Does CBD interact with prednisone, and if so, are there risks that should cause concern?

Prednisone is a prescription drug used to provide relief for inflamed areas of the body. It is also indicated to treat conditions, such as inflammation (swelling), severe allergies, arthritis, asthma, eye or vision problems, blood or bone marrow problems, and stomach or bowel problems (1). 

Moreover, doctors prescribe prednisone to help patients with lupus, skin conditions, endocrine problems, kidney problems, ulcerative colitis, adrenal problems, and flare-ups of multiple sclerosis. 

Prednisone is a corticosteroid, or a cortisone-like medicine or steroid. This drug works on the immune system to help relieve swelling, redness, itching, and allergic reactions.

However, this medicine may cause changes in mood or behavior for some patients. Symptoms to watch for include depression, trouble with sleeping, a false or unusual sense of well-being, mood swings, and personality changes while taking this medicine (2).

Can CBD Be Taken With Prednisone?

Taking CBD along with prednisone could either decrease the effects of cannabidiol or increase the amount of prednisone entering the bloodstream.

Whenever one takes CBD or any medicine, it passes through the digestive system to the liver, where an enzymatic pathway, called the cytochrome P450 (CYP450) family of enzymes, metabolizes or breaks down the substance ingested. 

Liver enzymes CYP450 process about 60% of all medications. One of these, CYP3A4, metabolizes prednisone to make it available to the body (3).

Studies have demonstrated that CBD strongly inhibits the activity of CYP3A4 liver enzymes (4).

Meanwhile, prednisone is a weak inducer of CYP3A4 (5). Still, prednisone may increase how quickly the liver breaks down CBD when they are taken in combination. 

In particular, the effects of taking CBD along with prednisone could either decrease the effects of cannabidiol or increase the amount of prednisone entering the bloodstream.

The increased prednisone concentration can amplify the drug’s many side effects and raise the risk of severe symptoms, such as dizziness or fainting, blurred vision, irregular or pounding heartbeat, increased thirst or urination, irritability, and unusual tiredness or weakness (6).

Thus, medical experts advise those taking CBD and prednisone to be cautious with this combination (7).

Can CBD Replace Prednisone?

No study explicitly says CBD can be used in place of prednisone. However, studies have shown that CBD possesses many potential therapeutic benefits that may help with some symptoms or conditions for which prednisone is indicated. 

Prednisone is sometimes prescribed for bone marrow problems, which is important for the health of blood cells. Meanwhile, studies have shown that CBD promotes the structural health of bones

The effect of CBD on bones was also demonstrated by a 2015 study that investigated the properties of cannabidiol concerning bone-related conditions. Data showed that CBD led to an improvement in fracture healing (8).

Like prednisone, CBD can help with skin conditions. A study published in the journal Trends in Pharmacological Sciences has suggested the existence of a functional endocannabinoid system (ECS) in the skin and implicated it in various biological processes (9). 

CBD impacts the TRPV-1 and GPR55 receptors (10). Both receptors are found in the skin and play a role in pain signaling and inflammation.

CBD has also been shown to help with mood swings, depression, dizziness, and sleeping difficulty, which may be the side effects from taking prednisone. 

A study published in the Journal of Psychopharmacology found that CBD may decrease anxiety levels in individuals with a social anxiety disorder (SAD). 

Results indicated that, relative to placebo, CBD was associated with significantly decreased subjective anxiety (11). 

In another study, results showed that CBD could theoretically induce rapid-acting antidepressant-like effects and enhance neurotransmission (12). Neurotransmission is the process of communication between nerve cells.

In a 2019 study published in The Permanente Journal, sleep and anxiety scores were measured in human subjects, and the findings showed that CBD could hold benefits for anxiety-related disorders (13).

Meanwhile, CBD’s antiemetic properties, which prevent nausea and vomiting, are incredibly helpful. 

A 2014 review from the European Journal of Pharmacology established the potential of cannabis to limit or prevent nausea and vomiting from a wide range of causes (14). 

More importantly, the powerful anti-inflammatory properties of CBD could help with some of the same disorders  that prednisone treats. 

CBD’s anti-inflammatory characteristics have been shown in several human and animal studies, like that of a 2014 study published in the Journal of Clinical Investigation and a 2012 research conducted by authors from the Department of Pathology, School of Veterinary Medicine in the University of São Paulo, Brazil (15).

Other studies have demonstrated that the anti-inflammatory and immunosuppressive actions of CBD may be of use in treating rheumatoid arthritis and the associated pain (16).

Meanwhile, research published in the Free Radical Biology & Medicine Journal by George Booz of the University of Mississippi Medical Center showed that CBD, which may interact with the endocannabinoid system, is a promising prototype for anti-inflammatory drug development (17).  

Conclusion

CBD “is generally well tolerated with a good safety profile,” the World Health Organization (WHO) states in a critical review (18).

Still, it is not clear how much to take or how often a person should use it for any particular problem. 

