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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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.
Keto pills use a powerful fat burning ketone, Beta-hydroxybutyrate (BHB), which has been modified to produce the same fat burning results as the actual keto diet. Taking the keto pill daily will allow the BHB to start the keto process in your body. Your body will go into ketosis with a simple pill instead of having to eat certain foods to change your body’s fuel source from carbs to ketones. 

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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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It is important to weigh out the pros and cons of any formula before you decide to use it for long term. When you look at a supplement, the first thing that should come to your mind is the ingredients and the possible side effects. So, base your pros and cons on these two factors. After that, you can check the credibility of the company and the reviews of customers who have used the supplement before you. All these things help you learn about the supplement in detail.

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Many of our existing anticonvulsant medications exert effects on inhibitory neurotransmission, and more specifically, by enhancing synaptic levels of γ-aminobutyric acid (GABA) or modulating post-synaptic GABAA receptors (Meldrum & Rogawski, 2007; White et al., 2007). Examples of such agents include tiagabine, vigabatrin, benzodiazepines, barbiturates, felbamate, and topiramate. Thus, given the wealth of information regarding GABAergic neurotransmission, one possibility is that the KD, perhaps through ketone bodies, might be responsible for elevating synaptic levels of GABA, which would then yield an inhibitory (and potentially anticonvulsant) effect.
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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Untuk memperdalam ilmunya, beliau selalu aktif mengikuti pelatihan mengenai gizi dan nutrisi hingga asupan nutrisi untuk penderita penyakit metabolik dan degeneratif. Pada tahun 2019, beliau mendapatkan sertifikasi dari Harvard Medical School dalam mengikuti pelatihan mengenai “Obesity Medicine.” Beberapa kali beliau juga aktif menjadi narasumber acara mengenai gizi di televisi, radio, surat kabar, sosial media, hingga seminar. Di tengah aktivitasnya, beliau kini menjadi tim medis di Persatuan Atletik Seluruh Indonesia. Dokter Raissa bisa ditemui di tempat praktik pribadinya di Sawo 15 Menteng, atau di RS Pondok Indah - Puri Indah dan di RS Metropolitan Medical Center.

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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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