Epilepsy is a disorder of the brain that causes recurrent episodes called seizures. A seizure is sometimes described as an electrical storm in the brain leading to abnormal movements, sensations, and states of consciousness. In reality, however, it is more orderly than a storm. During a seizure, nerves function in an abnormally synchronized manner, a kind of lockstep that can continue for seconds or minutes. The results range from mild changes in awareness to violent convulsions.
Isolated seizures can occur for many reasons. The term
is applied when a person has recurrent seizures with no known treatable cause. If the seizure occurs in a localized part of the brain, it is called a
partial seizure. If it affects much of brain, it is called a
The most common forms of generalized seizures are absence seizures (petit mal) and tonic-clonic seizures (grand mal). Petit mal seizures involve a brief lapse of consciousness that occurs suddenly and lasts for a brief time before disappearing; there are usually no symptoms afterward. A grand mal seizure involves: loss of consciousness, convulsions of the body, tongue biting, and often urination. A state of confusion follows the seizure.
Partial seizures come in three main varieties. They can be simple (involving just an arm, for example) or complex (involving more complicated movements and loss of consciousness). Finally, some may turn into generalized seizures. There are several medications used to treat epilepsy, generally with considerable success. Most of these drugs can cause significant side effects, though. Fortunately, some of these side effects may be partially correctable through nutrient supplementation (see the
There are no well-established herbs or supplements for the treatment of epilepsy. However, a number of supplements may be useful for treating nutritional deficiencies caused by anticonvulsant drugs. Besides herbs and supplements, the ketogenic diet might be helpful for controlling seizures in children.
Note: Epilepsy is far too serious a condition for self-treatment. For this reason, none of the treatments listed below should be used without the advice and supervision of a doctor.
Before drug treatments for epilepsy were invented, scientists noticed that fasting tends to reduce seizure frequency. Subsequent investigation pinned down a metabolic state called ketosis as the causative factor. Ketosis occurs during fasting and also while consuming a diet high in fat and very low in carbohydrates (the ketogenic diet).
When effective anticonvulsant drugs were developed, the ketogenic diet fell into disfavor, but in recent years medical interest has returned. Today, the diet is seeing increased use in the treatment of people who do not respond fully to standard medications. Most studies have involved children because they tend to be more agreeable than adults to the diet.
Evidence suggests that the ketogenic diet may almost completely stop seizures in about half of all children with epilepsy and reduce seizure frequency less dramatically in another third.1-6 Unfortunately, the ketogenic diet can cause side effects, such as fatigue, nausea, reduced immunity, mental confusion, dehydration, constipation, and increased tendency to bruise.2,3,7-13 Major side effects seen occasionally with certain forms of the ketogenic diet include kidney stones, gallstones, impaired liver function, severe hypoproteinemia (dangerously low levels of protein in the blood), and kidney injury.14
Vitamin and mineral deficiency may also occur with some ketogenic diets, but the use of a
multivitamin/multimineral supplement can easily prevent this.15
Many drugs can impair the body’s ability to absorb or metabolize certain nutrients; however, anticonvulsants are particular offenders. Meaningful evidence indicates that common anticonvulsants interfere with the body’s handling of
vitamin D, and
vitamin K. In addition, one anticonvulsant, valproic acid, affects the nutrient-like substance
carnitine. For these reasons, it is often recommended that people using anticonvulsants take supplements that provide these nutrients.
However, there’s a potential catch to correcting such “nutrient depletions.” In some cases, taking the nutrient can impair the absorption or alter the metabolism of anticonvulsant drugs. In other cases, it is possible that nutrient depletion is part of how the anticonvulsant operates! For this reason, physician supervision is essential when taking any supplements.
For more information, see the full articles on
Folate (also known as folic acid) is a B vitamin that plays an important role in many vital aspects of health. Unfortunately, most drugs used for preventing seizures can reduce levels of folate in the body.16-21 In turn, low serum folate levels can cause elevated levels of homocysteine, possibly increasing the risk of heart disease.22
Low folate levels are also linked to increased risk of a variety of birth defects. Because anticonvulsant drugs deplete folate, babies born to women taking anticonvulsants are at increased risk for such birth defects.
