The fatty acids then flow into the bloodstream and are taken up by body tissues.  Once in the cells, the fatty acids are transported into the mitochondria of the cell to be metabolized carbon by carbon in a process called beta-oxidation. As glucose levels fall and fatty acid levels in the blood rise, the liver cells ramp up beta-oxidation which increases the amounts of a molecule called Acetyl-CoA. As the level of Acetyl-CoA rises, it is shunted to a process called ketogenesis. Ketogenesis generates a ketone body called acetoacetate first, and this ketone is then converted into the two other types of ketones: beta-hydroxybutyrate, and acetone.  Meanwhile, the glycerol part of the fat molecule gets converted into glucose in a process called gluconeogenesis, which means "make new sugar".
To understand exogenous ketones, you should know that there are three types of ketones: beta-hydroxybutyrate (BHB), acetoacetate (ACA) and acetone, and all three are the normal by-products of fat breakdown by your body. In much the same way as glucose, ketones can be used by your tissues, especially your brain, diaphragm and heart and are actually a far more efficient fuel source than glucose.
Epilepsy is one of the most common neurological disorders after stroke,[7] and affects around 50 million people worldwide.[8] It is diagnosed in a person having recurrent, unprovoked seizures. These occur when cortical neurons fire excessively, hypersynchronously, or both, leading to temporary disruption of normal brain function. This might affect, for example, the muscles, the senses, consciousness, or a combination. A seizure can be focal (confined to one part of the brain) or generalised (spread widely throughout the brain and leading to a loss of consciousness). Epilepsy can occur for a variety of reasons; some forms have been classified into epileptic syndromes, most of which begin in childhood. Epilepsy is considered refractory (not yielding to treatment) when two or three anticonvulsant drugs have failed to control it. About 60% of patients achieve control of their epilepsy with the first drug they use, whereas around 30% do not achieve control with drugs. When drugs fail, other options include epilepsy surgery, vagus nerve stimulation, and the ketogenic diet.[7]
The brain is composed of a network of neurons that transmit signals by propagating nerve impulses. The propagation of this impulse from one neuron to another is typically controlled by neurotransmitters, though there are also electrical pathways between some neurons. Neurotransmitters can inhibit impulse firing (primarily done by γ-aminobutyric acid, or GABA) or they can excite the neuron into firing (primarily done by glutamate). A neuron that releases inhibitory neurotransmitters from its terminals is called an inhibitory neuron, while one that releases excitatory neurotransmitters is an excitatory neuron. When the normal balance between inhibition and excitation is significantly disrupted in all or part of the brain, a seizure can occur. The GABA system is an important target for anticonvulsant drugs, since seizures may be discouraged by increasing GABA synthesis, decreasing its breakdown, or enhancing its effect on neurons.[7]

Once inside the mitochondrion, the dominant way that the bound fatty acids are used as fuel in cells is through β-oxidation, which cleaves two carbons off of the acyl-CoA molecule in every cycle to form acetyl-CoA.[24] Acetyl-CoA enters the citric acid cycle, where it undergoes an aldol condensation with oxaloacetate to form citric acid; citric acid then enters the tricarboxylic acid cycle (TCA), which harvests a very high energy yield per carbon in the original fatty acid.[25][26]


The ketogenic diet is usually initiated in combination with the patient's existing anticonvulsant regimen, though patients may be weaned off anticonvulsants if the diet is successful. Some evidence of synergistic benefits is seen when the diet is combined with the vagus nerve stimulator or with the drug zonisamide, and that the diet may be less successful in children receiving phenobarbital.[18]
“For events longer than 60 minutes, consuming 0.7 g carbohydrates·kg-1 body weight·h-1 (approximately 30-60 g·h-1) has been shown unequivocally to extend endurance performance. Consuming carbohydrates during exercise is even more important in situations when athletes have not carbohydrate-loaded, not consumed pre-exercise meals, or restricted energy intake for weight loss. Carbohydrate intake should begin shortly after the onset of activity; [and continue] at 15- to 20-min intervals throughout the activity.”
If you remain under your optimal net carbs limit, then you should enter ketosis within 2 to 3 days. But it can take up to 7 days. The fastest way to get into ketosis is to exercise on an empty stomach, in order to accelerate the depletion of glycogen in your body. You can also do a Fat Fast for a few days (eating more fat) to speed up the rate at which you enter ketosis AND start to cut out refined carbs (like sugar) before you go for full ketosis. Another option is to do a water fast, (only drinking water) which also speeds up getting into ketosis.
Lemons are also keto-friendly, so go ahead and add a spritz of lemon juice to your ice water. One typical lemon wedge has about 0.5  g of net carbohydrates and only 0.2 g of sugar. The fruit also offers  3.7 mg of vitamin C, which is 6.2 percent of the DV. Lemon water contains antioxidants that fight free radicals, and it also promotes healthy digestion, according to the Cleveland Clinic.
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