Epidyolex 100 mg/ml oral solution – Summary of Product Characteristics (SmPC) by GW Pharma Ltd CBD has been shown to reduce the severity & frequency of seizures. Check out the best CBD oils for epilepsy & information on dosage.
Epidyolex 100 mg/ml oral solution
Each ml of oral solution contains 100 mg cannabidiol.
Excipients with known effect
Each ml of solution contains:
79 mg anhydrous ethanol
736 mg refined sesame oil
0.0003 mg benzyl alcohol
For the full list of excipients, see section 6.1.
Clear, colourless to yellow solution
Epidyolex is indicated for use as adjunctive therapy of seizures associated with Lennox-Gastaut syndrome (LGS) or Dravet syndrome (DS), in conjunction with clobazam, for patients 2 years of age and older.
Epidyolex is indicated for use as adjunctive therapy of seizures associated with tuberous sclerosis complex (TSC) for patients 2 years of age and older.
Epidyolex should be initiated and supervised by physicians with experience in the treatment of epilepsy.
For LGS and DS
The recommended starting dose of cannabidiol is 2.5 mg/kg taken twice daily (5 mg/kg/day) for one week. After one week, the dose should be increased to a maintenance dose of 5 mg/kg twice daily (10 mg/kg/day). Based on individual clinical response and tolerability, each dose can be further increased in weekly increments of 2.5 mg/kg administered twice daily (5 mg/kg/day) up to a maximum recommended dose of 10 mg/kg twice daily (20 mg/kg/day).
Any dose increases above 10 mg/kg/day, up to the maximum recommended dose of 20 mg/kg/day, should be made considering individual benefit and risk and with adherence to the full monitoring schedule (see section 4.4).
The recommended starting dose of cannabidiol is 2.5 mg/kg taken twice daily (5 mg/kg/day) for one week. After one week, the dose should be increased to a dose of 5 mg/kg twice daily (10 mg/kg/day) and the clinical response and tolerability should be assessed. Based on individual clinical response and tolerability, each dose can be further increased in weekly increments of 2.5 mg/kg administered twice daily (5 mg/kg/day) up to a maximum recommended dose of 12.5 mg/kg twice daily (25 mg/kg/day).
Any dose increases above 10 mg/kg/day, up to the maximum recommended dose of 25 mg/kg/day, should be made considering individual benefit and risk and with adherence to the full monitoring schedule (see section 4.4).
The dosage recommendations for LGS, DS and TSC are summarised in the following table:
Table 1: Dosage recommendations
Starting dose – first week
2.5 mg/kg taken twice daily (5 mg/kg/day)
5 mg/kg twice daily (10 mg/kg/day)
5 mg/kg twice daily (10 mg/kg/day)
Further titration as applicable (incremental steps)
weekly increments of 2.5 mg/kg administered twice daily (5 mg/kg/day)
Maximal recommended dose
10 mg/kg twice daily (20 mg/kg/day)
12.5 mg/kg twice daily (25 mg/kg/day)
Each Epidyolex carton is supplied with:
– Two 1 ml syringes graduated in 0.05 ml increments (each 0.05 ml increment corresponds to 5 mg cannabidiol)
– Two 5 ml syringes graduated in 0.1 ml increments (each 0.1 ml increment corresponds to 10 mg cannabidiol)
If the calculated dose is 100 mg (1 ml) or less, the smaller 1 ml oral syringe should be used.
If the calculated dose is more than 100 mg (1 ml), the larger 5 ml oral syringe should be used.
The calculated dose should be rounded to the nearest graduated increment.
If cannabidiol has to be discontinued, the dose should be decreased gradually. In clinical trials, cannabidiol discontinuation was achieved by reducing the dose by approximately 10% per day for 10 days. A slower or faster down titration may be required, as clinically indicated, at the discretion of the prescriber.
In the case of one or more missed doses, the missed doses should not be compensated. Dosing should be resumed at the existing treatment schedule. In the case of more than 7 days’ missed doses, re-titration to the therapeutic dose should be made.
Clinical trials of cannabidiol in the treatment of LGS, DS and TSC did not include a sufficient number of patients aged above 55 years to determine whether or not they respond differently from younger patients.
In general, dose selection for an elderly patient should be cautious, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other concurrent therapy (see sections 4.4 under hepatocellular injury and 5.2).
Cannabidiol can be administered to patients with mild, moderate, or severe renal impairment without dose adjustment (see section 5.2). There is no experience in patients with end-stage renal disease. It is not known if cannabidiol is dialysable.
Cannabidiol does not require dose adjustment in patients with mild hepatic impairment (Child-Pugh A).
Caution should be used in patients with moderate (Child-Pugh B) or severe hepatic impairment (Child-Pugh C). A lower starting dose is recommended in patients with moderate or severe hepatic impairment. The dose titration should be performed as detailed in the table below.
Table 2: Dose adjustments in patients with moderate or severe hepatic impairment
Starting Dose For LGS, DS and TSC
Maintenance Dose For LGS and DS
Second Week For TSC
Maximal Recommended Dose For LGS and DS
Maximal Recommended Dose For TSC
1.25 mg/kg twice daily
2.5 mg/kg twice daily
5 mg/kg twice daily
6.25 mg/kg twice daily
0.5 mg/kg twice daily
1 mg/kg twice daily
2 mg/kg twice daily
2.5 mg/kg twice daily
*Higher doses of cannabidiol may be considered in patients with severe hepatic impairment where the potential benefits outweigh the risks.
With LGS and DS
There is no relevant use of cannabidiol in children aged below 6 months. The safety and efficacy of cannabidiol in children aged 6 months to 2 years have not yet been established. No data are available.
There is no relevant use of cannabidiol in children aged below 1 month. The safety and efficacy of cannabidiol in children aged 1 month to 2 years have not yet been established. Currently available data in patients aged 1 to 2 years are described in section 5.1 but no recommendation on a posology can be made.
Dose adjustments of other medicinal products used in combination with cannabidiol
A physician experienced in treating patients who are on concomitant antiepileptic drugs (AEDs) should evaluate the need for dose adjustments of cannabidiol or of the concomitant medicinal product(s) to manage potential drug interactions (see sections 4.4 and 4.5).
Method of administration
Food may increase cannabidiol levels and therefore it should be taken consistently either with or without food, including the ketogenic diet. When taken with food, a similar composition of food should be considered, if possible (see section 5.2).
