So, the natural question arises, do ketone bodies affect inhibitory (or excitatory) neurotransmission? Unfortunately, the answer is (at least for now) a fairly convincing no. Thio and colleagues (2000) showed that acute application of BHB and ACA did not affect: (1) excitatory post-synaptic potentials (EPSPs) and population spikes in CA1 pyramidal neurons after Schaffer collateral stimulation; (2) spontaneous epileptiform activity in the hippocampal-entorhinal cortex slice seizure model; and (3) whole-cell currents evoked by glutamate, kainate, and GABA in cultured hippocampal neurons.

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Furthermore, if the KD increases GABA levels in the brain, then such an effect is approximated by vigabatrin, an irreversible inhibitor of the degradative enzyme GABA-transaminase, as well as by tiagabine, a GABA re-uptake blocker that interferes with presnaptic GABA transporters (White et al., 2007). Yet, the anticonvulsant profile of the KD is distinct from that of vigabatrin and tiagabine (Hartman et al., 2007). The general approach of deriving another pill that enhances brain GABA levels may not be relevant or viable, since many seizure types seem to be exacerbated by agents that contribute to enhanced tonic inhibition, and extrasynaptic GABA receptors that mediate tonic inhibition are more sensitive to elevated ambient GABA concentrations (Sazgar & Bourgeois, 2005). Indeed, increased GABAergic inhibition in the cortex appears to underlie the mechanism of synchronization and seizure generation in two mouse models of autosomal dominant nocturnal frontal lobe epilepsy (Klassen et al, 2006)

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Over the past decade, much progress has been made in understanding the mechanisms of ketogenic diet (KD) action. From the complex systemic and metabolic changes induced by the KD have emerged innovative hypotheses attempting to link biochemical adaptations to its clinical effects. Despite such developments, the fundamental question of how the KD works remains as elusive as ever. At present, it is unclear which of many potential mechanisms proposed thus far are directly relevant to the clinical effects of the KD. It is unlikely that these numerous hypotheses can be unified into a single mechanism (or a final common pathway). Nevertheless, it may be instructive to consider each of these putative mechanisms in turn and ask the following question: If the mechanism or target in question is a critical determinant of the anticonvulsant efficacy of the KD, then would a similar intervention known to be based on that mechanism yield a comparable effect? Perhaps answering this question for each mechanistic speculation might help substantiate (or invalidate) that particular hypothesis. Can the KD be packaged into a pill? At present, the answer is likely “no.” We have yet to discover a “magic bullet” that completely mirrors the anticonvulsant (and potential neuroprotective) effects of the KD. However, without a clearer understanding of the mechanistic elements comprising the complex metabolic puzzle posed by the KD, we would be left only with empiric observations, and to wonder curiously how a high-fat diet can exert such profound clinical effects.
As mentioned above, this product uses a ketone called BHB. BHB is short for Beta-hydroxybutyrate, which your body makes naturally. It’s supposed to increase your energy and burn fat simultaneously. There are no studies, however, that verify these claims. Keto Pills attempt to simulate this process, but there is little evidence right now that corroborates these theories. There is some promising research for exogenous ketones. For example, this study concludes that exogenous ketone drinks effectively achieve ketosis. It should be mentioned that Keto Pills are not the same thing, so the comparison is a little unclear. Ketosis, by the way, is just a way of referring to the metabolic process of burning fat instead of carbohydrates for energy.
“With the start of the keto diet, the body switches from using sugar as a source of energy to using the body’s stored fat,” Rahnama explained. “In the process of breaking down fat, the body produces ketones, which are then removed by the body through frequent and increased urination. This may lead to dehydration and flu-like symptoms, such as fatigue, dizziness, irritability, nausea, and muscle soreness.”

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Alternatively, if simple calorie restriction is sufficient to prevent seizure activity in patients, why not decrease total caloric intake, and not bother with the high-fat KD? However, from yet another perspective, one could consider combining the KD and calorie restriction (as has been done in animal studies). In rats fed a calorie-restricted KD, Bough and colleagues (2003) demonstrated exhibited greater paired-pulse inhibition in the dentate gyrus, elevated maximal dentate activation threshold, and an absence of “spreading depression”-like events compared with ad libitum-fed controls. These results suggest that treatment with a calorie-restricted KD may produce both anticonvulsant and anti-epileptogenic 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.

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Even though there are many new supplements that are being made and released every day, Regal Keto remains the ultimate popular one because it has some matchless features that other formulas are deprived of. The supplement helps to trim your body and make it more attractive and handsome. Since the formula is ketosis-based, it helps in losing weight and also keeping the body active. If you try to lose weight by using a diet plan, you will feel that you get tired because you are not eating much and that can leave you exhausted. On the other hand, Regal Keto does not have any effect like this because it induces the burning of fat and that makes the body more energized due to high energy content that is present in lipids.

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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 …
The earliest demonstration of direct in vivo effects of ketone bodies was made by Keith in the early 1930’s, when he determined that acetoacetate, when administered intraperitoneally in rabbits, prevented seizures induced by thujone (1933), a convulsant constituent found in many essential oils and an antagonist of GABAA receptors (Höld et al., 2000). This seminal observation was later confirmed in an audiogenic seizure-susceptible mouse model (Rho et al., 2002). More intriguingly, however, Likhodii and colleagues (2003) established the broad anticonvulsant properties of acetone in four different animal models, and when injected intraperitoneally, produced plasma and cerebrospinal fluid (CSF) concentrations consistent with those used to suppress seizures. These results confirmed and extended historical observations supporting an anticonvulsant action for acetone, through as yet undetermined mechanisms (Likhodii & Burnham, 2002). And in further support of this, other investigators found that acetone was detectable (up to a concentration of 0.7 mM) in the brains of fully controlled KD-treated patients with epilepsy using proton magnetic resonance spectroscopy (Seymour et al, 1999).

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