8 replies to this topic

[Lovetolearn]

My cousin has recently been diagnosed with epilepsy. Are there any supplements out there that would have a chance of alleviating the symptoms, I.e. seizures and headaches? I tried to do a search on the forum but didn't really see anything plus I'm posting from my phone and its a real pain .

[YBC]

Look into black cummin (nigella sativa). I don't know if it could do anything for epilepsy that conventional meds can't, although it has other benifits as well.

[medievil]

GABA, serotonine, glutmate and other neurotransmitters all play a role in epilepsy, for example serotonine withdrawal brainzaps is convulsant activity, increasing serotonine could theoretically help.

[zorba990]

L-Taurine

[nootrope]

A ketogenic diet (high in fat, lots of coconut oil)... Bacopa or gotu kola maybe. But these may not be nearly as effective as conventional medicine in severe cases.

[brundall]

My wife has epilepsy and we have been trying for a few years to get a handle on it. She used to have her complex partial seizures about 4 times per month but since we tried the following mix of supplements they are now down to around once per 3 months which has greatly improved her quality of life. She takes the following daily:

Magnesium 500mg
Taurine 500mg
L -Theanine 150mg (raises GABA levels in the brain)
Vinpocetine 10mg (improves blood flow to the brain)

Another supplement that she hasn't tried yet but has shown a history of being helpful for epilepsy is Bacopa. Good luck with your cousin.

[Lovetolearn]

Wow thank you for all the replies. I will do some research on some of the suggestions here. Much appreciated

[YBC]

Nutmeg has shown some promise as well:

Abstract The purpose of this study was to investigate the anticonvulsant activity of the volatile oil of nutmeg, the dried seed kernel of Myristica fragrans Houtt, using well-established animal seizure models and to evaluate its potential for acute toxicity and acute neurotoxicity. The volatile oil of nutmeg (nutmeg oil) was tested for its effects in maximal electroshock, subcutaneous pentylenetetrazole, strychnine and bicuculline seizure tests. All the experiments were performed at the time of peak effect of nutmeg oil. Nutmeg oil showed a rapid onset of action and short duration of anticonvulsant effect. It was found to possess significant anticonvulsant activity against electroshock-induced hind limb tonic extension. It exhibited dose dependent anticonvulsant activity against pentylenetetrazole-induced tonic seizures. It delayed the onset of hind limb tonic extensor jerks induced by strychnine. It was anticonvulsant at lower doses, whereas weak proconvulsant at a higher dose against pentylenetetrazole and bicuculline induced clonic seizures. Nutmeg oil was found to possess wide therapeutic margin, as it did not induce motor impairment when tested up to 600 mL/kg in the inverted screen acute neurotoxicity test. Furthermore, the LD₅₀ (2150 mL/kg) value was much higher than its anticonvulsant doses (50-300 mL/kg). The results indicate that nutmeg oil may be effective against grand mal and partial seizures, as it prevents seizure spread in a set of established animal models. Slight potentiation of clonic seizure activity limits its use for the treatment of myoclonic and absence seizures. Copyright © 2008 John Wiley & Sons, Ltd.

Nigella sativa still has the most promise imo:

Abstract Summary: The anticonvulsant effects of thymoquinone, the major constituent of Nigella sativa seeds, were investigated using pentylenetetrazole (PTZ)- and maximal electroshock (MES)-induced seizure models. We also studied the effect of thymoquinone on pentobarbital-induced hypnosis, locomotor activity, and motor coordination. In PTZ-induced seizure, the intraperitoneally injection of thymoquinone with doses of 40 and 80 mg/kg, prolonged the onset of seizures and reduced the duration of myoclonic seizures. The protective effect of thymoquinone against mortality was 71.4% and 100% in the mentioned doses, respectively. In MES model, thymoquinone failed to reduce the duration of seizure, whereas exhibited a complete protection against mortality. In PTZ model, flumazenil (10 mg/kg, ip), an antagonist of benzodiazepine (BZD) site in the GABAA-BZD receptor complex, inhibited the prolongation of seizure latency, but did not show any effect on the duration of myoclonic seizures. Also, pretreatment with naloxone (0.1 and 0.3 mg/kg, ip) inhibited the prolongation of myoclonic seizure latency and antagonized the reduction of myoclonic seizure duration induced by thymoquinone (40 and 80 mg/kg) in the PTZ model. Moreover, thymoquinone (40 and 80 mg/kg) did not have any hypnosis effect in the pentobarbital-induced hypnosis, but impaired the motor coordination and reduced the locomotor activity. These results indicate that thymoquinone may have anticonvulsant activity in the petit mal epilepsy probably through an opioid receptor-mediated increase in GABAergic tone. ]