Oral administration is recommended; however, when necessary, nasogastric and gastrostomy tubes may be acceptable routes for enteral administration.
For further information on the use of feeding tubes see section 6.6.
Hypersensitivity to the active substance or to any of the excipients listed in section 6.1.
Patients with transaminase elevations greater than 3 times the upper limit of normal (ULN) and bilirubin greater than 2 times the ULN (see section 4.4).
Cannabidiol can cause dose-related elevations of liver transaminases (alanine aminotransferase [ALT] and/or aspartate aminotransferase [AST]) (see section 4.8). The elevations typically occur in the first two months of treatment initiation; however, there were cases observed up to 18 months after initiation of treatment, particularly in patients taking concomitant valproate.
In clinical trials, the majority of ALT elevations occurred in patients taking concomitant valproate. Concomitant use of clobazam also increased the incidence of transaminase elevations, although to a lesser extent than valproate. Dose adjustment or discontinuation of valproate or dose adjustment of clobazam should be considered if transaminase elevations occur.
Resolution of transaminase elevations occurred with discontinuation of cannabidiol or reduction of cannabidiol and/or concomitant valproate in about two-thirds of the cases. In about one-third of the cases, transaminase elevations resolved during continued treatment with cannabidiol, without dose reduction.
Patients with baseline transaminase levels above the ULN had higher rates of transaminase elevations when taking cannabidiol. In some patients, a synergistic effect of concomitant treatment with valproate upon baseline elevated transaminases resulted in a higher risk of transaminase elevations.
In an uncontrolled study in patients in a different non-epilepsy indication, 2 elderly patients experienced elevations of alkaline phosphatase levels above 2 times the ULN in combination with transaminase elevations. The elevations resolved after discontinuation of cannabidiol.
In general, transaminase elevations of greater than 3 times the ULN in the presence of elevated bilirubin without an alternative explanation are an important predictor of severe liver injury. Early identification of elevated transaminase may decrease the risk of a serious outcome. Patients with elevated baseline transaminase levels above 3 times the ULN, or elevations in bilirubin above 2 times the ULN, should be evaluated prior to initiation of cannabidiol treatment.
Prior to starting treatment with cannabidiol, obtain serum transaminases (ALT and AST) and total bilirubin levels.
Serum transaminases and total bilirubin levels should be obtained at 1 month, 3 months, and 6 months after initiation of treatment with cannabidiol, and periodically thereafter or as clinically indicated.
Upon changes in cannabidiol dose above 10 mg/kg/day or changes in medicinal products (dose change or additions) that are known to impact the liver, this monitoring schedule should be restarted.
Patients with identified baseline elevations of ALT or AST and patients who are taking valproate should have serum transaminases and total bilirubin levels obtained at 2 weeks, 1 month, 2 months, 3 months, and 6 months after initiation of treatment with cannabidiol, and periodically thereafter or as clinically indicated. Upon changes in cannabidiol dose above 10 mg/kg/day or changes in medicinal products (dose change or additions) that are known to impact the liver, this monitoring schedule should be restarted.
If a patient develops clinical signs or symptoms suggestive of hepatic dysfunction, serum transaminases and total bilirubin should be promptly measured and treatment with cannabidiol should be interrupted or discontinued, as appropriate. Cannabidiol should be discontinued in any patients with elevations of transaminase levels greater than 3 times the ULN and bilirubin levels greater than 2 times the ULN. Patients with sustained transaminase elevations of greater than 5 times the ULN should also have treatment discontinued. Patients with prolonged elevations of serum transaminases should be evaluated for other possible causes. Dose adjustment of any co-administered medicinal product that is known to affect the liver should be considered (e.g., valproate and clobazam) (see section 4.5).
Somnolence and sedation
Cannabidiol can cause somnolence and sedation, which occur more commonly early in treatment and may diminish with continued treatment. The occurrence was higher for those patients on concomitant clobazam (see sections 4.5 and 4.8). Other CNS depressants, including alcohol, can potentiate the somnolence and sedation effect.
Increased seizure frequency
As with other AEDs, a clinically relevant increase in seizure frequency may occur during treatment with cannabidiol, which may require adjustment in dose of cannabidiol and/or concomitant AEDs, or discontinuation of cannabidiol, should the benefit-risk be negative. In the phase 3 clinical trials investigating LGS, DS and TSC, the observed frequency of status epilepticus was similar between the cannabidiol and placebo groups.
Suicidal behaviour and ideation
Suicidal behaviour and ideation have been reported in patients treated with AEDs in several indications. A meta-analysis of randomised placebo-controlled trials with AEDs has shown a small increased risk of suicidal behaviour and ideation. The mechanism of this risk is not known, and the available data do not exclude the possibility of an increased risk for cannabidiol.
Patients should be monitored for signs of suicidal behaviour and ideation and appropriate treatment should be considered. Patients and caregivers of patients should be advised to seek medical advice should any signs of suicidal behaviour and ideation emerge.
Cannabidiol can cause weight loss or decreased weight gain (see section 4.8). In LGS, DS and TSC patients, this appeared to be dose-related. In some cases, decreased weight was reported as an adverse event (see Table 3). Decreased appetite and weight loss may result in slightly reduced height gain. Continuous weight loss/absence of weight gain should be periodically checked to evaluate if cannabidiol treatment should be continued.
Sesame oil in the formulation
This medicinal product contains refined sesame oil which may rarely cause severe allergic reactions.
Benzyl alcohol in the formulation
This medicinal product contains 0.0003 mg/ml benzyl alcohol corresponding to 0.0026 mg per maximal Epidyolex dose (Epidyolex 12.5 mg/kg per dose (TSC) for an adult weighing 70 kg).
Benzyl alcohol may cause allergic reactions.
Populations not studied
Patients with clinically significant cardiovascular impairment were not included in the TSC clinical development programme.
CYP3A4 or CYP2C19 inducers
The strong CYP3A4/2C9 inducing agent rifampicin (600 mg administered once daily) decreased plasma concentrations of cannabidiol and of 7-hydroxy-cannabidiol (7-OH-CBD; an active metabolite of cannabidiol) by approximately 30% and 60%, respectively. Other strong inducers of CYP3A4 and/or CYP2C19, such as carbamazepine, enzalutamide, mitotane, St. John’s wort , when administered concomitantly with cannabidiol, may also cause a decrease in the plasma concentrations of cannabidiol and of 7-OH-CBD by a similar amount. These changes may result in a decrease in the effectiveness of cannabidiol. Dose adjustment may be necessary.