However, the case for taking extra folate is complicated by the fact that high folate levels may speed up the normal breakdown of phenytoin
and possibly other anticonvulsants. This could lead to breakthrough seizures. For this reason, folate supplementation during anticonvulsant therapy should always be supervised by a physician.
Numerous anticonvulsants can reduce body levels of the essential vitamin
biotin, probably by interfering with its absorption.23,24
Valproic acid may affect biotin to a lesser extent than other anticonvulsants.
It is not clear whether this biotin deficiency actually causes any problems. Nonetheless, it is not good to be short on any essential nutrient, and for this reason biotin supplementation has been recommended during long-term anticonvulsant therapy. Keep in mind, though, that the action of anticonvulsant drugs may be at least
partly related to their effect on biotin levels. For this reason, physician supervision is strongly advised before adding biotin to an anticonvulsant regimen.
Many anticonvulsant drugs increase the risk of
osteoporosis and other bone disorders.25,26
This is believed to be due in part to the fact that they impair calcium metabolism (see also the sections on vitamin D and vitamin K below). Effects on calcium may also
increase the tendency toward seizures by lowering blood levels of calcium.26
Calcium supplementation may thus be beneficial for people taking anticonvulsant drugs. However, some studies indicate that antacids containing calcium carbonate interfere with the absorption of phenytoin and perhaps other anticonvulsants.27,28
For this reason, calcium supplements and anticonvulsant drugs should be taken several hours apart.
Anticonvulsant drugs may interfere with the activity of
vitamin D; this may be another contributing factor to anticonvulsant-induced bone problems.29-31
Vitamin D supplementation may help prevent bone loss.79 Adequate sunlight exposure may also help because sunlight causes the body to manufacture the vitamin D.32
Phenytoin, carbamazepine, phenobarbital, and primidone speed up the normal breakdown of
vitamin K into inactive byproducts, thus depriving the body of active vitamin K. Use of these anticonvulsants by pregnant mothers can lead to vitamin K deficiencies in their unborn babies, resulting in bleeding disorders or facial-bone abnormalities in the newborns.33,34
For this reason, mothers who take these anticonvulsants may need vitamin K supplementation during pregnancy.
In other circumstances, anticonvulsants seldom deplete vitamin K enough to cause bleeding problems. However, vitamin K deficiency may contribute to anticonvulsant-induced osteoporosis.
Valproic acid (Depakene) and possibly other anticonvulsants may reduce the body’s levels of the substance
For this reason it has been suggested that people using these drugs should take supplemental carnitine. However, there is no evidence as yet that
taking carnitine will provide any noticeable benefit; the one study that did attempt to evaluate this possibility failed to discern any meaningful effect.45
traditional Chinese herbal remedies known by the Japanese names saiko-keishi-to and sho-saiko-to have also been suggested for epilepsy, but the supporting evidence for their use remains highly preliminary.46-48
Both of these combination treatments consist of bupleurum, peony root, pinellia root, cassia bark,
ginger root, jujube fruit,
Asian ginseng root, Asian skullcap root, and
licorice root, but the proportions vary.
A double-blind study performed in Iran reportedly found that use of an extract of the seed of the
Nigella sativa plant helped control seizures in children.80
Weak evidence suggests that the amino acid
taurine might offer modest, short-term benefits in epilepsy.49-51
Results are inconsistent regarding whether the use of
fish oil can decrease seizure frequency in people with epilepsy.68,81
Several studies by a single research group hint that the supplement
melatonin may improve quality of life in children with epilepsy.52, 69-72
People with epilepsy have lower-than-normal levels of the mineral
manganese in their blood.53
This suggests (but doesn't prove) that manganese supplements might be helpful for epilepsy
Other supplements sometimes suggested for epilepsy (but with no meaningful supporting evidence) include
glycine. Herbs traditionally regarded as “nervines” or nerve-relaxants are also sometimes proposed, such as the following:
However, there is no meaningful evidence that they can help, and some of these herbs present significant safety concerns.
Note: Most herbs used for epilepsy are sedatives, as are many anticonvulsant drugs. Combination treatment could lead to dangerous over-sedation. People with epilepsy should, therefore, seek medical supervision before using any herbs or supplements.
