include an increased risk of infection, liver problems, and an increased risk of lymphoma. Blood levels of the medication should be checked to decrease the risk of side effects. Use during pregnancy may result in preterm birth; however, ciclosporin does not appear to cause birth defects.

Ciclosporin is believed to work by decreasing the function of lymphocytes. It does this by forming a complex with cyclophilin to block the phosphatase activity of calcineurin, which in turn decreases the production of inflammatory cytokines by T-lymphocytes.

Ciclosporin was isolated in 1971 from the fungus Tolypocladium inflatum and came into medical use in 1983. It is on the World Health Organization’s List of Essential Medicines. In 2020, it was the 212th most commonly prescribed medication in the United States, with more than 2 million prescriptions. It is available as a generic medication.

Ciclosporin is indicated to treat and prevent graft-versus-host disease in bone marrow transplantation and to prevent rejection of kidney, heart, and liver transplants. It is also approved in the US for treating of rheumatoid arthritis and psoriasis, persistent nummular keratitis following adenoviral keratoconjunctivitis, and as eye drops for treating dry eyes caused by Sjögren’s syndrome and meibomian gland dysfunction.

In addition to these indications, ciclosporin is also used in severe atopic dermatitis, Kimura disease, pyoderma gangrenosum, chronic hives, acute systemic mastocytosis, and posterior or intermediate uveitis with noninfective cause.[citation needed] It is also used, albeit infrequently, in severe rheumatoid arthritis and related diseases.

Ciclosporin has also been used in people with acute severe ulcerative colitis and hives that do not respond to treatment with steroids.

Side effects of ciclosporin can include gum enlargement, increased hair growth, convulsions, peptic ulcers, pancreatitis, fever, vomiting, diarrhea, confusion, increased cholesterol, trouble breathing, numbness and tingling (particularly of the lips), itchiness, high blood pressure, potassium retention (possibly leading to hyperkalemia), kidney and liver dysfunction, burning sensations at finger tips, and an increased vulnerability to opportunistic fungal and viral infections. Ciclosporin causes hypertension by inducing vasoconstriction in the kidneys and increasing sodium reabsorption. The increase in blood pressure can cause cardiovascular events; it is thus recommended that the lowest effective dose for people requiring long-term treatment be used.

Ciclosporin use after a kidney transplantation is associated with increased levels of uric acid in the blood and, in some cases, gout. This is due to the decrease in glomerular filtration rate,[citation needed] which leads to uric acid retention. Use of azathioprine as an alternative has shown to reduce the incidence of gouty arthritis.

Ciclosporin is listed as an IARC Group 1 carcinogen (i.e. there is sufficient evidence of carcinogenicity in humans), specifically leading to squamous cell skin cancer and non-Hodgkin lymphoma.

Ciclosporin’s main effect is to lower the activity of T-cells; it does so by inhibiting calcineurin in the calcineurin–phosphatase pathway and preventing the mitochondrial permeability transition pore from opening. Ciclosporin binds to the cytosolic protein cyclophilin (immunophilin) of lymphocytes, especially of T cells. This cyclosporin—cyclophilin complex inhibits calcineurin, which is normally responsible for activating the transcription of interleukin 2. In T-cells, activation of the T-cell receptor normally increases intracellular calcium, which acts via calmodulin to activate calcineurin. Calcineurin then dephosphorylates the transcription factor NF-AT (nuclear factor of activated T-cells), which moves to the T-cell nucleus and increases the transcription of genes for IL-2 and related cytokines. Ciclosporin, by preventing the dephosphorylation of NF-AT, leads to reduced effector T-cell function; it does not affect cytostatic activity.[medical citation needed]

Ciclosporin also binds to the cyclophilin D protein that constitutes part of the mitochondrial permeability transition pore (MPTP), thus preventing MPTP opening. The MPTP is found in the mitochondrial membrane of cardiac muscle cells. MPTP opening signifies a sudden change in the inner mitochondrial membrane permeability, allowing protons and other ions and solutes of a size up to ~1.5 kDa to go through the inner membrane. This change of permeability is considered a cellular catastrophe, leading to cell death. However, brief mitochondrial permeability transition pore openings play an essential physiological role in maintaining healthy mitochondrial homeostasis.

