Ketogenic Diet

Ketogenic diet - Wikipedia, the free encyclopedia
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Ketogenic diet
From Wikipedia, the free encyclopedia
The ketogenic diet is a high-fat, adequateprotein, low-carbohydrate diet that in medicine is

used primarily to treat diicult-to-control
(refractory) epilepsy in children. The diet forces
the body to burn fats rather than carbohydrates.
Normally, the carbohydrates contained in food are
converted into glucose, which is then transported
around the body and is particularly important in
fueling brain-function. However, if there is very
little carbohydrate in the diet, the liver converts
fat into fatty acids and ketone bodies. The ketone
bodies pass into the brain and replace glucose as
an energy source. An elevated level of ketone
bodies in the blood, a state known as ketosis, leads
to a reduction in the frequency of epileptic
seizures.[1]
Testing for ketone bodies in

urine
The original therapeutic diet for paediatric epilepsy provides just enough protein
for body growth and repair, and suicient calories[Note 1] to maintain the correct
weight for age and height. This classic ketogenic diet contains a 4:1 ratio by
weight of fat to combined protein and carbohydrate. This is achieved by excluding
high-carbohydrate foods such as starchy fruits and vegetables, bread, pasta,
grains and sugar, while increasing the consumption of foods high in fat such as
nuts, cream and butter.[1] Most dietary fat is made of molecules called long-chain
triglycerides (LCTs). However, medium-chain triglycerides (MCTs)made from
fatty acids with shorter carbon chains than LCTsare more ketogenic. A variant
of the classic diet known as the MCT ketogenic diet uses a form of coconut oil,
which is rich in MCTs, to provide around half the calories. As less overall fat is
needed in this variant of the diet, a greater proportion of carbohydrate and
protein can be consumed, allowing a greater variety of food choices.[2][3]
The classic therapeutic ketogenic diet was developed for treatment of paediatric
epilepsy in the 1920s and was widely used into the next decade, but its popularity
waned with the introduction of eective anticonvulsant drugs. In the mid-1990s,
Hollywood producer Jim Abrahams, whose son's severe epilepsy was eectively
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 lm starring Meryl Streep. The foundation
sponsored a multicentre research study, the results of whichannounced in
1996marked the beginning of renewed scientic interest in the diet. [1]
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Almost half of children and young people with epilepsy who have tried some form
of this diet saw the number of seizures drop by at least half, and the eect
persists even after discontinuing the diet.[4] The most common adverse eect is
constipation, aecting about 30% of patientsthis was due to uid restriction,
which was once a feature of the diet, but this led to increased risk of kidney
stones, and is no longer considered benecial.[4][5] There is some evidence that
adults with epilepsy may benet from the diet, and that a less strict regimen, such
as a modied Atkins diet, is similarly eective.[1] Clinical trials and studies in
animal models (including C. elegans[6]) suggest that ketogenic diets provide
neuroprotective and disease-modifying benets for a number of adult
neurodegenerative disorders.[7][8] As of 2012, there is limited clinical trial data in
these areas, and, outside of paediatric epilepsy, use of the ketogenic diet remains
at the research stage.[5][9][10]
Contents
1 Epilepsy
2 History
2.1 Fasting
2.2 Diet
2.3 Anticonvulsants and decline
2.4 MCT diet
2.5 Revival
3 Eicacy
3.1 Trial design
3.2 Outcomes
4 Indications and contra-indications
5 Interactions
6 Adverse eects
7 Implementation
7.1 Initiation
7.2 Maintenance
7.3 Discontinuation
8 Variants
8.1 Classic
8.2 MCT oil
8.3 Modied Atkins
8.4 Low glycemic index treatment
8.5 Prescribed formulations
8.6 Worldwide
9 Mechanism of action
9.1 Seizure pathology
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10
11
12
13
14
15
9.2 Seizure control