A special form of
electromagnetic therapy called rTMS has shown promise for epilepsy. In a double-blind, placebo-controlled trial, 24 participants with epilepsy localized to a specific part of the brain and not fully responsive to drug treatment were given twice daily treatment with rTMS or sham rTMS for a week.54
The results showed a mild reduction in seizures among the participants given real rTMS. However, the benefits rapidly disappeared when treatment was stopped.
Weak evidence hints that
food allergen identification and avoidance
may be helpful for people with both
Acupuncture showed promise of reducing seizure frequency in some people with epilepsy in a review of 17 randomized trials with 1,538 people. The trials compared acupuncture (alone or with medication) to placebo or sham acupuncture; or medications or no treatment. Although some had a lower frequency rate of seizures with acupuncture alone or with medications, the quality of the trials was low, reducing the reliability of results. Current evidence does not support the use of acupuncture as treatment for epilepsy.84
Yoga has also been studied as a potential treatment. A review of 2 randomized trials involving 50 people found mixed results. One trial comparing real yoga to sham yoga or no treatment found that real yoga did reduce the frequency and duration of seizures. But, another trial did not support the use of yoga. The researchers all emphasized the need for more studies.83, 85
Numerous herbs and supplements have been associated with unexpected or unexpectedly severe seizures.67
In most cases, however, the evidence linking any particular natural product to increased seizure activity remains circumstantial. Some of the more worrisome potential “pro-seizure” agents are discussed here. In addition, we discuss herbs and supplements that may interact with medications used for seizures. See also the discussion of
Ginkgo seeds contain a seizure-promoting substance called 4-methoxypyridoxine (MPN).57
seeds are seldom used today, seizures have also been reported with the use of the more normal form of the herb: ginkgo leaf extract.58,59,73
One possible explanation is that ginkgo-leaf products may have been contaminated ginkgo seeds. Another possibility has been proposed as well: ginkgo may affect the brain in ways similar to tacrine, a drug also used to improve memory and which has been associated with seizures. Finally, it has been suggested that ginkgo might impair the effectiveness of dilantin and depakote. Regardless of the explanation, people with epilepsy should probably avoid ginkgo.
Many anti-epilepsy drugs work by blocking the effects of a substance called glutamate; for this reason, high dosages of the closely-related amino acid
could conceivably overwhelm these drugs and pose a risk to people with epilepsy.
Manufacturers of the supplement
warn that it might increase seizure risk.
Tea made from the herb
is thought to be safe, but hyssop essential oil, like most
essential oils, is toxic in excessive doses. Some of the constituents of hyssop oil are thought to increase risk of seizures.74,75
For this reason, hyssop essential oil should not be used by people with epilepsy.
Japanese star-anise contains substances that can trigger seizure activity.76-78
Some evidence hints that the supplement
5-HTP could potentially exacerbate or initiate a seizure-related illness called myoclonic seizure disorder.60,61
Grapefruit juice slows the body's normal breakdown of several drugs, including the anticonvulsant
carbamazepine, allowing it to build up to potentially dangerous levels in the blood; this effect can last for 3 days or more following the last glass of juice.62
ipriflavone might increase levels of carbamazepine and phenytoin, potentially raising the risk of side effects.63
white willow, also known as willow bark, is used to treat pain and fever. White willow contains a substance closely related to aspirin known as salicin. Aspirin is known to increase phenytoin levels and toxicity during long-term use of both drugs.64
This raises the concern that white willow might have similar effects on phenytoin, though this has not been proven.
Nicotinamide appears to increase blood levels of carbamazepine and primidone, possibly requiring a reduction in drug dosage to prevent toxic effects.65
Early reports suggested the possibility that the supplement
gamma-linolenic acid (GLA) might worsen temporal lobe epilepsy.66
However, there has been no later confirmation of this.
Prasad AN, Stafstrom CF, Holmes GL. Alternative epilepsy therapies: the ketogenic diet, immunoglobulins, and steroids.
Vining EPG, Freemen JM, Ballaban-Gil K, et al. A multicenter study of the efficacy of the ketogenic diet.
Freeman JM, Vining EP, Pillas DJ, et al. The efficacy of the ketogenic diet-1998: a prospective evaluation of intervention in 150 children.
Neelam GK, Koehler AN, McGhee B, et al. The ketogenic diet in refractory epilepsy: the experience of Children’s Hospital of Pittsburgh.
Mak SC, Chi CS, Wan CJ. Clinical experience of ketogenic diet on children with refractory epilepsy.