Cannabidiol is a substrate for UGT1A7, UGT1A9 and UGT2B7. No formal drug-drug interaction studies have been conducted with cannabidiol in combination with UGT inhibitors, therefore caution should be taken when co-administering drugs that are known inhibitors of these UGTs. Dose reduction of cannabidiol and/or the inhibitor may be necessary when given in combination.
Concomitant AED treatments
The pharmacokinetics of cannabidiol are complex and may cause interactions with the patient’s concomitant AED treatments. cannabidiol and/or concomitant AED treatment should therefore be adjusted during regular medical supervision and the patient should be closely monitored for adverse drug reactions. In addition, monitoring of plasma concentrations should be considered.
The potential for drug-drug interactions with other concomitant AEDs has been assessed in healthy volunteers and patients with epilepsy for clobazam, valproate stiripentol. Although no formal drug-drug interaction studies have been performed for other AEDs, phenytoin and lamotrigine are addressed based on in vitro data.
When cannabidiol and clobazam are co-administered, bi-directional PK interactions occur. Based on a healthy volunteer study, elevated levels (3- to 4-fold) of N-desmethylclobazam (an active metabolite of clobazam) can occur when combined with cannabidiol, likely mediated by CYP2C19 inhibition, with no effect on clobazam levels. In addition, there was an increased exposure to 7-OH-CBD, for which plasma area under the curve (AUC) increased by 47% (see section 5.2). Increased systemic levels of these active substances may lead to enhanced pharmacological effects and to an increase in adverse drug reactions. Concomitant use of cannabidiol and clobazam increases the incidence of somnolence and sedation compared with placebo (see sections 4.4 and 4.8). Reduction in dose of clobazam should be considered if somnolence or sedation are experienced when clobazam is co-administered with cannabidiol.
Concomitant use of cannabidiol and valproate increases the incidence of transaminase enzyme elevations (see section 4.4). The mechanism of this interaction remains unknown. If clinically significant increases of transaminases occur, cannabidiol and/or concomitant valproate should be reduced or discontinued in all patients until a recovery of transaminase elevations are observed (see section 4.4). Insufficient data are available to assess the risk of concomitant administration of other hepatotoxic medicinal products and cannabidiol (see section 4.4).
Concomitant use of cannabidiol and valproate increases the incidence of diarrhoea and events of decreased appetite. The mechanism of this interaction is unknown.
When cannabidiol was combined with stiripentol in a healthy volunteer trial there was an increase in stiripentol levels of 28% for maximum measured plasma concentration (Cmax) and 55% for AUC. In patients, however, the effect was smaller, with an increase in stiripentol levels of 17% in Cmax and 30% in AUC. The clinical importance of these results has not been studied. The patient should be closely monitored for adverse drug reactions.
Exposure to phenytoin may be increased when it is co-administered with cannabidiol, as phenytoin is largely metabolised via CYP2C9, which is inhibited by cannabidiol in vitro. There have not been any clinical studies formally investigating this interaction. Phenytoin has a narrow therapeutic index, so combining cannabidiol with phenytoin should be initiated with caution and if tolerability issues arise, dose reduction of phenytoin should be considered.
Lamotrigine is a substrate for UGT enzymes including UGT2B7 which is inhibited by cannabidiol in vitro. There have not been any clinical studies formally investigating this interaction. Lamotrigine levels may be elevated when it is co-administered with cannabidiol.
Mammalian target of rapamycin (mTOR) or calcineurin inhibitors
No dedicated drug-drug interaction studies have been conducted with mTOR inhibitors (e.g., everolimus) or calcineurin inhibitors (e.g., tacrolimus). In view of potential interaction which may lead to increased plasma concentrations of mTOR inhibitors/calcineurin inhibitors, these medications should be co-administered with caution and monitoring of the mTOR/ calcineurin inhibitor blood level should be considered.
Potential for cannabidiol to affect other medicinal products
CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, UGT1A9, and UGT2B7 Substrates
In vivo data from steady-state dosing with cannabidiol (750 mg twice daily) when co-administered with a single dose of caffeine (200 mg), a sensitive CYP1A2 substrate, showed increased caffeine exposure by 15% for Cmax and 95% for AUC compared to when caffeine was administered alone. These data indicate that cannabidiol is a weak inhibitor of CYP1A2. Similar modest increases in exposure may be observed with other sensitive CYP1A2 substrates (e.g., theophylline or tizanidine). The clinical importance of these findings has not been studied. The patient should be closely monitored for adverse drug reactions.
In vitro data predict drug-drug interactions with CYP2B6 substrates (e.g., bupropion, efavirenz), uridine 5′ diphospho-glucuronosyltransferase 1A9 (UGT1A9) (e.g., diflunisal, propofol, fenofibrate), and UGT2B7 (e.g., gemfibrozil, morphine, lorazepam) when co-administered with cannabidiol. Co-administration of cannabidiol is also predicted to cause clinically significant interactions with CYP2C8 (repaglinide) and CYP2C9 (e.g., warfarin) substrates.
In vitro data have demonstrated that cannabidiol inhibits CYP2C19, which may cause increased plasma concentrations of medicines that are metabolised by this isoenzyme such as clobazam and omeprazole. Dose reduction should be considered for concomitant medicinal products that are sensitive CYP2C19 substrates or that have a narrow therapeutic index.
Because of potential inhibition of enzyme activity, dose reduction of substrates of UGT1A9, UGT2B7, CYP2C8, and CYP2C9 should be considered, as clinically appropriate, if adverse reactions are experienced when administered concomitantly with cannabidiol. Because of potential for both induction and inhibition of enzyme activity, dose adjustment of substrates of CYP1A2 and CYP2B6 should be considered, as clinically appropriate.
In vitro assessment of interaction with UGT enzymes
In vitro data suggest that cannabidiol is a reversible inhibitor of UGT1A9 and UGT2B7 activity at clinically relevant concentrations. The metabolite 7-carboxy-cannabidiol (7-COOH-CBD) is also an inhibitor of UGT1A1, UGT1A4 and UGT1A6-mediated activity in vitro. Dose reduction of the substrates may be necessary when cannabidiol is administered concomitantly with substrates of these UGTs.
