The relevance of leptin to seizure susceptibility was recently highlighted by Erbayat-Altay and colleagues (2008) who demonstrated a significantly decreased threshold in leptin-deficient ob/ob mice to pentylenetetrazol-induced seizures. Indeed, leptin itself inhibits seizures induced by 4-aminopyridine and pentyelenetrazole-induced, possibly through blockade of AMPA receptor-mediated synaptic transmission (Xu et al., 2008). If the limiting of AMPA receptor-mediated transmission is a critical factor, it should be recalled this can also be accomplished by topiramate. With respect to the KD, the leptin signaling system is believed to contribute to slow weight gain associated with chronic treatment in both rodents and humans (Thio et al., 2006). KD-fed juvenile rodents had higher serum leptin levels and lower insulin levels than control rats fed a standard diet.
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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One potential explanation for the anticonvulsant action of the KD argues that increased ATP synthesis should produce a positive bioenergetic balance, allowing stabilization of the resting membrane potential via enhanced activity of Na+-K+-ATPase (Bough & Rho, 2007). Several decades ago, De Vivo and colleagues (1978) reported that the KD increased the total quantity of bioenergetic substrates (such as adenosine triphosphate, or ATP) and elevated the energy charge in rat brain. These changes were purported to stabilize the cell membrane, especially in the face of excessive excitation. Consistent with these observations, a later human study utilizing magnetic resonance spectroscopic techniques indicated that patients with epilepsy fed a KD had elevated phosphocreatine to creatine levels in the brain (Pan et al., 1999). Recently, using cDNA microarray technology, increased expression of the mitochondrial ATP synthase β,D subunit in mouse brain was reported after KD treatment (Noh et al., 2004). And in the most comprehensive study of this kind to date, the KD was found to enhance mitochondrial biogenesis and significantly increase the number of transcripts encoding energy metabolism genes in rats (Bough et al., 2006). This increase in bioenergetic capacity enabled hippocampal slices from these animals to better withstand metabolic challenge from low glucose exposure. Taken together, the prevailing notion has been that increased energy production and reserve capacity enable greater resistance to neuronal hyperexcitability and hypersynchrony.
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).
Olahraga adalah cara diet sehat yang paling mudah untuk Anda lakukan. Mengatur porsi makan saja tidak akan sukses menurunkan berat badan jika tidak dibarengi olahraga rutin. Pasalnya, tubuh Anda tetap perlu membakar ekstra kalori yang masuk ke dalam tubuh, sekaligus juga membentuk otot. Kalau bukan dengan olahraga, dengan cara apa lagi lemak tubuh bisa dihilangkan?