While the relationships between seizure activity, oxidative stress and neuronal injury have yet to be clarified, previous studies have indicated that defects in antioxidant systems may contribute to seizure genesis and epileptogenesis (Cock, 2002; Patel, 2004; Liang & Patel, 2006; Shin et al, 2008). Earlier, the effects of a KD on mitochondrial ROS generation were discussed. Are there other mechanisms through which oxidative stress can be attenuated in epileptic brain?

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Dikalangan para penggiat diet dan olahragawan menu diet 1 minggu ini tengah menjadi perbincangan. apa benar bisa menurunkan berat badan atau tidak. memang tidak sedikit orang yang meragukannya tapi tidak perlu khawatir banyak yang sudah mencoba program diet ini hasilnya bagus. dan jika anda ingin waktu yang lebih lama bisa mencoba menu diet cara menurunkan berat badan 10kg ala Sheina Malsiana salah satu peserta X-Faxtor Indonesia dengan ukuran badan jumbo.

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Slimlinic Keto enhancements appear alongside keto diet. It will give you mental clarity and lift the digestion of the body. Slimlinic Keto supplement will expand the dimension of serotonin and enable the fats to go about as fuel for the body when contrasted with the starches. You will feel light because the fixings present in this item assume a heavenly job in the detoxification of substantial metals.

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In rats fed a KD, Ziegler et al (2003) found an increase in antioxidant activity using a luminol oxidation assay in the hippocampus, and a four-fold increase in glutathione peroxidase activity. Consistent with these findings, Jarrett et al (2008) recently reported an up-regulation of GSH biosynthesis in adolescent rats fed a KD. Furthermore, these investigators observed improved mitochondrial antioxidant status, and proposed that these changes were responsible for preventing mitochondrial DNA from oxidant-induced damage. Collectively, these studies suggest that the KD may indeed exert neuroprotective activity.

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Thus, if fatty acids (and perhaps more specifically, polyunsaturated fatty acids or PUFAs), enhance mitochondrial uncoupling, and if this basic downstream mechanism is responsible for both anticonvulsant and neuroprotective effects (which has yet to be demonstrated), then could taking a chemical uncoupler such as 2,4-dinitrophenol (DNP) render the same effects? Of course, it is well known that DNP, a potent mitochondrial uncoupler that greatly increases the basal metabolic rate, and once used to treat obesity in the 1930’s, has a major untoward side-effect profile – namely, high fever and the risk of death. Clearly, if mitochondrial uncoupling were to represent the essential target, then less potent (and less toxic) compounds are required, and novel delivery systems need to be developed.

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Informasi yg sangat bermanfaat untuk kita semua yg sedang mencari pola makan sehat yang juga mampu meregenerasi sel tubuh dan jauh dari penyakit dan sudah terbukti dari living proof keto warriors (orang yg berjuang menjalankan pola makan sehat ketogenic)..Dan kita harus open minded menerima informasi yang jauh berbeda dari info yangkita dapat selama ini…. 

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While the relationships between seizure activity, oxidative stress and neuronal injury have yet to be clarified, previous studies have indicated that defects in antioxidant systems may contribute to seizure genesis and epileptogenesis (Cock, 2002; Patel, 2004; Liang & Patel, 2006; Shin et al, 2008). Earlier, the effects of a KD on mitochondrial ROS generation were discussed. Are there other mechanisms through which oxidative stress can be attenuated in epileptic brain?

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While the relationships between seizure activity, oxidative stress and neuronal injury have yet to be clarified, previous studies have indicated that defects in antioxidant systems may contribute to seizure genesis and epileptogenesis (Cock, 2002; Patel, 2004; Liang & Patel, 2006; Shin et al, 2008). Earlier, the effects of a KD on mitochondrial ROS generation were discussed. Are there other mechanisms through which oxidative stress can be attenuated in epileptic brain?

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Given these findings, it is not surprising that investigators have studied the effects of dietary supplementation with PUFAs alone, to determine whether these substrates can render an anticonvulsant effect. Early case reports suggested that seizures might be better controlled with this approach (Schlanger et al., 2002). However, a recent randomized trial in adult patients with epilepsy failed to demonstrate superiority of a PUFA supplement (EPA) plus DHA, 2.2 mg/day in a 3:2 ratio) over placebo (Bromfield et al., 2008). Thus, the jury is still out as to whether PUFAs alone can mirror the clinical effects of the KD. 

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