Ethanol in the formulation
Each ml of Epidyolex contains 79 mg of ethanol, equivalent to 10% v/v anhydrous ethanol, i.e., up to 691.3 mg ethanol/ per maximal single Epidyolex dose (12.5 mg/kg) for an adult weighing 70 kg (9.9 mg ethanol/ kg). For an adult weighing 70 kg, this is equivalent to 17 ml of beer, or 7 ml of wine per dose.
There are only limited data from the use of cannabidiol in pregnant women. Studies in animals have shown reproductive toxicity (see section 5.3).
As a precautionary measure, cannabidiol should not be used during pregnancy unless the potential benefit to the mother clearly outweighs the potential risk to the foetus.
There are no clinical data on the presence of cannabidiol or its metabolites in human milk, the effects on the breastfed infant, or the effects on milk production.
Studies in animals have shown toxicological changes in lactating animals, when the mother was treated with cannabidiol (see section 5.3).
There are no human studies on excretion of cannabidiol in breast milk. Given that cannabidiol is highly protein bound and will likely pass freely from plasma into milk, as a precaution, breast-feeding should be discontinued during treatment.
No human data on the effect of cannabidiol on fertility are available.
No effect on reproductive ability of male or female rats was noted with an oral dose of up to 150 mg/kg/day cannabidiol (see section 5.3).
Cannabidiol has major influence on the ability to drive and operate machines because it may cause somnolence and sedation (see section 4.4). Patients should be advised not to drive or operate machinery until they have gained sufficient experience to gauge whether it adversely affects their abilities (see section 4.8).
Summary of the safety profile
Adverse reactions reported with cannabidiol in the recommended dose range of 10 to 25 mg/kg/day are shown below.
The most common adverse reactions are somnolence, decreased appetite, diarrhoea, pyrexia, fatigue, and vomiting.
The most frequent cause of discontinuations was transaminase elevation.
Tabulated list of adverse reactions
Adverse reactions reported with cannabidiol in placebo-controlled clinical studies are listed in the table below by System Organ Class and frequency.
Table 3: Tabulated list of adverse reactions
System Organ Class
Adverse reactions from clinical trials
Infections and infestations
Pneumonia a , Urinary tract infection
Metabolism and nutrition disorders
Nervous system disorders
Respiratory, thoracic and mediastinal disorders
AST increased, ALT increased, GGT increased
Skin and subcutaneous tissue disorders
General disorders and administration site conditions
a Grouped Terms: Pneumonia: Pneumonia, Pneumonia RSV, Pneumonia mycoplasmal, Pneumonia adenoviral, Pneumonia viral, Aspiration pneumonia; Somnolence: Somnolence, Sedation.
Description of selected adverse reactions
Cannabidiol can cause dose-related elevations of ALT and AST (see section 4.4).
In controlled studies for LGS, DS (receiving 10 or 20 mg/kg/day) and for TSC (receiving 25 mg/kg/day), the incidence of ALT elevations above 3 times the ULN was 12% in cannabidiol-treated patients compared with < 1% in patients on placebo.
Less than 1% of cannabidiol -treated patients had ALT or AST levels greater than 20 times the ULN. There have been cases of transaminase elevations associated with hospitalisation in patients taking cannabidiol.
Risk Factors for Hepatocellular injury
Concomitant Valproate and Clobazam, Dose of cannabidiol and Baseline Transaminase Elevations
Concomitant Valproate and Clobazam
In cannabidiol-treated patients receiving doses of 10, 20, and 25 mg/kg/day, the incidence of ALT elevations greater than 3 times the ULN was 23% in patients taking both concomitant valproate and clobazam, 19% in patients taking concomitant valproate (without clobazam), 3% in patients taking concomitant clobazam (without valproate), and 3% in patients taking neither drug.
ALT elevations greater than 3 times the ULN were reported in 15% of patients taking cannabidiol 20 or 25 mg/kg/day compared with 3% in patients taking cannabidiol 10 mg/kg/day.
The risk of ALT elevations was higher at dosages higher than the 25 mg/kg/day in the controlled study in TSC.
Baseline transaminase elevations
In controlled trials (see section 5.1) in patients taking cannabidiol 20 or 25 mg/kg/day, the frequency of treatment-emergent ALT elevations greater than 3 times the ULN was 29% (80% of these were on valproate) when ALT was above the ULN at baseline, compared to 12% (89% of these were on valproate) when ALT was within the normal range at baseline. A total of 5% of patients (all on valproate) taking cannabidiol 10 mg/kg/day experienced ALT elevations greater than 3 times the ULN when ALT was above the ULN at baseline, compared with 3% of patients (all on valproate) in whom ALT was within the normal range at baseline.
Somnolence and sedation
Somnolence and sedation (including lethargy) events have been observed in controlled trials (see section 4.4) with cannabidiol in LGS, DS and TSC, including 29% of cannabidiol-treated patients (30% of patients taking cannabidiol 20 or 25 mg/kg/day and 27% of patients taking cannabidiol 10 mg/kg/day). These adverse reactions were observed at higher incidences at dosages above 25 mg/kg/day in the controlled study in TSC. The rate of somnolence and sedation (including lethargy) was higher in patients on concomitant clobazam (43% in cannabidiol-treated patients taking clobazam, compared with 14% in cannabidiol-treated patients not on clobazam).
In the controlled trial in TSC patients, an increased frequency of adverse events associated with seizure worsening was seen at doses above 25 mg/kg/day. Although no clear pattern was established, the adverse events reflected increased seizure frequency or intensity, or new seizure types. The frequency of adverse events associated with seizure worsening was 11% for patients taking 25 mg/kg/day cannabidiol and 18% for patients taking cannabidiol doses greater than 25 mg/kg/day, compared to 9% in patients taking placebo.
Cannabidiol can cause weight loss or decreased weight gain (see section 4.4). In LGS, DS and TSC patients, the decrease in weight appeared to be dose-related, with 21% of patients on cannabidiol 20 or 25 mg/kg/day experiencing a decrease in weight of ≥ 5%, compared to 7% in patients on cannabidiol 10 mg/kg/day. In some cases, the decreased weight was reported as an adverse event (see Table 3 above). Decreased appetite and weight loss may result in slightly reduced height gain.
