Polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA, C22: 6ω-3), arachidonic acid (AA, C20: 4ω-3), or eicosapentaenoic acid (EPA, C20: 5ω-3) have been reported to suppress voltage-gated sodium channels and L-type calcium channels in seizure-prone structures such as the hippocampus (Vreugdenhil et al., 1996). The KD produces elevations of both AA and DHA in serum (Fraser et al., 2003; Cunnane et al., 2002) and brain (Taha et al., 2005) of patients and animals, respectively, suggesting that these substrates might exert anticonvulsant effects by inhibiting sodium and calcium channels, like many anticonvulsant drugs (Xiao et al., 1997, 1998).
Jo is the creative food photographer and stylist behind healthy eating blog, Modern Food Stories. Jo's a testament that once you find the right approach for you, you can overcome poor health through the healing power of food. She believes the secret to radiant health starts and ends with a healthy gut so all her recipes are grain, gluten and refined sugar free. Most are also dairy-free.
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Trim Pill Keto helped me attain the very best body ever. I was From slimming straps to crash diets, I have tried what not, however, the problem was still there. Luckily, I got to learn about Trim Pill Keto from among my friends, and I thought to give it a go. I began using it, and this is the consequence — I’m now very slim, healthy and more beautiful. Not only this, I feel energetic and active during the day, and can comfortably wear my favorite outfits.
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The Trim Pill Keto a remarkable weight loss supplement Reduces the extra weight to give you a slim and trim body. It eliminates the Excess fat by the process of ketosis. It is a Well-known substitute for a ketogenic diet. The constant use of Trim Pill Keto with no jump to 90 days Generates skyrocket changes. It reduces the desire by the secretion of serotonin hormone. The super beneficial formula burns off the fat to reduce the weight harmlessly. It accelerates the metabolism by releasing energy that is senile. This energy keeps you active for a long.
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The scientific rationale for elucidating mechanisms of disease pathogenesis or of therapeutic interventions has been traditionally based upon the lofty goal of discovering novel treatments, ones that would be more efficacious than existing options and also be devoid of side-effects altogether. Moreover, in epilepsy research, disease prevention or modification has become the “holy grail”, such that we are no longer complacent with symptomatic treatment and increasing attention is being given to understanding the processes of anti-epileptogenesis itself. Researchers in the field of the ketogenic diet (KD) have also embraced these tenets and recently embarked on that all-too-familiar Quixotic journey, with the ultimate aim of reducing the “difficult” KD regimen to a simple pill. If achieved, this result would represent an ironic recapitulation of the early history of the KD in the United States. Although the KD experienced an initial surge of interest following its introduction in the early 1920’s, it was relegated to near obscurity by the emergence of a familiar drug known as phenytoin. Henceforth, until the mid 1990’s, clinicians – for obvious practical reasons – found it simpler to prescribe a pill rather than an exacting diet.
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Resep Cheesecake Pablo Keto ini saya modifikasi dari resepnya Yuda Bustara. Crust yang harusnya dari pastry saya ganti dengan campuran tepung keto dan tepung almond. Untuk cheesecakenya sendiri bahannya hampir sama, hanya saja gula saya ganti dengan pemanis Diabetasol dan saya tambahkan perasan jeruk lemon agar terasa lebih segar. Berhubung crustnya agak rapuh jadi harap …
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Over the past decade, much progress has been made in dissecting apart the mechanisms underlying the anticonvulsant (and potentially, neuroprotective) effects of the KD (Gasior et al., 2006; Bough & Rho, 2007). The complex systemic and metabolic changes induced by a high-fat, low-carbohydrate diet – not surprisingly – provide fertile ground for very innovative and speculative hypotheses linking certain adaptations to a net anticonvulsant effect, ones that by necessity take researchers back to the earlier days of introductory biochemistry and human physiology. While many intriguing concepts and research data have been reviewed systematically in the context of the international symposium from which this supplement stems, the fundamental question of how the KD works remains as tantalizing as ever.
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Brokoli bisa Anda andalkan sebagai salah satu makanan diet sehat. Hal ini karena brokoli rendah kalori namun kaya akan vitamin, serat, serta mineral. Bayangkan, satu gelas yang penuh dengan potongan brokoli hanya mengandung 30 kalori saja. Sementara untuk kandungan serat, brokoli memiliki serat sebanyak 5 gram yang dapat membantu Anda kenyang seharian.
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?
So the question remains, can the KD be packaged into a pill? At this stage, given our state of knowledge, the likely answer is NO. Then, could we take a polypharmacy approach and develop a number of pills, each with a distinct mechanistic target? Such a strategy would not be too different than what is practiced by adults – and especially, the elderly – who are by both necessity and choice on multi-drug regimens and/or multi-nutritional supplements, again with the goal of achieving health and warding off the ravages of aging and disease. There is likely no “magic bullet” that completely mirrors the anticonvulsant (and potential neuroprotective) effects of the KD; the same could be said for the treatment of the epilepsies – a group of related conditions with widely divergent etiologies, and hence a multiplicity of underlying pathophysiological mechanisms. Nevertheless, without dissecting the component pieces of the complex metabolic puzzle posed by the KD, we would again be left with only empiric observations, and to wonder curiously how a high-fat diet can exert such profound clinical effects.
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