Other applications
See also
Notes
References
Further reading
External links
Epilepsy
Epilepsy is one of the most common neurological disorders after stroke,[11] and
aects at least 50million people worldwide.[12] It is diagnosed in a person having
recurrent unprovoked seizures. These occur when cortical neurons re
excessively, hypersynchronously, or both, leading to temporary disruption of
normal brain function. This might aect, for example, the muscles, the senses,
consciousness, or a combination. A seizure can be focal (conned to one part of
the brain) or generalised (spread widely throughout the brain and leading to a
loss of consciousness). Epilepsy may occur for a variety of reasons; some forms
have been classied 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 will achieve
control of their epilepsy with the rst drug they use, whereas about 30% do not
achieve control with drugs. When drugs fail, other options include epilepsy
surgery, vagus nerve stimulation and the ketogenic diet.[11]
History
The ketogenic diet is a mainstream therapy that does not use pharmaceutical
drugs, which was developed to reproduce the success and remove the limitations
of the non-mainstream use of fasting to treat epilepsy.[Note 2] Although popular in
the 1920s and 30s, it was largely abandoned in favour of new anticonvulsant
drugs.[1] Most individuals with epilepsy can successfully control their seizures
with medication. However, 2030% fail to achieve such control despite trying a
number of dierent drugs.[9] For this group, and for children in particular, the
diet has once again found a role in epilepsy management.[1][13]
Fasting
Physicians of ancient Greece treated diseases, including epilepsy, by altering their
patients' diet. An early treatise in the Hippocratic Corpus, On the Sacred Disease,
covers the disease; it dates from c.400 BC. Its author argued against the
prevailing view that epilepsy was supernatural in origin and cure, and proposed
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that dietary therapy had a rational and physical

basis.[Note 3] In the same collection, the author of
Epidemics describes the case of a man whose
epilepsy is cured as quickly as it had appeared,
through complete abstinence of food and
drink.[Note 4] The royal physician Erasistratus
declared, "One inclining to epilepsy should be
made to fast without mercy and be put on short
rations."[Note 5] Galen believed an "attenuating
diet"[Note 6] might aord a cure in mild cases and
be helpful in others.[14]
The rst modern study of fasting as a treatment for
epilepsy was in France in 1911.[15] Twenty
epilepsy patients of all ages were "detoxied" by
consuming a low-calorie vegetarian diet, combined
A news report of Dr Hugh
with periods of fasting and purging. Two beneted
Conklin's "water diet"
enormously, but most failed to maintain
treatment from 1922
compliance with the imposed restrictions. The diet
improved the patients' mental capabilities, in
contrast to their medication, potassium bromide, which dulled the mind.[16]
Around this time, Bernarr Macfadden, an American exponent of physical culture,
popularised the use of fasting to restore health. His disciple, the osteopathic
physician Hugh Conklin, of Battle Creek, Michigan, began to treat his epilepsy
patients by recommending fasting. Conklin conjectured that epileptic seizures
were caused when a toxin, secreted from the Peyer's patches in the intestines,
was discharged into the bloodstream. He recommended a fast lasting 18 to
25days to allow this toxin to dissipate. Conklin probably treated hundreds of
epilepsy patients with his "water diet" and boasted of a 90% cure rate in children,
falling to 50% in adults. Later analysis of Conklin's case records showed 20% of
his patients achieved freedom from seizures and 50% had some improvement. [13]
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 H. Rawle Geyelin
reported his experiences to the American Medical Association convention. He had
seen Conklin's success rst-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 Howland, the parent of one of Conklin's
successful patients and a wealthy New York corporate lawyer, gave his brother
John a gift of $5,000 to study "the ketosis of starvation". As professor of
paediatrics at Johns Hopkins Hospital, John Howland used the money to fund
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research undertaken by neurologist Stanley Cobb and his assistant William G.

Lennox.[13]
Diet
In 1921, Rollin Woodyatt reviewed the research on diet and diabetes. He reported
that three water-soluble compounds, -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. Russel 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 benets of fasting in a dietary
therapy that could be maintained indenitely. His trial on a few epilepsy patients
in 1921 was the rst use of the ketogenic diet as a treatment for epilepsy. [13]
Wilder's colleague, paediatrician Mynie Peterman, later formulated the classic
diet, with a ratio of one gram of protein per kilogram of body weight in children,
1015g of carbohydrate per day, and the remainder of calories from fat.
Peterman's work in the 1920s established the techniques for induction and
maintenance of the diet. Peterman documented positive eects (improved
alertness, behaviour and sleep) and adverse eects (nausea and vomiting due to
excess ketosis). The diet proved to be very successful in children: Peterman
reported in 1925 that 95% of 37 young patients had improved seizure control on
the diet and 60% became seizure-free. By 1930, the diet had also been studied in
100 teenagers and adults. Cliord Barborka, also from the Mayo Clinic, reported
that 56% of those older patients improved on the diet and 12% became
seizure-free. Although the adult results are similar to modern studies of children,
they did not compare as well to contemporary studies. Barborka concluded that
adults were least likely to benet from the diet, and the use of the ketogenic diet
in adults was not studied again until 1999.[13][17]
Anticonvulsants and decline

