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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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One of the nagging unresolved questions regarding ketone bodies is whether they correlate with seizure control. Recent studies have suggested that under certain conditions and in specific models, blood levels of ketones do not in fact correlate well with anticonvulsant effects (Hartman & Vining, 2007). However, ketone levels are known to vary considerably during the circadian cycle, mostly as a consequence of feeding schedules and subsequent metabolism of foodstuffs (DeGasquet et al., 1977). Despite numerous studies highlighting ketonemia following KD treatment, we still do not know what the true brain concentrations are, especially in the microenvironment of the highly metabolically active synapse. Moreover, there are other studies suggesting that high ketone body levels are not necessary for clinical efficacy of a high-fat diet against medically refractory epilepsies (Pfeifer & Thiele, 2005).
Jadi Anda benar-benar lebih khawatir tentang roti daripada burger? ya saya berpikir tentang hal itu bisakah Anda melakukan ini? ya saya benar-benar melakukannya dan Anda tahu sedang dan saya menyukainya. Apakah terstruktur, saya butuh aturan, saya pasti aturan ya. baik saya kira saya tertarik tetapi saya akan jika saya bisa berbicara secara terbuka tentang beberapa kekhawatiran saya.

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Resep Tumis Bunga Pepaya Kangkung Khas Manado ini kesukaan saya dan suami. Di awal-awal mencoba menbuat sendiri, saya tidak tahu caranya agar bunga pepaya tidak pahit. Saya pikir sama caranya dengan mengolah pare, agar tidak pahit diremas-remas dengan garam terlebih dahulu. Meskipun pahitnya berkurang, tapi bentuk bunga pepaya jadi tidak bagus. Ternyata ada cara yang …

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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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