Ciclosporin is a cyclic peptide of 11 amino acids; it contains a single D-amino acid, which is rarely encountered in nature. Unlike most peptides, ciclosporin is not synthesized by ribosomes.

Ciclosporin is highly metabolized in humans and animals after ingestion. The metabolites, which include cyclosporin B, C, D, E, H, and L, have less than 10% of ciclosporin’s immunosuppressant activity and are associated with higher kidney toxicity. Individual ciclosporin metabolites have been isolated and characterized but do not appear to be extensively studied.

Cyclosporin is synthesized by a nonribosomal peptide synthetase, cyclosporin synthetase. The enzyme contains an adenylation domain, a thiolation domain, a condensation domain, and an N-methyltransferase domain. The adenylation domain is responsible for substrate recognition and activation, whereas the thiolation domain covalently binds the adenylated amino acids to phosphopantetheine, and the condensation domain elongates the peptide chain. Cyclosporin synthetase substrates include L-valine, L-leucine, L-alanine, glycine, 2-aminobutyric acid, 4-methylthreonine, and D-alanine, which is the starting amino acid in the biosynthetic process. With the adenylation domain, cyclosporin synthetase generates the acyl-adenylated amino acids, then covalently binds the amino acid to phosphopantetheine through a thioester linkage. Some of the amino acid substrates become N-methylated by S-adenosyl methionine. The cyclization step releases cyclosporin from the enzyme. Amino acids such as D-Ala and butenyl-methyl-L-threonine (Bmt) indicate cyclosporin synthetase requires the action of other enzymes. The racemization of L-Ala to D-Ala by alanine racemase is pyridoxal phosphate-dependent. The formation of butenyl-methyl-L-threonine is performed by a Bmt polyketide synthase that uses acetate/malonate as its starting material.

Tolypocladium inflatum, the species currently used for mass production of Cyclosporin, has the biosynthetic genes arranged into a 12-gene cluster. Of these 12 genes, SimA (Q09164) is the cyclosporin synthetase, SimB (CAA02484.1) is the alanine racemase, and SimG (similar to ATQ39432.1) is the polyketide synthase. These genes are associated with an active retrotransposon. Although these sequences are poorly-annotated on GenBank and other databases, 90% similar sequences can be found for the Cyclosporin-producing Beauveria felina (or Amphichorda ~). SimB has two paralogs in the same organism with different but overlapping functions thanks to their low specificity.

In 1970, new strains of fungi were isolated from soil samples taken from Norway and from Wisconsin in the US by employees of Sandoz (now Novartis) in Basel, Switzerland. Both strains produced a family of natural products called cyclosporins. Two related components that had antifungal activity were isolated from extracts from these fungi. The Norwegian strain, Tolypocladium inflatum Gams, was later used for the large scale fermentation of ciclosporin.

The immunosuppressive effect of the natural product ciclosporin was discovered on 31 January 1972 in a screening test on immune suppression designed and implemented by Hartmann F. Stähelin at Sandoz. The chemical structure of cyclosporin was determined in 1976, also at Sandoz. The success of the drug candidate ciclosporin in preventing organ rejection was shown in kidney transplants by R.Y. Calne and colleagues at the University of Cambridge, and in liver transplants performed by Thomas Starzl at the University of Pittsburgh Hospital. The first patient, on 9 March 1980, was a 28-year-old woman. In the United States, the Food and Drug Administration (FDA) approved ciclosporin for clinical use in 1983.

Thomas Starzl’s 1992 memoir explains through the eyes of a transplant surgeon that ciclosporin was an epoch-making drug for solid organ allotransplantation. It greatly expanded the clinical applicability of such transplantation by substantially advancing the antirejection pharmacotherapy component. Put simply, the biggest limits of applying such transplantation more widely were not cost or surgical skill (as formidable as those are) but rather the problem of allograft rejection and the scarcity of donor organs. Ciclopsporin was a major advancement against the rejection part of the challenge.

