Antojos de grasa

Baicalin, the primary flavonoid from Baikal skullcap (Scutellaria baicalensis), has demonstrated neuroprotective and anticonvulsant properties in animal seizure models. Studies show baicalin reduces hippocampal cell loss, mossy fiber sprouting, and oxidative damage in epileptic rodents, though direct seizure frequency reduction may not be the primary observed effect. It is recognized in peer-reviewed epilepsy research as a beneficial adjuvant.

Black cumin (Nigella sativa) has recognized traditional anticonvulsant use and has been tested in clinical trials. A double-blind crossover trial in children with refractory epilepsy found that thymoquinone (1 mg/kg, the main bioactive of Nigella sativa) significantly decreased mean seizure frequency versus placebo. Animal studies confirm anticonvulsant activity via opioid-mediated GABAergic enhancement.

Seed extracts of C. crista demonstrated significant anticonvulsant activity in multiple standard preclinical seizure models including pentylenetetrazole (PTZ), maximal electroshock, strychnine, and picrotoxin-induced convulsions in rodents. Medium and high doses (600–800 mg/kg) were effective.

Cannabidiol (CBD) is an FDA-approved treatment (Epidiolex®) for Dravet syndrome and Lennox-Gastaut syndrome, two severe forms of epilepsy. Landmark double-blind, placebo-controlled RCTs (GWPCARE1 and related trials) demonstrated mean seizure reductions of 39–67% in drug-resistant patients. CBD acts via GPR55 antagonism, TRPV1 desensitization, and adenosine reuptake inhibition rather than cannabinoid receptors.

Caprylic acid (C8) is the principal active fatty acid in the medium-chain triglyceride ketogenic diet (MCT-KD), a clinically established therapy for drug-resistant epilepsy. Animal studies confirm direct anticonvulsant activity independent of ketosis, and it potentiates valproate. Human use of the MCT-KD is supported by decades of paediatric clinical experience, though large RCTs specific to caprylic acid alone remain limited.

Chrysin demonstrates anticonvulsant activity in pentylenetetrazole (PTZ)-induced convulsions in rats, reducing lipid peroxidation and protein carbonylation. Its GABAergic mechanism—the same underlying its anxiolytic effects—provides pharmacological plausibility. All evidence is preclinical.

MCTs from coconut oil contribute to ketone production. The classical MCT-based ketogenic diet is an established, evidence-based treatment for drug-resistant childhood epilepsy. Whole coconut oil has lower MCT density than refined MCT oil used clinically, but it is a dietary source supporting ketogenesis relevant to epilepsy management.

CoQ10 has preclinical and mechanistic evidence supporting its use as adjunctive therapy in epilepsy. Animal studies show CoQ10 reduces seizure severity in PTZ and pilocarpine models, augments the effects of antiepileptic drugs like phenytoin and valproate, and protects against seizure-induced oxidative damage and neuronal loss. CoQ10 deficiency is linked to epileptic manifestations.

Daidzin has demonstrated antiepileptic/anticonvulsant activity in experimental animal models, attributed to its GABAergic mechanism. Multiple peer-reviewed studies consistently identify antiepileptic activity as a core neurological property. No human clinical trials have been conducted.

DHA, the primary omega-3 fatty acid of brain tissue, exerts anti-epileptic effects by increasing seizure latency in PTZ models and elevating cortical seizure thresholds. In a comparative clinical trial, epileptic patients receiving DHA (417 mg/day) had significantly fewer monthly seizures (11.9) than placebo (16.6). A 2025 meta-analysis of RCTs confirms omega-3/DHA supplementation reduces seizures in adults with drug-resistant epilepsy.

EPA has been tested as adjunctive anti-seizure therapy in clinical trials. In a 57-patient comparative trial, epileptic patients receiving EPA (386 mg/day) had 9.7 monthly seizures versus 16.6 in the placebo group and more seizure-free days. A 2025 meta-analysis of six RCTs confirmed significant seizure reductions with omega-3 (including EPA) supplementation in adults with drug-resistant epilepsy.

Folinic acid is the established treatment for cerebral folate deficiency (CFD) syndromes, including FOLR1-mutation–related folate transporter deficiency and folinic acid-responsive seizures (FARS) of the neonatal period. Clinical case series and reports document dramatic seizure reduction and developmental improvement with folinic acid therapy. It is not a general antiepileptic but has specific, well-documented efficacy in folate-transport–related epilepsies.