Cannabidiol can cause dose-related diarrhoea. In controlled trials in LGS and DS, the frequency of diarrhoea was 13% in patients receiving 10 mg/kg/day cannabidiol and 21% in patients receiving 20 mg/kg/day cannabidiol, compared to 10% in patients receiving placebo. In a controlled trial in TSC, the frequency of diarrhoea was 31% in patients receiving 25 mg/kg/day cannabidiol and 56% in patients receiving doses greater than 25 mg/kg/day cannabidiol, compared to 25% in patients receiving placebo.
In the clinical trials, the first onset of diarrhoea was typically in the first 6 weeks of treatment with cannabidiol. The median duration of diarrhoea was 8 days. The diarrhoea led to cannabidiol dose reduction in 10% of patients, temporary dose interruption in 1% of patients and permanent discontinuation in 2% of patients.
Cannabidiol can cause decreases in haemoglobin and haematocrit. In LGS, DS and TSC patients, the mean decrease in haemoglobin from baseline to end of treatment was −0.36 g/dL in cannabidiol-treated patients receiving 10, 20, or 25 mg/kg/day. A corresponding decrease in haematocrit was also observed, with a mean change of −1.3% in cannabidiol-treated patients.
Twenty-seven percent (27%) of cannabidiol-treated patients with LGS and DS and 38% of cannabidiol-treated patients (25 mg/kg/day) with TSC developed a new laboratory-defined anaemia during the course of the study (defined as a normal haemoglobin concentration at baseline, with a reported value less than the lower limit of normal at a subsequent time point).
Increases in creatinine
Cannabidiol can cause elevations in serum creatinine. The mechanism has not yet been determined. In controlled studies in healthy adults and in patients with LGS, DS and TSC, an increase in serum creatinine of approximately 10% was observed within 2 weeks of starting cannabidiol. The increase was reversible in healthy adults. Reversibility was not assessed in studies in LGS, DS or TSC.
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via Yellow Card Scheme at www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.
Experience with doses higher than the recommended therapeutic dose is limited. Mild to moderate diarrhoea and somnolence have been reported in healthy adult subjects taking a single dose of 6000 mg; this equates to a dose of over 85 mg/kg for a 70 kg adult. These adverse reactions resolved upon study completion.
Management of overdose
In the event of overdose the patient should be observed and appropriate symptomatic treatment given, including monitoring of vital signs.
Pharmacotherapeutic group: antiepileptics, other antiepileptics; ATC code: N03AX24
Mechanism of action
The precise mechanisms by which cannabidiol exerts its anticonvulsant effects in humans are unknown. Cannabidiol does not exert its anticonvulsant effect through interaction with cannabinoid receptors. Cannabidiol reduces neuronal hyper-excitability through modulation of intracellular calcium via G protein-coupled receptor 55 (GPR55) and transient receptor potential vanilloid 1 (TRPV-1) channels, as well as modulation of adenosine-mediated signalling through inhibition of adenosine cellular uptake via the equilibrative nucleoside transporter 1 (ENT-1).
In patients, there is a potential additive anticonvulsant effect from the bi-directional pharmacokinetic interaction between cannabidiol and clobazam, which leads to increases in circulating levels of their respective active metabolites, 7-OH-CBD (approximately 1.5-fold) and N-CLB (approximately 3-fold) (see sections 4.5, 5.1 and 5.2).
Adjunctive therapy in patients with Lennox-Gastaut syndrome (LGS)
The efficacy of cannabidiol for the adjunctive therapy of seizures associated with Lennox-Gastaut syndrome (LGS) was evaluated in two randomised, double-blind, placebo-controlled, parallel-group studies (GWPCARE3 and GWPCARE4). Each study consisted of a 4-week baseline period, a 2-week titration period and a 12-week maintenance period. Mean age of the study population was 15 years and 94% were taking 2 or more concomitant AEDs (cAEDs) during the trial. The most commonly used cAEDs (> 25% of patients) in both trials were valproate, clobazam, lamotrigine, levetiracetam, and rufinamide. Approximately 50% of the patients were taking concomitant clobazam. Of the patients that were not taking clobazam, the majority had previously taken and subsequently discontinued clobazam treatment.
The primary endpoint was the percentage change from baseline in drop seizures per 28 days over the treatment period for the cannabidiol group compared to placebo. Drop seizures were defined as atonic, tonic, or tonic-clonic seizures that led or could have led to a fall or injury. Key secondary endpoints were the proportion of patients with at least a 50% reduction in drop seizure frequency, the percentage change from baseline in total seizure frequency, and Subject/Caregiver Global Impression of Change at the last visit.
Subgroup analyses were conducted on multiple factors, including cAEDs. Results of the subgroup analysis of patients treated with clobazam compared to patients treated without clobazam, indicated that there is residual statistical uncertainty regarding the treatment effect of cannabidiol in patients not taking clobazam. In this population, efficacy has not been established.
Table 4 summarises the primary endpoint of percent reduction from baseline in drop seizures, and the key secondary measure of proportion of patients with at least a 50% reduction in drop seizure frequency, as well as results of the subgroup analysis for these outcome measures in patients treated with concomitant clobazam.
Table 4:Primary and ≥50% responder key secondary outcome measures and subgroup analysis in LGS studies
Subgroup With Clobazam
DROP SEIZURES PER 28 DAYS
Percentage Reduction from Baseline a
Difference or Percent Reduction Compared with Placebo (95% CI), p-value b
≥ 50% REDUCTION IN DROP SEIZURES (RESPONDER ANALYSIS)
Percentage of ≥ 50% Responders, p-value d
CI=95% confidence interval.
a Data for the overall population are presented as median percent reduction from baseline. Data for the with clobazam subgroup are presented as percent reduction from baseline estimated from a negative binomial regression analysis.
b Overall data are presented as estimated median difference and p-value from a Wilcoxon rank-sum test. Data for the with clobazam subgroup are estimated from a negative binomial regression analysis.
c Nominal p-value.
d The Overall p-value is based on a Cochran-Mantel-Haenszel test; the nominal p-values for the with clobazam subgroup are based on logistic regression analysis.
Additional secondary outcome measures in the subgroup of patients treated with concomitant clobazam
Cannabidiol was associated with an increase in the percentage of subjects experiencing a greater than or equal to 75% reduction in drop seizure frequency during the treatment period in each trial (11% 10 mg/kg/day cannabidiol, 31% to 36% 20 mg/kg/day cannabidiol, 3% to 7% placebo).
