In 1921, Rollin Turner Woodyatt reviewed the research on diet and diabetes. He reported that three water-soluble compounds, β-hydroxybutyrate, acetoacetate, and acetone (known collectively as ketone bodies), were produced by the liver in otherwise healthy people when they were starved or if they consumed a very low-carbohydrate, high-fat diet.[10] Dr. Russell Morse Wilder, at the Mayo Clinic, built on this research and coined the term "ketogenic diet" to describe a diet that produced a high level of ketone bodies in the blood (ketonemia) through an excess of fat and lack of carbohydrate. Wilder hoped to obtain the benefits of fasting in a dietary therapy that could be maintained indefinitely. His trial on a few epilepsy patients in 1921 was the first use of the ketogenic diet as a treatment for epilepsy.[10]
There are three instances where there’s research to back up a ketogenic diet, including to help control type 2 diabetes, as part of epilepsy treatment, or for weight loss, says Mattinson. “In terms of diabetes, there is some promising research showing that the ketogenic diet may improve glycemic control. It may cause a reduction in A1C — a key test for diabetes that measures a person’s average blood sugar control over two to three months — something that may help you reduce medication use,” she says.

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Sleep enough – for most people at least seven hours per night on average – and keep stress under control. Sleep deprivation and stress hormones raise blood sugar levels, slowing ketosis and weight loss a bit. Plus they might make it harder to stick to a keto diet, and resist temptations. So while handling sleep and stress will not get you into ketosis on it’s own, it’s still worth thinking about.

The nerve impulse is characterised by a great influx of sodium ions through channels in the neuron's cell membrane followed by an efflux of potassium ions through other channels. The neuron is unable to fire again for a short time (known as the refractory period), which is mediated by another potassium channel. The flow through these ion channels is governed by a "gate" which is opened by either a voltage change or a chemical messenger known as a ligand (such as a neurotransmitter). These channels are another target for anticonvulsant drugs.[7]
One of the most basic and most profound benefits of a ketogenic diet is that it drastically lowers inflammation (1). This is mainly due to the reduced amount of free radical production that occurs when burning ketones for energy instead of glucose. Less inflammation allows for more energy production and an overall more efficiently functioning body. This allows for a heightened ability of the body to heal in many different aspects.
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keto diet before and after


One of the most basic and most profound benefits of a ketogenic diet is that it drastically lowers inflammation (1). This is mainly due to the reduced amount of free radical production that occurs when burning ketones for energy instead of glucose. Less inflammation allows for more energy production and an overall more efficiently functioning body. This allows for a heightened ability of the body to heal in many different aspects.
During the 1920s and 1930s, when the only anticonvulsant drugs were the sedative bromides (discovered 1857) and phenobarbital (1912), the ketogenic diet was widely used and studied. This changed in 1938 when H. Houston Merritt, Jr. and Tracy Putnam discovered phenytoin (Dilantin), and the focus of research shifted to discovering new drugs. With the introduction of sodium valproate in the 1970s, drugs were available to neurologists that were effective across a broad range of epileptic syndromes and seizure types. The use of the ketogenic diet, by this time restricted to difficult cases such as Lennox–Gastaut syndrome, declined further.[10]

The day before admission to hospital, the proportion of carbohydrate in the diet may be decreased and the patient begins fasting after his or her evening meal.[19] On admission, only calorie- and caffeine-free fluids[37] are allowed until dinner, which consists of "eggnog"[Note 8] restricted to one-third of the typical calories for a meal. The following breakfast and lunch are similar, and on the second day, the "eggnog" dinner is increased to two-thirds of a typical meal's caloric content. By the third day, dinner contains the full calorie quota and is a standard ketogenic meal (not "eggnog"). After a ketogenic breakfast on the fourth day, the patient is discharged. Where possible, the patient's current medicines are changed to carbohydrate-free formulations.[19]


Long-term use of the ketogenic diet in children increases the risk of slowed or stunted growth, bone fractures, and kidney stones.[18] The diet reduces levels of insulin-like growth factor 1, which is important for childhood growth. Like many anticonvulsant drugs, the ketogenic diet has an adverse effect on bone health. Many factors may be involved such as acidosis and suppressed growth hormone.[38] About one in 20 children on the ketogenic diet develop kidney stones (compared with one in several thousand for the general population). A class of anticonvulsants known as carbonic anhydrase inhibitors (topiramate, zonisamide) are known to increase the risk of kidney stones, but the combination of these anticonvulsants and the ketogenic diet does not appear to elevate the risk above that of the diet alone.[39] The stones are treatable and do not justify discontinuation of the diet.[39] Johns Hopkins Hospital now gives oral potassium citrate supplements to all ketogenic diet patients, resulting in one-seventh of the incidence of kidney stones.[40] However, this empiric usage has not been tested in a prospective controlled trial.[9] Kidney stone formation (nephrolithiasis) is associated with the diet for four reasons:[39]

Metabolic Syndrome Limited research, including a study published in November 2017 in the journal Diabetes & Metabolic Syndrome: Clinical Research & Reviews, has suggested that adults with metabolic disease following keto shed more weight and body fat compared with those on a standard American diet, which is heavy in processed food and added sugars. (6)

In the mid-1990s, Hollywood producer Jim Abrahams, whose son's severe epilepsy was effectively controlled by the diet, created the Charlie Foundation to promote it. Publicity included an appearance on NBC's Dateline programme and ...First Do No Harm (1997), a made-for-television film starring Meryl Streep. The foundation sponsored a multicentre research study, the results of which—announced in 1996—marked the beginning of renewed scientific interest in the diet.[1]
To say that the keto diet has become one of the most popular diets of recent years is a complete understatement. Case in point: There are more than one million searches on Google every month for the keto diet. It’s unique because the fad diet has captured the interest of people who want to lose weight — and there’s no shortage of reported success stories to be found.

There is a reason why we store hundreds of thousands of calories in the form of fat in our body and only about 2000 calories in the form of glucose (with only a small amount of this useable by the brain). The reason is simple - The body prefers fat as its fuel source. Mark Sisson explains this in his article ‘A metabolic Paradigm Shift, or Why Fat is the Preferred Fuel for Human Consumption’.

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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]

It seems strange that a diet that calls for more fat can raise “good” cholesterol and lower “bad” cholesterol, but ketogenic diets are linked to just that. It may be because the lower levels of insulin that result from these diets can stop your body from making more cholesterol. That means you’re less likely to have high blood pressure, hardened arteries, heart failure, and other heart conditions. It's unclear, however; how long these effects last.

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When you eat less than 50 grams of carbs a day, your body eventually runs out of fuel (blood sugar) it can use quickly. This typically takes 3 to 4 days. Then you’ll start to break down protein and fat for energy, which can make you lose weight. This is called ketosis. It's important to note that the ketogenic diet is a short term diet that's focussed on weight loss rather than the pursuit of health benefits. 
Insulin is a hormone that lets your body use or store sugar as fuel. Ketogenic diets make you burn through this fuel quickly, so you don’t need to store it. This means your body needs -- and makes -- less insulin. Those lower levels may help protect you against some kinds of cancer or even slow the growth of cancer cells. More research is needed on this, though.
Polycystic Ovary Syndrome (PCOS) Because women with the infertility condition PCOS are at a greater risk for diabetes and obesity, some clinicians recommend the keto diet, says Taylor Moree, RD, LD, of Balance Fitness and Nutrition in Atlanta. But PCOS is no different from most health conditions mentioned here: Long-term research on the safety is needed.

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