Acta Paediatr Taiwan.
Lefevre F, Aronson N. Ketogenic diet for the treatment of refractory epilepsy in children: a systematic review of efficacy.
Wing RR, Vazquez JA, Ryan CM. Cognitive effects of ketogenic weight-reducing diets.
Int J Obes Relat Metab Disord.
Woody RC, Steele RW, Knapple WL, et al. Impaired neutrophil function in children with seizures treated with the ketogenic diet.
Hassan AM, Keene DL, Whiting SE, et al. Ketogenic diet in the treatment of refractory epilepsy in childhood.
Herzberg GZ, Fivush BA, Kinsman SL, et al. Urolithiasis associated with the ketogenic diet.
Swink TD, Vining EP, Freeman JM. The ketogenic diet: 1997.
Bloom WL, Azar GJ. Similarities of carbohydrate deficiency and fasting: weight loss, electrolyte excretion, and fatigue.
Arch Intern Med.
Berry-Kravis E, Booth G, Taylor A, et al. Bruising and the ketogenic diet: evidence for diet-induced changes in platelet function.
Ballaban-Gil K, Callahan C, O'Dell C, et al. Complications of the ketogenic diet.
Berkowitz VJ. A view on high-protein, low-carb diets [Letter response].
J Am Diet Assoc.
Kishi T, Fujita N, Eguchi T, et al. Mechanism for reduction of serum folate by antiepileptic drugs during prolonged therapy.
J Neurol Sci.
Reynolds EH. Mental effects of anticonvulsants, and folic acid metabolism.
Hendel J, Dam M, Gram L, et al. The effects of carbamazepine and valproate on folate metabolism.
Acta Neurol Scand.
Berg MJ, Stumbo PJ, Chenard CA, et al. Folic acid improves phenytoin pharmacokinetics.
J Am Diet Assoc.
Lewis DP, Van Dyke DC, Willhite LA, et al. Phenytoin-folic acid interaction.
Lewis DP, Van Dyke DC, Stumbo PJ, et al. Drug and environmental factors associated with adverse pregnancy outcomes. Part I: Antiepileptic drugs, contraceptives, smoking, and folate.
Arenz A, Klein M, Fiehe K. Occurrence of neurotoxic 4'-O-methylpyridoxine in Ginkgo biloba leaves, ginkgo medications and Japanese ginkgo food.
Said HM, Redha R, Nylander W. Biotin transport in the human intestine: inhibition by anticonvulsant drugs.
Am J Clin Nutr.
Krause KH, Bonjour JP, Berlit P, et al. Biotin status of epileptics.
Ann N Y Acad Sci.
Wahl TO, Gobuty AH, Lukert BP. Long-term anticonvulsant therapy and intestinal calcium absorption.
Clin Pharmacol Ther.
Weinstein RS, Bryce GF, Sappington LJ, et al. Decreased serum ionized calcium and normal vitamin D metabolite levels with anticonvulsant drug treatment.
J Clin Endocrinol Metab.
Carter BL, Garnett WR, Pellock JM, et al. Effect of antacids on phenytoin bioavailability.
Ther Drug Monit.
McElnay JC, Uprichard G, Collier PS. The effect of activated dimethicone and a proprietary antacid preparation containing this agent on the absorption of phenytoin.
Br J Clin Pharmacol.
Hahn TJ, Hendin BA, Scharp CR, et al. Effect of chronic anticonvulsant therapy on serum 25-hydroxycalciferol levels in adults.
N Engl J Med.
Jubiz W, Haussler MR, McCain TA, et al. Plasma 1,25-dihydroxyvitamin D levels in patients receiving anticonvulsant drugs.
J Clin Endocrinol Metab.
Brodie MJ, Boobis AR, Dollery CT, et al. Rifampicin and vitamin D metabolism.
Clin Pharmacol Ther.
Williams C, Netzloff M, Folkerts L, et al. Vitamin D metabolism and anticonvulsant therapy: effect of sunshine on incidence of osteomalacia.
South Med J.
Cornelissen M, Steegers-Theunissen R, Kollee L, et al. Increased incidence of neonatal vitamin K deficiency resulting from maternal anticonvulsant therapy.
Am J Obstet Gynecol.