High doses of CBD may also interact with other medications, such as blood thinners, antidepressants, and immune suppressors (19).

Thus, individuals should be cautious when supplementing their existing medications with CBD. 

Do not take other pharmaceuticals unless they have been discussed with a medical professional. 

More importantly, before using CBD as a remedy for specific symptoms or conditions, consult with a doctor experienced in cannabis use for advice.

Medically reviewed DR. WIEGMANN on 06-22-2020


  1. Mayo Clinic. (2020, Feb 1). Prednisone. Retrieved from https://www.mayoclinic.org/drugs-supplements/prednisone-oral-route/side-effects/drg-20075269?p=1.
  2. Mayo Clinic. (2020, Feb 1). Prednisone. Retrieved from https://www.mayoclinic.org/drugs-supplements/prednisone-oral-route/side-effects/drg-20075269?p=1.
  3. PharmGKB. Prednisone. Retrieved from https://www.pharmgkb.org/chemical/PA451100.
  4. Yamaori S, Ebisawa J, Okushima Y, Yamamoto I, Watanabe K. Potent inhibition of human cytochrome P450 3A isoforms by cannabidiol: role of phenolic hydroxyl groups in the resorcinol moiety. Life Sci. 2011;88(15-16):730–736. DOI:10.1016/j.lfs.2011.02.017.
  5. Marcantonio EE, Ballard J, Gibson CR, et al. Prednisone has no effect on the pharmacokinetics of CYP3A4 metabolized drugs – midazolam and odanacatib. J Clin Pharmacol. 2014;54(11):1280–1289. DOI:10.1002/jcph.338.
  6. Mayo Clinic. (2020, Feb 1). Prednisone. Retrieved from https://www.mayoclinic.org/drugs-supplements/prednisone-oral-route/side-effects/drg-20075269?p=1.
  7. MedlinePlus. (2020, Jan 21). Cannabidiol. Retrieved from https://medlineplus.gov/druginfo/natural/1439.html.
  8. Kogan NM, Melamed E, Wasserman E, et al. Cannabidiol, a Major Non-Psychotropic Cannabis Constituent Enhances Fracture Healing and Stimulates Lysyl Hydroxylase Activity in Osteoblasts. J Bone Miner Res. 2015;30(10):1905–1913. DOI:10.1002/jbmr.2513.
  9. Bíró T, Tóth BI, Haskó G, Paus R, Pacher P. The endocannabinoid system of the skin in health and disease: novel perspectives and therapeutic opportunities. Trends Pharmacol Sci. 2009;30(8):411–420. DOI:10.1016/j.tips.2009.05.004.
  10. Sharir H, Abood ME. Pharmacological characterization of GPR55, a putative cannabinoid receptor. Pharmacol Ther. 2010;126(3):301–313. DOI:10.1016/j.pharmthera.2010.02.004; Costa B, Giagnoni G, Franke C, Trovato AE, Colleoni M. Vanilloid TRPV1 receptor mediates the antihyperalgesic effect of the nonpsychoactive cannabinoid, cannabidiol, in a rat model of acute inflammation. Br J Pharmacol. 2004;143(2):247–250. DOI:10.1038/sj.bjp.0705920.
  11. Crippa JA et al.Neural basis of anxiolytic effects of cannabidiol (CBD) in generalized social anxiety disorder: a preliminary report.J Psychopharmacol. 2011 Jan;25(1):121-30. DOIi: 10.1177/0269881110379283. Epub 2010 Sep 9. DOI: 10.1177/0269881110379283.
  12. Linge R et al. Cannabidiol induces rapid-acting antidepressant-like effects and enhances cortical 5-HT/glutamate neurotransmission: role of 5-HT1A receptors. Neuropharmacology. 2016 Apr;103:16-26. doi: 10.1016/j.neuropharm.2015.12.017. Epub 2015 Dec 19.DOI: 10.1016/j.neuropharm.2015.12.017.
  13. Shannon S, Lewis N, Lee H, Hughes S. Cannabidiol in Anxiety and Sleep: A Large Case Series. Perm J. 2019;23:18–041. DOIi:10.7812/TPP/18-041.
  14. Sharkey KA, Darmani NA, Parker LA. Regulation of nausea and vomiting by cannabinoids and the endocannabinoid system. Eur J Pharmacol. 2014;722:134–146. DOI:10.1016/j.ejphar.2013.09.068.
  15. Oláh A, Tóth BI, Borbíró I, et al. Cannabidiol exerts sebostatic and antiinflammatory effects on human sebocytes. J Clin Invest. 2014;124(9):3713–3724. DOI:10.1172/JCI64628; Ribeiro A et al. Cannabidiol, a non-psychotropic plant-derived cannabinoid, decreases inflammation in a murine model of acute lung injury: role for the adenosine A(2A) receptor. Eur J Pharmacol. 2012 Mar 5;678(1-3):78-85. DOI: 10.1016/j.ejphar.2011.12.043. Epub 2012 Jan 12.
  16. Blake DR, Robson P, Ho M, Jubb RW, McCabe CS. Preliminary assessment of the efficacy, tolerability and safety of a cannabis-based medicine (Sativex) in the treatment of pain caused by rheumatoid arthritis. Rheumatology (Oxford) 2006;45:50–52; Malfait AM, Gallily R, Sumariwalla PF, Malik AS, Andreakos E, Mechoulam R, Feldmann M. The nonpsychoactive cannabis constituent cannabidiol is an oral anti-arthritic therapeutic in murine collagen-induced arthritis. Proc. Natl. Acad. Sci. U. S. A. 2000;97:9561–9566.
  17. Booz GW. Cannabidiol as an emergent therapeutic strategy for lessening the impact of inflammation on oxidative stress. Free Radic Biol Med. 2011;51(5):1054–1061. DOI:10.1016/j.freeradbiomed.2011.01.007.
  18. Expert Committee on Drug Dependence Fortieth Meeting. Cannabidiol (CBD) Critical Review Report. June 2018. Retrieved from https://www.who.int/medicines/access/controlled-substances/CannabidiolCriticalReview.pdf.
  19. Harvard Health Publishing. (2019, Oct). Know the facts about CBD products. Retrieved from https://www.health.harvard.edu/staying-healthy/know-the-facts-about-cbd-products.