GE is one of the oldest documented TCM treatments for epilepsy and convulsions, and preclinical evidence for anticonvulsant/anti-epileptic properties is extensive. A 2016 ScienceDirect review specifically examined 'Gastrodia elata and epilepsy: Rationale and therapeutic potential.' Clinical use for epilepsy is documented in China.

Glutamic acid is mechanistically central to epilepsy: excess glutamatergic excitation via NMDA, AMPA, and kainate receptors underlies seizure generation and propagation. Clinical studies show elevated plasma glutamic acid in epileptic patients and their relatives. A small clinical trial found that oral glutamic acid reduced seizure frequency by over 40% in uncontrolled epilepsy patients.

Multiple preclinical studies demonstrate broad-spectrum anticonvulsant activity for Huperzine A across diverse seizure models, including genetic absence epilepsy, Dravet syndrome mouse models, and kainic acid-induced temporal lobe epilepsy. No human clinical trials have been published, but the mechanistic and animal data are robust. Clinical trials in Dravet syndrome have been planned.

Aegle marmelos extracts have been studied in preclinical models of epilepsy and convulsion, with multiple pharmacological reviews documenting anticonvulsant activity. AM is reported to produce beneficial effects in epilepsy through CNS mechanisms, including neuroinflammation reduction and antioxidant neuroprotection.

L-serine is the established treatment for seizures in serine-deficiency disorders (PHGDH, PSAT1, PSPH deficiencies), where patients may have up to 60–70 tonic-clonic seizures per day; L-serine supplementation causes significant seizure reduction or complete cessation in virtually all patients. L-serine treatment has also been associated with improvements in EEG and seizure frequency in GRIN-related epileptic encephalopathies involving NMDA-receptor loss-of-function.

Luteolin reduces seizure severity, frequency, and duration in multiple animal seizure models (PTZ, kainic acid) and preserves hippocampal neuronal integrity. It modulates GADD45B, MAPK, NF-κB, and PKA/CREB/BDNF pathways. Evidence is preclinical; no human trials have been conducted.

Magnesium is a well-recognized anticonvulsant agent, with intravenous magnesium an established treatment for eclamptic seizures. Magnesium deficiency is associated with increased epilepsy risk, and studies suggest that children with low serum magnesium have up to 75% response rates to magnesium supplementation with reduced seizure frequency. Magnesium helps maintain neuronal connections and inhibits excessive firing.

Human and animal studies document lower blood manganese levels in people with epilepsy, and manganese is a cofactor for glutamine synthetase—critical to regulating excitatory glutamate in the brain. MnSOD activity in mitochondria also modulates seizure susceptibility. Direct therapeutic evidence from human supplementation trials is absent.

The MCT ketogenic diet is a clinically established variant of ketogenic dietary therapy for drug-resistant epilepsy, particularly in children. Developed in the 1970s, it permits more dietary carbohydrate by deriving 30–60% of fat calories from MCT oil, achieving equivalent seizure control to the classical ketogenic diet. An early study reported >50% seizure reduction in two-thirds of treated children over 10 weeks.

Melatonin has been investigated as adjunctive therapy for epilepsy in multiple small clinical trials. A 2023 randomized double-blind placebo-controlled trial found melatonin significantly reduced the severity of epileptic seizures. Mechanistically, melatonin modulates neuronal activity by reducing glutamatergic and enhancing GABAergic neurotransmission, and its metabolite kynurenic acid is an endogenous anticonvulsant.

NAC has clinical evidence primarily in myoclonic epilepsy of the Unverricht-Lundborg type (progressive myoclonic epilepsy), where it has been used as an adjunctive treatment. A systematic review of NAC in psychiatry and neurology identified progressive myoclonic epilepsy as a condition with favorable clinical evidence. Broader anticonvulsant effects in other epilepsy types are primarily preclinical.

C. rotundus rhizome extract shows anticonvulsant activity in multiple rodent seizure models (MES- and PTZ-induced), with effects comparable to phenytoin and diazepam at 100 mg/kg oral dose. Flavonoids are considered the primary active constituents. Ethnobotanical use for epilepsy and convulsions is also documented.

Omega-3 fatty acids (particularly EPA and DHA) have been studied in multiple RCTs for epilepsy. A 2025 meta-analysis of six RCTs found a significant reduction of 9.49 seizures per month in adults with drug-resistant epilepsy receiving omega-3 supplementation. Proposed mechanisms include elevation of seizure thresholds, modulation of neuronal excitability, and dampening of neuroinflammatory cytokines.