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 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 eective across a broad range of
epileptic syndromes and seizure types. The use of the ketogenic diet, by this time
restricted to diicult cases such as LennoxGastaut syndrome, declined
further.[13]
MCT diet
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In the 1960s, it was discovered that medium-chain

triglycerides (MCTs) produce more ketone bodies
per unit of energy than normal dietary fats (which
are mostly long-chain triglycerides).[18] MCTs are
more eiciently absorbed and are rapidly
transported to the liver via the hepatic portal
system rather than the lymphatic system.[19] The
severe carbohydrate restrictions of the classic
ketogenic diet made it diicult for parents to
produce palatable meals that their children would
tolerate. In 1971, Peter Huttenlocher devised a
ketogenic diet where about 60% of the calories
came from the MCT oil, and this allowed more
protein and up to three times as much
carbohydrate as the classic ketogenic diet. The oil
was mixed with at least twice its volume of
skimmed milk, chilled, and sipped during the meal
or incorporated into food. He tested it on twelve
Medium-chain triglyceride
children and adolescents with intractable seizures.
(MCT) oil emulsion
Most children improved in both seizure control and
alertness, results that were similar to the classic
ketogenic diet. Gastrointestinal upset was a
problem, which led one patient to abandon the diet, but meals were easier to
prepare and better accepted by the children.[18] The MCT diet replaced the
classic ketogenic diet in many hospitals, though some devised diets that were a
combination of the two.[13]
Revival
The ketogenic diet achieved national media exposure in the US in October 1994,
when NBC's Dateline television programme reported the case of Charlie
Abrahams, son of Hollywood producer Jim Abrahams. The two-year-old suered
from epilepsy that had remained uncontrolled by mainstream and alternative
therapies. Abrahams discovered a reference to the ketogenic diet in an epilepsy
guide for parents and brought Charlie to John Freeman at Johns Hopkins
Hospital, which had continued to oer the therapy. Under the diet, Charlie's
epilepsy was rapidly controlled and his developmental progress resumed. This
inspired Abrahams to create the Charlie Foundation to promote the diet and fund
research.[13] A multicentre prospective study began in 1994, the results were
presented to the American Epilepsy Society in 1996 and were published [20] in
1998. There followed an explosion of scientic interest in the diet. In 1997,
Abrahams produced a TV movie, ...First Do No Harm, starring Meryl Streep, in
which a young boy's intractable epilepsy is successfully treated by the ketogenic
diet.[1]
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By 2007, the ketogenic diet was available from around 75 centres in 45 countries,
and less restrictive variants, such as the modied Atkins diet, were in use,
particularly among older children and adults. The ketogenic diet was also under
investigation for the treatment of a wide variety of disorders other than
epilepsy.[1]
Eicacy
The ketogenic diet reduces seizure frequency by more than 50% in half of the
patients who try it and by more than 90% in a third of patients. [5] Three-quarters
of children who respond do so within two weeks, though experts recommend a
trial of at least three months before assuming it has been ineective. [9] Children
with refractory epilepsy are more likely to benet from the ketogenic diet than
from trying another anticonvulsant drug.[1] There is some evidence that
adolescents and adults may also benet from the diet.[9]
Trial design
Early studies reported high success rates: in one study in 1925, 60% of patients
became seizure-free, and another 35% of patients had a 50% reduction in seizure
frequency. These studies generally examined a cohort of patients recently treated
by the physician (what is known as a retrospective study) and selected patients
who had successfully maintained the dietary restrictions. However, these studies
are diicult to compare to modern trials. One reason is that these older trials
suered from selection bias, as they excluded patients who were unable to start
or maintain the diet and thereby selected from patients who would generate
better results. In an attempt to control for this bias, modern study design prefers
a prospective cohort (the patients in the study are chosen before therapy begins)
in which the results are presented for all patients regardless of whether they
started or completed the treatment (known as intent-to-treat analysis).[21]
Another dierence between older and newer studies is that the type of patients
treated with the ketogenic diet has changed over time. When rst developed and
used, the ketogenic diet was not a treatment of last resort; in contrast, the
children in modern studies have already tried and failed a number of
anticonvulsant drugs, so may be assumed to have more diicult-to-treat epilepsy.
Early and modern studies also dier because the treatment protocol has changed.
In older protocols, the diet was initiated with a prolonged fast, designed to lose
510% body weight, and heavily restricted the calorie intake. Concerns over child
health and growth led to a relaxation of the diet's restrictions. [21] Fluid restriction
was once a feature of the diet, but this led to increased risk of constipation and
kidney stones, and is no longer considered benecial.[5]
Outcomes
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A study with an intent-to-treat prospective design was published in 1998 by a