More Info

Less Info

HYPOCALCAEMIA

    DEFINITION

    Abnormally low concentration of calcium in the blood (Total calcium

    < 2.20 mmol/L or 8.8 mg/dL).

    The ionized calcium is a more accurate reflection of calcium status,

    especially in patients with low serum albumin. The normal ionized

    calcium is from 1.12 to 1.23 mmol/L ( 2.24 to 2.46 meq/L, 4.48 to 4.92

    mg/dL).

    TOXIC CAUSES

    Ethylene glycol

    Fluorides and fluorosilicates

    Hydrofluoric acid (ingestion or skin contact)

    Oxalic acid and soluble oxalates

    Phosphate enemas

    Valproic acid

    NON-TOXIC CAUSES

    Hypoparathyroidism

    Malabsorption

    Pancreatitis

    Renal failure

    Vitamin D deficiency

    CLINICAL FEATURES

    Severe hypocalcaemia may appear within an hour of acute ingestion of

    hydrofluoric acid, fluorides, fluorosilicates or oxalic acid. 

    Paraesthesias, tetany, and convulsions are often present.  The

    electrocardiograph shows a widened or prolonged QT interval and large

    or peaked T waves.  Dysrhythmias and cardiac arrest may occur.

    DIFFERENTIAL DIAGNOSIS:

    Congenital QT prolongation syndrome

    Type Ia antiarrhythmic agents

    Tetanus

    Hyperventilation

    Strychnine

    Seizures

    RELEVANT INVESTIGATIONS

    Total and ionized serum calcium concentration

    Serum electrolytes: magnesium, phosphate, sodium and potassium

    concentration

    Renal function (urea, creatinine)

    Acidbase status (blood gases, serum bicarbonate)

    Electrocardiograph (QT interval and T wave morphology)

    Consider amylase, valproic acid, ethylene glycol levels in appropriate

    circumstances.

    TREATMENT

    After acute ingestion of hydrofluoric acid, fluorides, fluorosilicates

    or oxalic acid, calcium salts should be given orally or by gastric

    tube as soon as possible (50 mL of 10% calcium gluconate; 1 mL/kg in

    children).  Calcium acts as a chelating agent in the stomach. 

    Magnesium (e.g., magnesium hydroxide found in liquid antacid

    preparations) may also be helpful for fluoride ingestion. 

    Extensive skin contamination by hydrofluoric acid, fluorides,

    fluorosilicates or oxalic acid may lead to systemic toxicity and

    severe hypocalcaemia.

    In all patients with suspected or confirmed hypocalcaemia, perform

    continuous cardiac monitoring, and give intravenous  calcium 

     gluconate (10 to 15 mL over 3 to 5 minutes, 0.01 to 0.02 mL/kg in

    children). Further doses of calcium salts depend on serum calcium

    concentration and ECG.  The required dose of calcium salt may be from

    3 g to 20 g on the first day.  Calcium chloride may also be used, but

    contains approximately 3 times the amount of calcium per mL. 

    CLINICAL COURSE AND MONITORING

    Sudden cardiac arrest can occur – provide continuous

    electrocardiographic monitoring (QT interval, T waves). 

    Serum calcium and ionized calcium concentrations.

    Some of the causes of hypocalcaemia may also lead to severe

    hyperkalaemia – measure serum potassium and electrolytes frequently.

    AUTHOR(S)/REVIEWERS

    Author:        Dr V. Danel, Unité de Toxicologie Clinique, Grenoble,

                   France.

    Peer review:   Cardiff 9/96: V Afanasiev, M Burger, T Della Puppa,

                   L Fruchtengarten, K Olsen, J Szajewski.

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