In each trial, patients receiving cannabidiol experienced a greater median percentage reduction in total seizures compared with placebo (53% 10 mg/kg/day, 64% to 66% 20 mg/kg/day, 25% for each placebo group; p=0.0025 for 10 mg/kg/day and p
Greater improvements in overall condition, as measured by Global Impression of Change scores at the last visit, were reported by caregivers and patients with both doses of cannabidiol (76% on 10 mg/kg/day, 80% for each group on 20 mg/kg/day, 31% to 46% on placebo; p=0.0005 for 10 mg/kg/day and p
Compared with placebo, cannabidiol was associated with an increase in the number of drop seizure-free days during the treatment period in each trial, equivalent to 3.3 days per 28 days (10 mg/kg/day) and 5.5 to 7.6 days per 28 days (20 mg/kg/day).
Adjunctive therapy in patients with Dravet syndrome
The efficacy of cannabidiol for the adjunctive therapy of seizures associated with Dravet syndrome (DS) was evaluated in two randomised, double-blind, placebo-controlled, parallel-group studies (GWPCARE2 and GWPCARE1). Each study consisted of a 4-week baseline period, a 2-week titration period and a 12-week maintenance period. Mean age of the study population was 9 years and 94% were taking 2 or more cAEDs during the trial. The most commonly used cAEDs (> 25% of patients) in both trials were valproate, clobazam, stiripentol, and levetiracetam. Approximately 65% of the patients were taking concomitant clobazam. Of the patients that were not taking clobazam, the majority had previously taken and subsequently discontinued clobazam treatment.
The primary endpoint was the change in convulsive seizure frequency during the treatment period (Day 1 to the end of the evaluable period) compared to baseline (GWPCARE2), and the percentage change from baseline in convulsive seizures per 28 days over the treatment period (GWPCARE1) for the cannabidiol groups compared to placebo. Convulsive seizures were defined as atonic, tonic, clonic, and tonic-clonic seizures. Key secondary endpoints for GWPCARE2 were the proportion of patients with at least a 50% reduction in convulsive seizure frequency, the change in total seizure frequency, and Caregiver Global Impression of Change at the last visit. The key secondary endpoint for GWPCARE1 was the proportion of patients with at least a 50% reduction in convulsive seizure frequency.
Subgroup analyses were conducted on multiple factors, including cAEDs. Results of the subgroup analysis of patients treated with clobazam compared to patients treated without clobazam, indicated that there is residual statistical uncertainty regarding the treatment effect of cannabidiol in patients not taking clobazam. In this population, efficacy has not been established.
Table 5 summarises the primary endpoint of percent reduction from baseline in convulsive seizures, and the key secondary measure of proportion of patients with at least a 50% reduction in convulsive seizure frequency, as well as results of the subgroup analysis for these outcome measures in patients treated with concomitant clobazam.
Table 5: Primary and ≥ 50% responder key secondary outcome measures and subgroup analysis in DS studies
CBD Oil for Seizures & Epilepsy: Benefits, Dosage, & Side Effects
Research suggests CBD is a safe and effective treatment for seizure disorders.
1 in 10 patients are seizure-free after taking CBD oil & 70% had dramatic reductions in symptoms.
Epilepsy is the fourth most common neurological disorder, according to the Epilepsy Foundation.
CBD is reported to be one of the most effective treatment options for this condition — even for types of epilepsy proven to be difficult to treat with conventional medicine.
In this article, we’ll discuss exactly how effective CBD is for treating epilepsy, which types of epilepsy CBD works best for, and how to source the right kind of CBD to use.
MEDICALLY REVIEWED BY
Carlos G. Aguirre, M.D., Pediatric Neurologist
Updated on March 23, 2022
Table of Contents
$49 – $229
Royal CBD Oil 30 mL
5 / 5
|Total CBD:||500 – 2500 mg|
|Potency:||16.6 – 83.3 mg/mL|
|Cost per mg CBD:||$0.12 – $0.18|
The Benefits of CBD Oil For Epilepsy
The benefits of CBD oil for epilepsy include:
- Alleviates convulsions
- Protects the neurons from damage
- Regulates excess brain activity
- Reduces brain inflammation
- Promotes GABA activity in the brain
Despite all the research we have in the effects of CBD for epileptic conditions, we still don’t know the exact mechanisms involved.
Seizures are incredibly complex, and the causes generally involve multiple separate organ dysfunctions combining to produce symptoms. Therefore, deciding which part of this interaction is improved with CBD is hard to pinpoint.
Here are the current theories based on clinical, in vivo, and in vitro research findings.
1. Reduces Epileptic Convulsions
Epileptic-induced rodents were given various concentrations of CBD. The highest-dose group (100 mg per kg) showed significant improvements in muscle contractions during seizures .
2. Regulates Electrical Activity in The Brain
Seizures are characterized by excessive and chaotic electrical activity in the brain.
Electrical activity is largely regulated by the vanilloid receptors (TRPV).
CBD and CBDV have both been shown to regulate these vanilloid receptors (TRPV1) in the brain .
When TRPV1 is overactivated for any reason, it induces epileptic seizures. CBD and CBDV have been found to control the overactivity of this receptor in the brain — potentially leading to fewer seizures.
3. Protects The Brain Cells
CBD and many other cannabinoids in the cannabis plant have been shown to have broad, non-specific neuroprotective effects on the brain. Some of these neuroprotective effects are thought to be partly responsible for CBD’s powerful anti-epileptic activity.
CBD is protective for other neurological conditions, including:
4. Inhibits Brain Inflammation
As with most neurological disorders, inflammation is a huge factor in epilepsy .
A lot of evidence suggests CBD is an effective anti-inflammatory compound for the brain — potentially alleviating one of the significant factors for neurological disorders such as epilepsy.
CBD is effective because its fat-soluble nature allows it to pass through the blood-brain barrier efficiently. It also offers anti-inflammatory effects through some different inflammatory messengers and immune-regulating cells [11, 12, 13].
What’s The Dose of CBD Oil For Seizures?
Figuring out the right dose of CBD for epilepsy is difficult — and will likely require some trial and error.
Everybody responds to CBD differently. Some people require high doses; others much lower. You won’t know for sure the ideal dose you need without experience.
In general, people with epilepsy require higher-than-average dosing to get the maximum amount of benefits from the compound. This is why we recommend buying a high-potency CBD oil. If you buy a low-potency CBD product and then realize you need a high dose to see any benefits, you’re likely to need to take the entire bottle for a single dose. High-potency oils last longer by delivering the same amount of CBD in a smaller amount of oil or capsules.