Pyridoxal-5-phosphate (PLP), the biologically active form of vitamin B6, treats specific types of epilepsy—particularly PNPO deficiency—that do not respond to pyridoxine itself. It is a recognized treatment for vitamin B6-dependent epilepsies and acts directly as the cofactor for GABA synthesis. Clinical evidence includes documented seizure freedom in patients with PLP-responsive genetic epilepsies.

P. foetida demonstrates anticonvulsant activity in preclinical models. This property is documented in multiple review sources alongside the plant's sedative-anxiolytic effects, suggesting a broader CNS-modulating pharmacological profile. The activity is attributed to flavonoids and iridoid glycosides.

Resveratrol has been investigated as adjunctive therapy for epilepsy due to its neuroprotective and antioxidant properties. Animal studies show that resveratrol pretreatment significantly attenuates mitochondrial complex I dysfunction and oxidative stress during status epilepticus. It is included among natural interventions that may benefit epileptic patients in clinical protocol literature, with mechanistic evidence from preclinical models.

Rosmarinic acid has demonstrated anticonvulsant properties in preclinical seizure models, attributed primarily to GABA transaminase inhibition (raising brain GABA levels) and inhibition of excitatory neurotransmitter pathways. These are well-characterized preclinical mechanisms; no human RCTs for epilepsy with RA have been conducted.

S. indicus extract demonstrates anticonvulsant activity in two rodent seizure models, protecting against both pentylenetetrazole- and maximal electroshock-induced convulsions. Traditional Ayurvedic use for epilepsy is explicit and well-documented.

A. calamus rhizome has documented anticonvulsant activity in multiple animal seizure models, including the Maximal Electro Shock model, with effects compared directly to phenytoin. Traditional use for epilepsy in Ayurveda, Chinese medicine, and Indian tribal communities is extensively documented.

Swertiamarin, the key secoiridoid from Swertia, demonstrated significant anticonvulsant activity in a pilocarpine-induced seizure mouse model, delaying seizure onset and reducing hippocampal neuroinflammation. Traditional Ayurvedic use for epilepsy is also well documented. This preclinical study provides direct scientific evidence for the link.

Taurine is an inhibitory neuromodulator that decreases seizure activity by binding to GABA-A receptors and glycine receptors, and by elevating glutamic acid decarboxylase activity. Published clinical data (Mantovani and DeVivo) document its effects on seizures in epileptic patients, though only approximately one-third of patients respond favorably. It is recognized in peer-reviewed reviews as a nutrient that may reduce seizure frequency.

The ethanolic extract of Tylophora indica leaves has been evaluated for anticonvulsant activity in validated animal seizure models (maximal electroshock and pentylenetetrazole models), showing complete prevention of seizures at 100 mg/kg. The mechanisms identified include blockade of sodium channels and T-type calcium channels, consistent with established antiepileptic drug mechanisms.

Vitamin B6 (pyridoxine) is an established treatment for pyridoxine-dependent epilepsy, a genetically-defined condition in which vitamin B6 administration results in cessation of seizures. It also plays a well-documented role in converting excitatory glutamate to inhibitory GABA. Low pyridoxine levels are associated with worsened seizure control across multiple epilepsy subtypes.

Vitamin E (alpha-tocopherol) has been evaluated as adjunctive therapy for epilepsy in multiple randomized trials. Ogunmakan et al.'s double-blind RCT found that over 60% of pediatric epilepsy patients had reduced seizure frequency after three months of combined vitamin E and antiepileptic drug therapy. A 2025 systematic review and meta-analysis evaluated multiple RCTs of vitamin E in epilepsy.

Amber (Hu Po) is a historically documented TCM treatment for epilepsy and convulsions, especially in children. Animal studies show succinic acid delays chemically induced convulsions in mice. No human clinical trials for epilepsy using amber exist.

Ashwagandha has a documented history of use in Ayurvedic medicine for epilepsy, listed consistently in traditional texts and modern Ayurvedic formulations. The NIH LiverTox database and MSKCC integrative medicine resource both acknowledge traditional Ayurvedic use for epilepsy. Proposed mechanisms involve GABAergic modulation, but human clinical trial evidence is absent.

In Eastern Europe and Asia, decoctions of asparagus rhizomes and roots have traditionally been used for epilepsy, as documented in the PMC-published comprehensive review of A. officinalis pro-health activity. No clinical evidence for anti-epileptic efficacy exists.

Bacopa (Bacopa monnieri, brahmi) has been used in Ayurvedic medicine for approximately 5,000 years, with epilepsy listed as one of its primary indications in the Charaka Samhita. Preclinical animal studies show significant anticonvulsant effects via GABAergic and glutamatergic modulation, and some small clinical studies report reduced seizure frequency, though large RCT evidence is lacking.

