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.
Memasuki hari ke lima ini menu dietnya sudah boleh makan nasi tapi jangan terlalu banyak cukup makan nasih putih 5 sendok saja, satu hari boleh makan 2 porsi tapi jangan pada saat makan malam. anda bisa menambahkan Tomat mentah atau di rebus 8 potong untuk menambah Gizi makanan yang dikonsumsi. dan yang paling penting jangan sampai lupa porsi minum air putih ditambah.
Bagaimana saya bisa kehilangan 28 pon cepat
Apakah kopi yang baik untuk Hep C
Thus, if fatty acids (and perhaps more specifically, polyunsaturated fatty acids or PUFAs), enhance mitochondrial uncoupling, and if this basic downstream mechanism is responsible for both anticonvulsant and neuroprotective effects (which has yet to be demonstrated), then could taking a chemical uncoupler such as 2,4-dinitrophenol (DNP) render the same effects? Of course, it is well known that DNP, a potent mitochondrial uncoupler that greatly increases the basal metabolic rate, and once used to treat obesity in the 1930’s, has a major untoward side-effect profile – namely, high fever and the risk of death. Clearly, if mitochondrial uncoupling were to represent the essential target, then less potent (and less toxic) compounds are required, and novel delivery systems need to be developed.
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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.
Apa perbedaan antara minyak MCT dan minyak kelapa
Saya tidak berpikir beberapa hal lain yang Anda bicarakan dalam acara ini karena mari kita perjelas jika Anda terjatuh dan Anda memiliki roti kecil dengan burger itu dan Anda mengambil karbohidrat, pada dasarnya Anda sekarang menggunakan diet tinggi kalori, tinggi lemak, yang merupakan kebalikan dari apa yang Anda inginkan pada steak sedikit, sedikit kesalahan untuk membuat masalah besar terjadi pada tubuh Anda. Jadi, bisakah Anda benar-benar ketat tentang rencana makan diet ketogenik ini .
Bagaimana Anda gula siram keluar dari tubuh Anda
What investigators have elucidated over the past decade or so is that a variety of molecular, genetic, cellular, and metabolic factors are likely contributory to the clinical effects of the KD. As a generalization, it is becoming widely accepted that the mechanistic underpinnings of the KD are likely multiple, parallel, and possibly synergistic (Bough & Rho, 2007).
Given these observations, would it be practical to package acetoacetate or acetone into a pill? While ketone bodies in situ are likely to influence local cellular bioenergetics, there are profound logistical constraints precluding ease of administration in humans to achieve comparable low millimolar concentrations observed in clinical practice (Hartman & Vining, 2007). Acetoacetate is highly unstable, as it has an immediate tendency to spontaneously decarboxylate, and acetone is a well known solvent that can cause significant mucosal irritation. Finally, oral ingestion of β-hydroxybutyrate formulations to achieve such concentrations may not be readily achievable (Smith et al., 2005). These considerations pose not insignificant challenges toward the design of a ketone pill.
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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.
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Bagaimana Anda mendapatkan cukup lemak pada diet keto
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Historically, many anticonvulsant medications have resulted from structural modifications of lead compounds that had themselves been discovered serendipitously. The mechanistic bases for their effectiveness have typically been elucidated post-hoc. At present, it is unclear which of many potential mechanisms reviewed in this supplement are relevant to the clinical effects of the KD. It would be far too difficult to integrate these numerous possibilities into a single unifying hypothesis (or a final common pathway), or to consider them simultaneously. Nevertheless, it might be instructive to consider each of these putative mechanisms one by one and ask a simple comparative 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 perhaps invalidate) that particular hypothesis.
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