With that said, we recommend starting at a low dose and building up gradually over time until you reach a dose that provides the level of relief you’re looking for.
Recommended strength for epilepsy: high strength
We’ve outlined the standard dosage schedule below based on weight and strength.
To learn how to calculate these doses yourself, check out our Guide to Dosing CBD.
CBD Dosage Calculator
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Tips for Getting the Most Out of CBD Supplements for Epilepsy:
- Always seek out high-quality CBD products to avoid contamination with heavy metals or pesticides — which can make epilepsy even worse
- Use full-spectrum extracts for the best results — research suggests these extracts are more effective than isolated or purified CBD products
- Increase the dose gradually — start with a low dose and build up to a higher dose until symptoms are reduced
- Combine CBD with other antiepileptic treatments and dietary changes — such as a ketogenic diet, regular exercise, and psychotherapy when appropriate
- Take CBD regularly — the effects are more pronounced after several weeks of regular use
What is Epilepsy?
Epilepsy is a spectrum of disorders involving the primary symptom: unprovoked seizures. Other health issues may or may not also be present. Everybody experiences epilepsy differently, and seizures can vary significantly in frequency and severity.
Some epileptic patients suffer from seizures one or two times per year, while others can experience nearly nonstop seizures throughout the day.
Seizures can involve whole-body convulsions (grand mal), remain confined to one limb (Jacksonian seizures), or involve lapses in consciousness (petit mal). We’ll include more on the different types of seizures later.
The seizure itself is the result of dysfunctional electrical activity in the brain — which can originate from anywhere in the brain. This abnormal electrical activity can remain confined to the area in which it started, or it can spread throughout the entire brain. In most cases, the latter is more severe.
People suffering from epilepsy usually have the condition for the rest of their life. However, it can come and go from one year to the next. Some people report being seizure-free for up to six years before having another seizure.
There are many different forms of epilepsy and numerous potential causes for each one. It can, therefore, be difficult for doctors to pinpoint the exact cause of the seizures in many cases.
Symptoms of Epilepsy
- Temporary confusion
- Prolonged staring
- Uncontrollable jerking movements
- Loss of consciousness
- A sudden sense of intense fear or anxiety
- Lapses in memory
What Causes Seizures & Epilepsy?
Seizures are the primary symptoms of epilepsy. Although epilepsy is characterized by recurring seizures, there are other causes, such as high fever or head injuries.
The brain is made up of billions of specialized cells called neurons. They’re designed to transfer messages throughout the brain and body using electrical impulses. To do this effectively, the neurons in the brain need to work together.
In the event of a seizure, large groups of neurons will send messages at the same time (hypersynchrony), disrupting normal brain function. This can cause changes in taste, vision, sound, smell, language, posture, memory, emotion, and consciousness.
Some seizures will affect the entire brain; others only specific regions. The severity of the electrical activity and how much of the brain is affected will determine the individual side-effects. Ultimately, no seizure is the same.
Causes of Seizures May Include:
There are different forms that seizures can happen depending on the individual and the type of epilepsy they have. Some people will experience one, two, or all three.
Three Types of Epilepsy
There are three different types of epilepsy.
The main differentiating factor for epilepsy is the types of seizures experienced, but there are other factors depending on the site of electrical dysfunction in the brain and the underlying cause of the condition.
Over the past decade, a group called the International League Against Epilepsy (ILAE) has been working hard to standardize the terminology used in diagnosing and describing epilepsy.
Here are the definitions listed in their 2017 outline.
1. Focal Onset
Focal onset epileptics experience abnormal electrical activity in only specific regions of the brain. They used to be called “partial seizures.”
There are four types of focal seizures:
- Focal-aware seizures — the patient is aware of the seizure while it’s taking place.
- Focal-impaired awareness seizures — the patient is unaware or unconscious during the seizure.
- Focal motor seizures — these involve movements such as rubbing hands together or twitching during the seizure.
- Focal non-motor seizures — these do not involve muscle twitches or movements, but instead shifts in thinking and emotions during the seizure. Waves of heat or cold, a racing heart, or intense emotions are common.
2. Generalized Onset
Generalized onset seizures involve abnormal electrical activity throughout both sides of the brain, resulting in widespread side effects throughout the body.
Within generalized onset epilepsies, there are two types — motor onset and non-motor onset.
Motor onset conditions used to be referred to as “grand mal” seizures — in some circles, they still are. They result in full-body seizures and an inability to control the body while the seizures are occurring. They can last anywhere from a few seconds to a few hours. CBD is useful for these types of seizures due to its ability to relax muscle contractions around the body.
Non-motor onset seizure conditions are usually called “absence” seizures. They involve periods of staring into space or repetitive movements (such as tapping hands or licking lips). These types of seizures make it seem as though the person having the seizure is no longer there — hence the name “absence seizures.”
3. Unknown Onset
As the name implies, any seizure where the source of the seizure can’t be identified is referred to as having an unknown onset. These seizures are especially challenging to treat.
The new terminology outlined by the ILAE does not change the characterization of epileptic syndromes — of which there are quite a few.
The Most Common Epileptic Syndromes Include:
- Lennox-Gastaut Syndrome (LGS)
- Dravet Syndrome
- Juvenile Myoclonic Epilepsy (JME)
- Benign rolandic epilepsy (BRE)
- Childhood absence epilepsy (CAE)
- Infantile spasms (or West syndrome)
The Risks of Epilepsy
Epilepsy can endanger the safety of those affected. It can be risky to drive, work, or even cross the street. If a seizure comes on suddenly, those affected are unlikely to get out of harm’s way.
Conventional Treatment Options for Epilepsy
It’s important to remember that epilepsy is a spectrum. Certain medications or other treatment options tend to work better for some forms of epilepsy over others. In some cases, no conventional treatment works for the patient’s requirement — these are usually the people that begin using CBD.
Medications for Epilepsy Include:
Medical Marijuana for Epilepsy
It’s clear that marijuana is a useful supplement for different forms of epilepsy, including both generalized and focal, along with some epileptic syndromes.
Studies have shown that CBD is the active constituent of these effects. Interestingly, a meta-analysis recently showed that although any form of CBD offers benefits, a full-spectrum CBD extract containing a variety of other cannabinoids was more beneficial and had fewer side effects overall .