Abstract Introduction: Despite administration of numerous combinations of epileptic drugs, nearly 15% of childhood seizures are resistant to treatment and it is still a problem in pediatric practice. In traditional medicine, Nigella sativa was known to have anticonvulsant effects. Recent studies also have shown its anticonvulsant effects. Most of the properties of N. sativa or its extracts are mainly attributed to thymoquinone. It has been shown that thymoquinone has several therapeutic effects and no evidence of toxicity or side effects is reported. Materials and methods: In this pilot, double-blinded crossover clinical trial study on children with refractory epilepsy, thymoquinone with dose of 1mg/kg was administered as an adjunctive therapy and its effects on frequency of seizures were compared with those of a placebo. Twenty-two patients entered in the study. They were assigned in two groups and received either thymoquinone or placebo for a period of four weeks, and then during the two weeks of wash out period, they received only their pre-existing anti-epileptic drugs; then, after cross-overing, they received thymoquinone or placebo for a period of four weeks again. During these periods their effects on seizure frequency were investigated. Results: The reduction of frequency of seizures at the end of first period in comparison with the same period before the study demonstrated a significant difference between two groups (thymoquinone and placebo) (P=0.04). Also reduction of frequency of seizure has shown significant difference between two groups at the end of second period in comparison with end of first period (P=0.02). The parental satisfaction showed significant difference between the two groups at the end of the first period (P=0.03). Conclusion: It can be concluded that thymoquinone has anti-epileptic effects in children with refractory seizures.

[Lydiaunicorn]

(I know this is an old thread but I'll try posting my question here first as it is related to the topic...)

 

I am interested in trying taurine for my daughter's seizures and want to make sure it is safe for her. In this mouse study, it seems that taurine was helpful when injected but harmful when eaten? Would that mean the oral supplements you can purchse online would be harmful? Please help me understand.

 

 

Abstract

Parenteral injection of kainic acid (KA), a glutamate receptor agonist, causes severe and stereotyped behavioral convulsions in mice and is used as a rodent model for human temporal lobe epilepsy. The goal of this study is to examine the potential anti-convulsive effects of the neuro-active amino acid taurine, in the mouse model of KA-induced limbic seizures. We found that taurine (43 mg/Kg, s.c.) had a significant antiepileptic effect when injected 10 min prior to KA. Acute injection of taurine increased the onset latency and reduced the occurrence of tonic seizures. Taurine also reduced the duration of tonic-clonic convulsions and mortality rate following KA-induced seizures. Furthermore, taurine significantly reduced neuronal cell death in the CA3 region of the hippocampus, the most susceptible region to KA in the limbic system. On the other hand, supplementation of taurine in drinking water (0.05%) for 4 continuous weeks failed to decrease the number or latency of partial or tonic-clonic seizures. To the contrary, we found that taurine-fed mice showed increased susceptibility to KA-induced seizures, as demonstrated by a decreased latency for clonic seizures, an increased incidence and duration of tonic-clonic seizures, increased neuronal death in the CA3 region of the hippocampus and a higher post-seizure mortality of the animals. We suggest that the reduced susceptibility to KA-induced seizures in taurine-injected mice is due to an increase in GABA receptor function in the brain which increases the inhibitory drive within the limbic system. This is supported by our in vitro data obtained in primary neuronal cultures showing that taurine acts as a low affinity agonist for GABA(A) receptors, protects neurons against kainate excitotoxic insults and modulates calcium homeostasis. Therefore, taurine is potentially capable of treating seizure-associated brain damage.