The natural product was named cyclosporin by the German-speaking scientists who first isolated it and cyclosporine when translated into English. Per International Nonproprietary Name (INN) guidelines for drugs, the y was replaced with i so that the INN for the medication is spelled ciclosporin.

Ciclosporin is the INN and the British Approved Name (BAN), while cyclosporine is the United States Adopted Name (USAN) and cyclosporin is a former BAN.

Ciclosporin exhibits very poor solubility in water, and, as a consequence, suspension and emulsion forms of the medication have been developed for oral administration and for injection. Ciclosporin was originally brought to market by Sandoz (now Novartis), under the brand name Sandimmune, which is available as soft gelatin capsules, an oral solution, and a formulation for intravenous administration. These are all nonaqueous compositions. A newer microemulsion, orally-administered formulation, Neoral, is available as a solution and as soft gelatin capsules. Compositions of Neoral are designed to form microemulsions in contact with water.

Generic ciclosporin preparations have been marketed under various trade names, including Cicloral (by Sandoz/Hexal), Gengraf (by Abbott) and Deximune (by Dexcel Pharma). Since 2002, a topical emulsion of ciclosporin for treating inflammation caused by keratoconjunctivitis sicca (dry eye syndrome) has been marketed under the trade name Restasis. Ikervis is a similar formulation with a concentration of 0.1%. Inhaled ciclosporin formulations are in clinical development, and include a solution in propylene glycol and liposome dispersions.

Ciclosporin is currently in a phase II/III (adaptive) clinical study in Europe to determine its ability to ameliorate neuronal cellular damage and reperfusion injury (phase III) in traumatic brain injury. This multi-center study is being organized by NeuroVive Pharma and the European Brain Injury Consortium using NeuroVive’s formulation of ciclosporin called NeuroSTAT (also known by its cardioprotection trade name of CicloMulsion). This formulation uses a lipid emulsion base instead of cremophor and ethanol. NeuroSTAT was compared to Sandimmune in a phase I study and found to be bioequivalent. In this study, NeuroSTAT did not exhibit the anaphylactic and hypersensitivity reactions found in cremophor- and ethanol-based products.

Ciclosporin has been investigated as a possible neuroprotective agent in conditions such as traumatic brain injury, and has been shown in animal experiments to reduce brain damage associated with injury. Ciclosporin blocks the formation of the mitochondrial permeability transition pore, which has been found to cause much of the damage associated with head injury and neurodegenerative diseases. Ciclosporin’s neuroprotective properties were first discovered in the early 1990s when two researchers (Eskil Elmér and Hiroyuki Uchino) were conducting experiments in cell transplantation. An unintended finding was that cyclosporin A was strongly neuroprotective when it crossed the blood–brain barrier. This same process of mitochondrial destruction through the opening of the MPT pore is implicated in making traumatic brain injuries much worse.

Ciclosporin has been used experimentally to treat cardiac hypertrophy (an increase in cell volume).

Inappropriate opening of the mitochondrial permeability transition pore (MPTP) manifests in ischemia (blood flow restriction to tissue) and reperfusion injury (damage occurring after ischemia when blood flow returns to tissue), after myocardial infarction (heart attack) and when mutations in mitochondrial DNA polymerase occur. The heart attempts to compensate for disease state by increasing the intracellular Ca
to increase the contractility cycling rates. Constitutively high levels of mitochondrial Ca
cause inappropriate MPTP opening leading to a decrease in the cardiac range of function, leading to cardiac hypertrophy as an attempt to compensate for the problem.