Cornelissen M, Steegers-Theunissen R, Kollee L, et al. Supplementation of vitamin K in pregnant women receiving anticonvulsant therapy prevents neonatal vitamin K deficiency.
Am J Obstet Gynecol.
Hug C, McGraw CA, Bates SR, et al. Reduction of serum carnitine concentrations during anticonvulsant therapy with phenobarbital, valproic acid, phenytoin, and carbamazepine in children.
Chung S, Choi J, Hyun T, et al. Alterations in the carnitine metabolism in epileptic children treated with valproic acid.
J Korean Med Sci.
Melegh B, Trombitas K. Valproate treatment induces lipid globule accumulation with ultrastructual abnormalities of mitochondria in skeletal muscle.
Zelnik N, Fridkis I, Gruener N. Reduced carnitine and antiepileptic drugs: cause relationship or co-existence?
Coulter DL. Carnitine deficiency in epilepsy: risk factors and treatment.
J Child Neurol.
Melegh B, Pap M, Morava E, et al. Carnitine-dependent changes of metabolic fuel consumption during long-term treatment with valproic acid.
De Vivo DC, Bohan TP, Coulter DL, et al. L-carnitine supplementation in childhood epilepsy: current perspectives.
Matsuda I, Ohtani Y. Carnitine status in Reye and Reye-like syndromes.
Camina MF, Rozas I, Gomez M, et al. Short-term effects of administration of anticonvulsant drugs on free carnitine and acylcarnitine in mouse
serum and tissues.
Br J Pharmacol.
Rodriguez-Segade S, de la Pena CA, Tutor JC, et al. Carnitine deficiency associated with anticonvulsant therapy.
Clin Chim Acta.
Freeman JM, Vining EP, Cost S, et al. Does carnitine administration improve the symptoms attributed to anticonvulsant medications?: a double-blinded, crossover study.
1994;93(6 pt 1):893-895.
Yarnell EY, Abascal K. An herbal formula for treating intractable epilepsy: a review of the literature.
Alt Compl Ther.
Narita Y, Satowa H, Kokubu T, et al. Treatment of epileptic patients with the Chinese herbal medicine “saiko-keishi-to” (SK).
IRCS Med Sci.
Nagakubo S, Niwa S, Kumagai N, et al. Effects of TJ-960 on Sternberg’s paradigm results in epileptic patients.
Jpn J Psych Neur.
Durelli L, Mutani R. The current status of taurine in epilepsy.
Marchesi GF, Quattrini A, Scarpino O, et al. Therapeutic effects of taurine in epilepsy: a clinical and polyphysiographic study [in Italian; English abstract].
Riv Patol Nerv Ment.
Fukuyama Y, Ochiai Y. Therapeutic trial by taurine for intractable childhood epilepsies.
Fauteck JD, Schmidt H, Lerchl A, et al. Melatonin in epilepsy: First results of replacement therapy and first clinical results.
Biol Signals Recept.
Akram M, Sullivan C, Mack G, et al. What is the clinical significance of reduced manganese and zinc levels in treated epileptic patients?
Med J Aust.
Theodore WH, Hunter K, Chen R, et al. Transcranial magnetic stimulation for the treatment of seizures: A controlled study.
Egger J, Carter CM, Soothill JF, et al. Oligoantigenic diet treatment of children with epilepsy and migraine.
Kajiyama Y, Fujii K, Takeuchi H, et al. Ginkgo seed poisoning.
Granger AS. Ginkgo biloba precipitating epileptic seizures.
Gregory PJ. Seizure associated with Ginkgo biloba? [letter].
Ann Intern Med.
Coleman M. Myoclonus in the young after 5-hydroxytryptophan [letter].
N Engl J Med.
Hagan JJ, Hatcher JP, Slade PD. The role of 5-HT1D and 5-HT1A receptors in mediating 5-hydroxytryptophan induced myoclonic jerks in guinea pigs.
Eur J Pharmacol.
A to Z Drug Facts.
2nd ed. [book on CD-ROM]. St. Louis, MO: Facts and Comparisons; 2000.
Monostory K, Vereczkey L, Levai F, et al. Ipriflavone as an inhibitor of human cytochrome P450 enzymes.
Br J Pharmacol.
Inoue F, Walsh RJ. Folate supplements and phenytoin-salicylate interaction.
