As chronic obstructive pulmonary disease (COPD) advances, about 35% of patients experience severe weight loss called pulmonary cachexia, including diminished muscle mass.[31] Around 25% experience moderate to severe weight loss, and most others have some weight loss.[31] Greater weight loss is associated with poorer prognosis.[31] Theories about contributing factors include appetite loss related to reduced activity, additional energy required for breathing, and the difficulty of eating with dyspnea (labored breathing).[31]
After about two to seven days of following the keto diet, you go into something called ketosis, or the state your body enters when it doesn't have enough carbs for your cells to use for energy. That's when you start making ketones, or organic compounds that your bod then uses in place of those missing carbs. At this point, your body also starts burning fat for more energy, says Beth Warren, R.D., founder of Beth Warren Nutrition and author of Living A Real Life With Real Food.
Italiano: Perdere Peso, Español: bajar de peso, Deutsch: Abnehmen, Português: Perder Peso, Nederlands: Afvallen, Français: perdre du poids, Русский: сбросить вес, 中文: 减肥, Čeština: Jak zhubnout, Bahasa Indonesia: Menurunkan Berat Badan, 日本語: ダイエット, ไทย: ลดน้ำหนัก, Tiếng Việt: Giảm Cân, हिन्दी: वज़न कम करें (kaise vajan kam kare), 한국어: 체중 감량하는 법, Türkçe: Nasıl Kilo Verilir
On the ketogenic diet, carbohydrates are restricted and so cannot provide for all the metabolic needs of the body. Instead, fatty acids are used as the major source of fuel. These are used through fatty-acid oxidation in the cell's mitochondria (the energy-producing parts of the cell). Humans can convert some amino acids into glucose by a process called gluconeogenesis, but cannot do this by using fatty acids.[57] Since amino acids are needed to make proteins, which are essential for growth and repair of body tissues, these cannot be used only to produce glucose. This could pose a problem for the brain, since it is normally fuelled solely by glucose, and most fatty acids do not cross the blood–brain barrier. However, the liver can use long-chain fatty acids to synthesise the three ketone bodies β-hydroxybutyrate, acetoacetate and acetone. These ketone bodies enter the brain and partially substitute for blood glucose as a source of energy.[56]
It has totally regulated my appetite and normalised my relationship with food. My obsessive thoughts have completely subsided, my black and white thinking around food has gone, and I no longer binge! This is amazing. For the first time in my adult life I feel like I know what it is like to have a normal relatinoship with food. I eat when I eat, a range of healthy whole foods and occasional less healthy foods. In normal amounts. In manageable amounts. And when my meal is over, I stop! Normal for others, a seeming impossibility for me (and, I’m guessing, others with eating disorders).
^ Jump up to: a b c d e f g h i Payne, C; Wiffen, PJ; Martin, S (18 January 2012). Payne, Cathy (ed.). "Interventions for fatigue and weight loss in adults with advanced progressive illness". The Cochrane Database of Systematic Reviews. 1: CD008427. doi:10.1002/14651858.CD008427.pub2. PMID 22258985. (Retracted, see doi:10.1002/14651858.cd008427.pub3. If this is an intentional citation to a retracted paper, please replace {{Retracted}} with {{Retracted|intentional=yes}}.)
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]
The ketogenic diet is indicated as an adjunctive (additional) treatment in children and young people with drug-resistant epilepsy.[26][27] It is approved by national clinical guidelines in Scotland,[27] England, and Wales[26] and reimbursed by nearly all US insurance companies.[28] Children with a focal lesion (a single point of brain abnormality causing the epilepsy) who would make suitable candidates for surgery are more likely to become seizure-free with surgery than with the ketogenic diet.[9][29] About a third of epilepsy centres that offer the ketogenic diet also offer a dietary therapy to adults. Some clinicians consider the two less restrictive dietary variants—the low glycaemic index treatment and the modified Atkins diet—to be more appropriate for adolescents and adults.[9] A liquid form of the ketogenic diet is particularly easy to prepare for, and well tolerated by, infants on formula and children who are tube-fed.[5][30]
Conklin's fasting therapy was adopted by neurologists in mainstream practice. In 1916, a Dr McMurray wrote to the New York Medical Journal claiming to have successfully treated epilepsy patients with a fast, followed by a starch- and sugar-free diet, since 1912. In 1921, prominent endocrinologist Henry Rawle Geyelin reported his experiences to the American Medical Association convention. He had seen Conklin's success first-hand and had attempted to reproduce the results in 36 of his own patients. He achieved similar results despite only having studied the patients for a short time. Further studies in the 1920s indicated that seizures generally returned after the fast. Charles P. Howland, the parent of one of Conklin's successful patients and a wealthy New York corporate lawyer, gave his brother John Elias Howland a gift of $5,000 to study "the ketosis of starvation". As professor of paediatrics at Johns Hopkins Hospital, John E. Howland used the money to fund research undertaken by neurologist Stanley Cobb and his assistant William G. Lennox.[10]