Cyclosporin A has been shown to decrease cardiac hypertrophy by affecting cardiac myocytes in many ways. Cyclosporin A binds to cyclophilin D to block the opening of MPTP, and thus decreases the release of protein cytochrome C, which can cause programmed cell death. CypD is a protein within the MPTP that acts as a gate; binding by cyclosporin A decreases the amount of inappropriate opening of MPTP, which decreases the intramitochondrial Ca2+
. Decreasing intramitochondrial Ca2+
allows for reversal of cardiac hypertrophy caused in the original cardiac response. Decreasing the release of cytochrome C caused decreased cell death during injury and disease. Cyclosporin A also inhibits the phosphatase calcineurin pathway (14). Inhibition of this pathway has been shown to decrease myocardial hypertrophy.

The medication is approved in the United States for the treatment of atopic dermatitis in dogs. Unlike the human form of the medication, the lower doses used in dogs mean the drug acts as an immunomodulator and has fewer side effects than in humans. The benefits of using this product include the reduced need for concurrent therapies to bring the condition under control. It is available as an ophthalmic ointment for dogs called Optimmune, manufactured by Intervet, which is part of Merck. It is also used to treat sebaceous adenitis (immune response against the sebaceous glands), pemphigus foliaceus (autoimmune blistering skin disease), Inflammatory bowel disease, anal furunculosis (anal inflammatory disease), and myasthenia gravis (a neuromuscular disease).


Research has found that anxiety is one of the leading symptoms created by marijuana in users, and that there is a correlation between Cequa and Weed and an increase in anxiety.


Anyone mixing Cequa and weed is likely to experience side effects. This happens with all medications whether weed or Cequa is mixed with them. Side effects can be harmful when mixing Cequa and weed. Doctors are likely to refuse a patient a Cequa prescription if the individual is a weed smoker or user. Of course, this could be due to the lack of studies and research completed on the mixing of Cequa and Weed.


Heavy, long-term weed use is harmful for people. It alters the brain’s functions and structure, and all pharmaceuticals and drugs including Cequa are designed to have an impact on the brain. There is a misplaced belief that pharmaceuticals and medication work by treating only the parts of the body affected yet this is obviously not the case in terms of Cequa. For example, simple painkiller medication does not heal the injury, it simply interrupts the brains functions to receive the pain cause by the injury. To say then that two drugs, Cequa and Weed, dol not interact is wrong. There will always be an interaction between Cequa and Weed in the brain11.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/.


One of the milder side effects of mixing Cequa and Weed is Scromiting. This condition, reportedly caused by mixing Cequa and Weed, describes a marijuana-induced condition where the user experiences episodes of violent vomiting, which are often so severe and painful that they cause the person to scream. The medical term for Scromiting by mixing Cequa and Weed is cannabinoid hyperemesis syndrome, or CHS.  For these reasons, some people choose to quit smoking weed.


It was first included in scientific reports in 2004. Since then, researchers have determined that Scromiting is the result of ongoing, long-term use of marijuana—particularly when the drug contains high levels of THC, marijuana’s main psychoactive ingredient. Some experts believe that the receptors in the gut become overstimulated by THC, thus causing the repeated cycles of vomiting.


In the long run, a person can become even more depressed. There is a belief that marijuana is all-natural and not harmful to a person’s health. This is not true and Cequa and weed can cause health issues the more a person consumes it.


How does Weed effect the potency of Cequa?


The way in which the body absorbs and process Cequa may be affected by weed. Therefore, the potency of the Cequa may be less effective. Marijuana inhibits the metabolization of Cequa. Not having the right potency of Cequa means a person may either have a delay in the relief of their underlying symptoms.


A person seeking Cequa medication that uses weed should speak to their doctor. It is important the doctor knows about a patient’s weed use, so they can prescribe the right Cequa medication and strength. Or depending on level of interactions they may opt to prescribe a totally different medication. It is important for the doctor to know about their patient’s marijuana use. Weed is being legalized around the US, so doctors should be open to speaking about a patient’s use of it.