Bourgeois BF, Dodson WE, Ferrendelli JA. Interactions between primidone, carbamazepine, and nicotinamide.
Vaddadi KS. The use of gamma-linolenic acid and linoleic acid to differentiate between temporal lobe epilepsy and schizophrenia.
Tyagi A, Delanty N. Herbal remedies, dietary supplements, and seizures.
Yuen AW, Sander JW, Fluegel D, et al. Omega-3 fatty acid supplementation in patients with chronic epilepsy: A randomized trial.
Epilepsy Behav. 2005 Jul 7 [Epub ahead of print].
Gupta M, Aneja S, Kohli K. Add-on melatonin improves quality of life in epileptic children on valproate monotherapy: a randomized, double-blind, placebo-controlled trial.
Epilepsy Behav. 2004;5:316-321.
Gupta M, Aneja S, Kohli K, et al. Add-on melatonin improves sleep behavior in children with epilepsy: randomized, double-blind, placebo-controlled trial.
J Child Neurol. 2005;20:112-115.
Gupta M, Gupta YK, Agarwal S, et al. A randomized, double-blind, placebo controlled trial of melatonin add-on therapy in epileptic children on valproate monotherapy: effect on glutathione peroxidase and glutathione reductase enzymes.
Br J Clin Pharmacol.
Gupta M, Gupta YK, Agarwal S, et al. Effects of Add-on Melatonin Administration on Antioxidant Enzymes in Children with Epilepsy Taking Carbamazepine Monotherapy: A Randomized, Double-blind, Placebo-controlled Trial.
Kupiec T, Raj V. Fatal seizures due to potential herb-drug interactions with Ginkgo biloba.
J Anal Toxicol. 2006;29:755-758.
Hold KM, Sirisoma NS, Sparks SE, et al. Metabolism and mode of action of cis- and trans-3-pinanones (the active ingredients of hyssop oil).
Millet Y, Tognetti P, Lavaire-Perlovisi M, et al. [Experimental study of the toxic convulsant properties of commercial preparations of essences of sage and hyssop].
Rev Electroencephalogr Neurophysiol Clin. 1979;9:12-18.
Vandenberghe N, Pittion-Vouyouvitch S, Flesch F, Wagner M, et al. [An inaugural generalized tonic-clonic convulsive crisis following ingestion of Japanese star anise]
Presse Med. 2003;32:27-28.
Nakamura T, Okuyama E, Yamazaki M. Neurotropic components from star anise (Illicium verum Hook. fil.)
Chem Pharm Bull
(Tokyo). 1996;44:1908-1914. Erratum in:
Chem Pharm Bull
(Tokyo). 1996 ;44:2344.
Okuyama E, Nakamura T, Yamazaki M. Convulsants from star anise (Illicium verum Hook.F.).
Chem Pharm Bull
Mikati MA, Dib L, Yamout B, et al. Two randomized vitamin D trials in
ambulatory patients on anticonvulsants: Impact on bone.
Akhondian J, Parsa A, Rakhshande H. The effect of
Nigella sativa L.
(black cumin seed) on intractable pediatric seizures.
Med Sci Monit.
Bromfield E, Dworetzky B, Hurwitz S, et al. A randomized trial of polyunsaturated fatty acids for refractory epilepsy.
Ramaratnam S, Sridharan K.
Yoga for epilepsy. Cochrane Database Syst Rev.
Cheuk DK, Wong V. Acupuncture for epilepsy.
Cochrane Database Syst Rev.
Panebianco M, Sridharan K, Ramaratnam S. Yoga for epilepsy. Cochrane Database Syst Rev. 2015;5:CD001524
Last reviewed December 2015 by EBSCO CAM Review Board
EBSCO Information Services is fully accredited by URAC. URAC is an independent, nonprofit health care accrediting organization dedicated to promoting health care quality through accreditation, certification and commendation.
Please be aware that this information is provided to supplement the care provided by your physician. It is neither intended nor implied to be a substitute for professional medical advice. CALL YOUR HEALTHCARE PROVIDER IMMEDIATELY IF YOU THINK YOU MAY HAVE A MEDICAL EMERGENCY. Always seek the advice of your physician or other qualified health provider prior to starting any new treatment or with any questions you may have regarding a medical condition.
Copyright © EBSCO Information Services. All rights reserved.