For this reason, we recommend using a quality full-spectrum product over pharmaceutical versions such as Sativex® or Epidolex®, as well as CBD products made from 99.9% pure CBD isolates.
It’s likely the other cannabinoids in the full-spectrum extracts, along with the terpenes and various other phytochemicals, work synergistically to produce the associated benefits.
The Story of Charlotte Figi
Charlotte Figi is an American girl with a severe case of Dravet syndrome who changed the way we treat epilepsy forever.
When Charlotte was just six years old, her parents signed a “do not resuscitate” order for their little girl. This meant that in the event of an emergency that saw Charlotte stop breathing or her heart stops beating, medical professionals would not be allowed to step in and save her life.
Her symptoms were very severe — she’d often experience hundreds of seizures each week. She could barely speak, and her quality of life was at an all-time low.
Even after trying numerous medications, the Figis saw virtually no improvement in their daughter’s condition.
It wasn’t until 2011 that the Figis decided to try cannabis for their daughter — and it worked.
Here seizures dropped from 1200 per month to about 3 — and the ones she had were significantly less severe. She can now talk, play, and live a life much closer to “normal.”
The media attention that followed this story exploded and is arguably the catalyst that led to the establishment of the CBD market we’re now experiencing. This is because it was discovered that CBD was the compound responsible for treating Charlotte’s condition. Researchers flocked to test it out on other types of epilepsy, as well as other medical conditions.
Guide to Using CBD for Epilepsy
CBD is becoming one of the most common treatment options for epileptics. However, with poor regulations in the CBD market, there is an alarming amount of low-quality products containing contaminants such as heavy metals or pesticides that can damage the neurons and potentially make epilepsy symptoms worse.
There are also a lot of companies selling oils with specific amounts of CBD listed on the bottle — but when tested by third parties, they’re found to contain only a fraction of the amount advertised.
When it comes to using CBD for epilepsy, it’s critical that you use only high-quality, contaminant-free, and high-potency products.
It’s also been proven through meta-analysis that a full-spectrum extract rich in CBD and other cannabinoids and terpenes has the biggest impact on epileptic conditions .
For this reason, we recommend searching specifically for a product with at least 50 mg per mL of CBD that is made from certified organic hemp and has publicly listed third-party test results.
How to Get a Prescription for Medical Cannabis & CBD
Although every country has its own rules regarding the use of medical marijuana, most countries with a medical program will prescribe it for epilepsy.
The National Institute of Health and Clinical Excellence is working on official guidance for prescribing medical cannabis.
Epilepsy treatment is expected to be one of the primary focus points for this piece, which is expected to be completed at the end of 2020.
If your country (or state) doesn’t have a medical marijuana program, low-THC hemp extracts are an excellent alternative. These are classified as nutritional supplements in most countries and are non-psychoactive.
Finding the Right CBD Supplements for Epilepsy
There are so many different cannabis companies selling CBD oils, capsules, and topicals — it can be hard to separate the good from the bad.
As a general guide, always look for the following:
- Products containing full-spectrum extracts
- Potencies of at least 50 mg per mL
- Productos with third-party lab tests posted
- Products made from certified organic hemp
- Extracts containing low THC (less than 0.3%)
1. CBD Oils For Epilepsy
CBD oils are the most popular form of CBD because it simplifies dosing, it can be stored for long periods of time, it is one of the cheapest forms of CBD and has high bioavailability.
2. CBD Capsules For Epilepsy
CBD capsules provide another great option for people who want a simple way to get their dose without having to measure or taste CBD oil. However, capsules are slightly more expensive on average than oils.
3. CBD Edibles For Epilepsy
Edible CBD products are also available — but aren’t recommended for daily CBD supplementation due to the high sugar content and inconsistencies with dosing. These are great for occasional use to make your CBD use more interesting (and flavorful) but not ideal for everyday use.
4. CBD Vape Oils & E-Liquids For Epilepsy
CBD vape oils and vape pens are also an option, and many people with epilepsy choose to use this method to get their dose of CBD. The benefit with vape oils is that the CBD enters the bloodstream almost immediately, offering fast relief from symptoms.
Unless vaping irritates your lungs, or you’d rather avoid it altogether, keep some vape oil on hand to address symptom flare-ups promptly without having to wait for oils or capsules to absorb through the digestive tract.
CBD & Epilepsy: What the Research Says
Cannabidiol (CBD) is one of over 66 different cannabinoids found in the cannabis plant.
There are two main cannabinoids in the cannabis plant that account for more than half the total cannabinoid content. CBD is non-psychoactive (meaning it won’t make you feel high). It’s also the primary ingredient responsible for the antiepileptic effects of the cannabis plant.
A pharmaceutical CBD preparation — Epidolex (cannabidiol) — was approved in 2018 for the treatment of Lennox-Gastaut syndrome (LGS) and Dravet syndrome — two forms of epilepsy known for resisting treatment.
A recent meta-analysis involving 670 people with various forms of epilepsy found that 71% of people taking CBD-rich full-spectrum extracts experienced reduced seizure frequency .
Roughly 40% of the people in this study had the frequency of seizures cut in half, and a quarter had an incredible 70% drop in episodes.
Amazingly, 10% of the group were reported to be seizure-free at the end of the study.
CBD works — there’s no doubt about it. The hard part now is determining exactly how it works.
We’re still uncovering exactly how CBD is useful for treating epilepsy and seizures. Even GW Pharmaceuticals admits on its website that the mechanism of action isn’t clear. GW Pharmaceuticals is the creator of Sativex® — the new cannabinoid-based pharmaceutical that’s been gaining a lot of hype lately as a breakthrough new treatment for epilepsy.
There are a few good theories, however.
Final Verdict: Can CBD Help With Epilepsy & Seizures?
CBD is perhaps one of the most exciting new treatment options for epilepsy — including epileptic syndromes such as Dravet syndrome that are problematically resistant to treatment.
To get the most out of CBD supplementation for epilepsy, a high-quality, full-spectrum extract should be used. It’s also recommended to opt for a high-potency option because, in most cases, high doses are needed to get the same level of benefits reported in the scientific literature.
Check out some of our recent reviews to vet a company and their product before you make a purchase. Remember only to buy products that are made from certified organic hemp and have been tested for purity and potency by third-party labs.
If a product doesn’t check these boxes, it’s wise to avoid taking them for epilepsy. You don’t want to make symptoms worse.