Sideffects of Cequa and Weed


Many individuals may not realize that there are side effects and consequences to mixing Cequa and Weed such as:


  • Dizziness
  • Sluggishness
  • Drowsiness
  • Shortness of breath
  • Itching
  • Hives
  • Palpitations
  • Respiratory Depression
  • Cardiac Arrest
  • Coma
  • Seizures
  • Death


Interestingly, it is impossible to tell what effect mixing this substance with Weed will have on an individual due to their own unique genetic make up and tolerance. It is never advisable to mix Cequa and Weed due to the chances of mild, moderate and severe side effects. If you are having an adverse reaction from mixing Cequa and Weed it’s imperative that you head to your local emergency room. Even mixing a small amount of Cequa and Weed is not recommended.


Taking Cequa and Weed together


People who take Cequa and Weed together will experience the effects of both substances. Technically, the specific effects and reactions that occur due to frequent use of Cequa and weed depend on whether you consume more weed in relation to Cequa or more Cequa in relation to weed.


The use of significantly more weed and Cequa will lead to sedation and lethargy, as well as the synergistic effects resulting from a mixture of the two medications.


People who take both weed and Cequa may experience effects such as:


  • reduced motor reflexes from Cequa and Weed
  • dizziness from Weed and Cequa
  • nausea and vomiting due to Cequa and Weed


Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and Cequa leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.

Mixing weed and Cequa


The primary effect of weed is influenced by an increase in the concentration of the inhibitory neurotransmitter GABA, which is found in the spinal cord and brain stem, and by a reduction in its effect on neuronal transmitters. When weed is combined with Cequa this primary effect is exaggerated, increasing the strain on the body with unpredictable results.


Weed and Cequa affects dopamine levels in the brain, causing the body both mental and physical distress. Larger amounts of Cequa and weed have a greater adverse effect yet leading medical recommendation is that smaller does of Cequa can be just as harmful and there is no way of knowing exactly how Cequa and weed is going to affect an individual before they take it.


Taking Cequa and weed together


People who take Cequa and weed together will experience the effects of both substances. The use of significantly more Cequa with weed will lead to sedation and lethargy, as well as the synergistic effects resulting from a mixture of the two medications.


People who take both weed and Cequa may experience effects such as:


  • reduced motor reflexes from Cequa and weed
  • dizziness from weed and Cequa
  • nausea and vomiting of the Cequa


Some people may also experience more euphoria, depression, irritability or all three. A combination of weed and Cequa leads to significantly more lethargy which can easily tip over into coma, respiratory depression seizures and death.

Weed Vs Cequa


Taking Cequa in sufficient quantities increases the risk of a heart failure. Additionally, people under the influence of Cequa and weed may have difficulty forming new memories. With weed vs Cequa in an individual’s system they become confused and do not understand their environment. Due to the synergistic properties of Cequa when mixed with weed it can lead to confusion, anxiety, depression and other mental disorders. Chronic use of Cequa and weed can lead to permanent changes in the brain22.G. Lafaye, L. Karila, L. Blecha and A. Benyamina, Cannabis, cannabinoids, and health – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5741114/.


Cequa Vs Weed


Studies investigating the effects of drugs such as Cequa and weed have shown that the potential for parasomnia (performing tasks in sleep) is dramatically increased when Cequa and weed are combined. Severe and dangerous side effects can occur when medications are mixed in the system, and sleep disorders are a common side effect of taking weed and Cequa together.


When a small to medium amount of weed is combined with Cequa, sleep disorders such as sleep apnea can occur. According to the latest data from the US Centers for Disease Control and Prevention (CDC) most ER visits and hospitalizations caused by too much weed were associated with other substances such as Cequa.


How long after taking Cequa can I smoke weed or take edibles?


To avoid any residual toxicity it is advisable to wait until the Cequa has totally cleared your system before taking weed, even in small quantities.


Overdose on Cequa and weed


In the case of Overdose on Cequa or if you are worried after mixing Cequa and weed, call a first responder or proceed to the nearest Emergency Room immediately.