Cowpea roots are traditionally used for epilepsy in African traditional medicine, documented by Kew Science and ethnobotanical literature. No human clinical trial has validated this use, and no mechanistic data is available for anticonvulsant activity.

Animal studies show M. pruriens seed extract has dose-dependent anticonvulsant effects in maximal electroshock and pentylenetetrazole seizure models in mice, restoring brain GABA levels. Ayurvedic and Unani texts document its use for seizures. No human clinical trials for epilepsy have been published.

Asafoetida is listed as an anti-epileptic in Moroccan pharmacopeia (where gum is chewed as antiepileptic) and in multiple global traditional medicine systems. Preclinical data show ferulic acid (a key asafoetida constituent) has anticonvulsant effects via GABAergic and nitric oxide pathways in rodent seizure models.

Indigo (I. tinctoria) has an extensive documented history in Ayurvedic, Siddha, TCM, and homeopathic traditions for epilepsy and seizure disorders, and animal studies confirm anticonvulsant activity via GABA modulation. No human clinical trials have been conducted.

Kava (Piper methysticum) has been used traditionally as a sedative herb for seizures and is noted in authoritative herbalism and epilepsy literature as having potential antiepileptic action via GABA-A receptor modulation by kavalactones. It appears in clinical compendiums as a traditional seizure remedy. Animal studies support anticonvulsant activity, though liver toxicity concerns limit its use.

Traditional use of lemon balm for epilepsy is documented in multiple historical sources including Iranian, European, and Middle Eastern pharmacopoeias. GABA-T inhibition by rosmarinic acid provides a mechanistic rationale directly analogous to the anticonvulsant drug vigabatrin. However, no human clinical trial for epilepsy has been published.

A. vulgaris is documented in European Pharmacopoeia homeopathic preparations and multiple ethnomedicinal systems for epilepsy and convulsive disorders. GABA-A receptor modulation by Artemisia constituents provides a mechanistic basis for anticonvulsant activity. One source describes seizure reduction in epileptic patients through moxibustion therapy, but controlled clinical evidence is absent.

TC is listed in Ayurveda and Siddha systems for epilepsy. Preclinical evidence shows TC extract has anticonvulsant effects and enhances the efficacy of sub-therapeutic doses of phenytoin and valproate in animal models, suggesting potential adjunctive therapy use.

Passionflower (Passiflora incarnata) has been used traditionally in Native American and European folk medicine for seizure and nervous disorders. Preclinical studies show that Passiflora extracts elicit GABA currents in hippocampal neurons and demonstrate anticonvulsant effects in animal models without sedation. Human clinical trial data for epilepsy specifically are lacking.

Skullcap (Scutellaria lateriflora, American skullcap) has a documented history of traditional use for epilepsy in both Native American and European folk medicine. Preclinical studies confirm modest anticonvulsant efficacy in PTZ-induced seizure models, attributed to GABA-A receptor affinity of its flavonoid constituents (particularly baicalin and scutellarein). Human clinical trial data are limited.

Epilepsy is documented as a traditional indication for P. hydropiper in ethnomedicinal literature from South and Central Asia. The plant is noted for CNS depressant and sedative properties in traditional systems, providing the basis for this use.

Valerian root has one of the longest documented histories as an anticonvulsant herb. In 1592, Fabio Colonna reported that powdered valerian root controlled his own epilepsy; by the late 18th century, it was considered among the best available treatments for seizures in Europe. Preclinical studies support anticonvulsant activity via GABAergic mechanisms, though human clinical trial evidence is lacking.

MP is documented in traditional Ayurvedic medicine for neurological disorders including epilepsy. Preclinical studies demonstrate anticonvulsant activity in PTZ, MES, picrotoxin, strychnine, and pilocarpine-induced seizure models in rodents, with proposed mechanisms involving GABAergic enhancement and Nrf2-mediated neuroprotection. No human clinical trials exist.

Epilepsy is a primary traditional indication for Bacopa monnieri in Ayurvedic medicine, mentioned in historical texts and in Ayurvedic formulations such as Brahmi Ghrita. Preclinical studies support anticonvulsant activity, but dedicated human RCTs for epilepsy are lacking.

Epilepsy ('the falling sickness') is listed in John Gerard's 1597 Herball and other classic texts as a traditional indication for wood betony. This is a historical folk use with no modern scientific or clinical support.