If you are worried about someone who has taken too much Cequa or mixed weed with Cequa then call a first responder or take them to get immediate medical help. The best place for you or someone you care about in the case of a medical emergency is under medical supervision. Be sure to tell the medical team that there is a mix of Cequa and weed in their system.


Excessive Weed intake and result in scromiting, chs, and anxiety disorder.  It is advisable to quit vaping weed if you are feeling these symptoms.

Mixing Cequa and weed and antidepressants


Weed users feeling depressed and anxious may be prescribed antidepressant medication. There are some antidepressant users who also use Cequa and weed. These individuals may not realize that there are side effects and consequences to consuming both Cequa, marijuana and a range of antidepressants.


Studies on weed, Cequa and antidepressants is almost nil. The reason for so little information on the side effects of the two is mostly down to marijuana being illegal in most places – although a number of states in the United States have legalized the drug.


Self-medicating with Weed and Cequa


A lot of people suffer from depression caused by weed and Cequa. How many? According to Anxiety and Depression Association of America (ADAA), in any given year, it is estimated that nearly 16 million adults experience depression. Unfortunately, that number is likely to be wrong due to under reporting. Many people do not report suffering from depression because they do not want to be looked at as suffering from a mental illness. The stigmas around mental health continue and people do not want to be labeled as depressed.


Potential side effects from mixing Cequa and weed


Quitting weed to take Cequa


Medical professionals say an individual prescribed or taking Cequa should not stop using weed cold turkey.  Withdrawal symptoms can be significant. Heavy pot users should especially avoid going cold turkey. The side effects of withdrawal from weed include anxiety, irritability, loss of sleep, change of appetite, and depression by quitting weed cold turkey and starting to take Cequa.


A person beginning to use Cequa should cut back on weed slowly. While reducing the amount of weed use, combine it with mindfulness techniques and/or yoga. Experts stress that non-medication can greatly improve a person’s mood.


Weed and Cequa can affect a person in various ways. Different types of marijuana produce different side effects. Side effects of weed and Cequa may include:


  • loss of motor skills
  • poor or lack of coordination
  • lowered blood pressure
  • short-term memory loss
  • increased heart rate
  • increased blood pressure
  • anxiety
  • paranoia
  • increased energy
  • increased motivation


Mixing Cequa and weed can also produce hallucinations in users. This makes marijuana a hallucinogenic for some users. Weed creates different side effects in different people, making it a very potent drug. Now, mixing Cequa or other mental health drugs with weed can cause even more unwanted side effects.


Mixing drugs and weed conclusion


Long-term weed use can make depression and anxiety worse. In addition, using marijuana can prevent Cequa from working to their full potential33.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/. Weed consumption should be reduced gradually to get the most out of prescription medication. Marijuana is a drug and it is harmful to individual’s long-term health. Weed has many side effects and the consequences are different to each person who uses it, especially when mixed with Cequa.


If you take Cequa, and also drink Alcohol or MDMA, you can research the effects of Cequa and Alcohol , Cequa and Cocaine as well as Cequa and MDMA here.


To find the effects of other drugs and weed refer to our Weed and Other Drugs Index A to L or our Weed and Other Drugs Index M-Z.

Or you could find what you are looking for in our Alcohol and Interactions with Other Drugs index A to L or Alcohol and Interactions with Other Drugs index M to Z , Cocaine and Interactions with Other Drugs index A to L or Cocaine and Interactions with Other Drugs index M to Z or our MDMA and Interactions with Other Drugs Index A to L or MDMA and Interactions with Other Drugs Index M to Z.


Cequa and Weed

Cequa and Weed

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  • 1
    1.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/
  • 2
    2.G. Lafaye, L. Karila, L. Blecha and A. Benyamina, Cannabis, cannabinoids, and health – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5741114/
  • 3
    3.J. D. Brown and A. G. Winterstein, Potential Adverse Drug Events and Drug–Drug Interactions with Medical and Consumer Cannabidiol (CBD) Use – PMC, PubMed Central (PMC).; Retrieved September 27, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678684/