team from the Johns Hopkins Hospital[22] and followed-up by a report published
in 2001.[23] As with most studies of the ketogenic diet, there was no control group
(patients who did not receive the treatment). The study enrolled 150 children.
After three months, 83% of them were still on the diet, 26% had experienced a
good reduction in seizures, 31% had had an excellent reduction and 3% were
seizure-free.[Note 7] At twelve months, 55% were still on the diet, 23% had a good
response, 20% had an excellent response and 7% were seizure-free. Those who
had discontinued the diet by this stage did so because it was ineective, too
restrictive or due to illness, and most of those who remained were beneting from
it. The percentage of those still on the diet at two, three and four years was 39%,
20% and 12% respectively. During this period the most common reason for
discontinuing the diet was because the children had become seizure-free or
signicantly better. At four years, 16% of the original 150 children had a good
reduction in seizure frequency, 14% had an excellent reduction and 13% were
seizure-free, though these gures include many who were no longer on the diet.
Those remaining on the diet after this duration were typically not seizure-free but
had had an excellent response.[23][24]
It is possible to combine the results of several small studies to produce evidence
that is stronger than that available from each study alonea statistical method
known as meta-analysis. One of four such analyses, conducted in 2006, looked at
19 studies on a total of 1,084 patients.[25] It concluded that half the patients
achieved a 50% reduction in seizures and a third achieved a 90% reduction. [5]
A systematic review in 2012 found and analysed four randomized controlled trials
of ketogenic diet in children and young people with epilepsy, as well as six
prospective and ve retrospective studies.[4] The trials were done among children
and young people for whom drugs failed to control their seizures, and only one of
the trials compared a group assigned to ketogenic diet with a group not assigned
to one.[19] The other trials compared types of diets or ways of introducing them to
make them more tolerable.[4] Nearly 40% of the children and young people had
half or fewer seizures with the diet compared with the group not assigned to the
diet. Only about 10% were still on the diet after a few years. [4] Adverse eects
such as hunger and loss of energy in that trial were common, with about 30%
experiencing constipation.[19]
Indications and contra-indications

The ketogenic diet is indicated as an adjunctive (additional) treatment in children
with drug-resistant epilepsy.[27][28] It is approved by national clinical guidelines in
Scotland,[28] England and Wales[27] and reimbursed by nearly all US insurance
companies.[29] Children with a focal lesion (a single point of brain abnormality
causing the epilepsy) who would make suitable candidates for surgery are more
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likely to become seizure-free with surgery than

with the ketogenic diet.[9][30] In the UK, the
National Institute for Health and Clinical
Excellence advises that the diet should not be
recommended for adults with epilepsy.[27] About a
third of epilepsy centres that oer the ketogenic
diet also oer a dietary therapy to adults. Some
clinicians consider the two less restrictive dietary
variantsthe low glycemic index treatment and
the modied Atkins dietto 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.[3][31]
Advocates for the diet recommend that it be
seriously considered after two medications have
failed, as the chance of other drugs succeeding is
only 10%.[9][32][33] The diet can be considered
earlier for some epilepsy and genetic syndromes
where it has shown particular usefulness. These
include Dravet syndrome, infantile spasms,
myoclonic-astatic epilepsy and tuberous sclerosis
complex.[9][34]
Experts on the ketogenic diet

recommend it be strongly
considered for children with
uncontrolled epilepsy who
have tried and failed two or
three anticonvulsant drugs;[9]
most children who start the
ketogenic diet have failed at
least three times this
number.[26]
A survey in 2005 of 88 paediatric neurologists in the US found that 36% regularly

prescribed the diet after three or more drugs had failed; 24% occasionally
prescribed the diet as a last resort; 24% had only prescribed the diet in a few rare
cases; and 16% had never prescribed the diet. There are several possible
explanations for this gap between evidence and clinical practice.[35] One major
factor may be the lack of adequately trained dietitians, who are needed to
administer a ketogenic diet programme.[32]
Because the ketogenic diet alters the body's metabolism, it is a rst-line therapy
in children with certain congenital metabolic diseases such as pyruvate
dehydrogenase (E1) deciency and glucose transporter 1 deciency syndrome,
which prevent the body from using carbohydrates as fuel, leading to a
dependency on ketone bodies. The ketogenic diet is benecial in treating the
seizures and some other symptoms in these diseases and is an absolute
indication.[36] On the other hand, it is absolutely contraindicated in the treatment
of other diseases such as pyruvate carboxylase deciency, porphyria and other
rare genetic disorders of fat metabolism.[9] A person with a disorder of fatty acid
oxidation is unable to metabolise fatty acids, which replace carbohydrates as the
major energy source on the diet. On the ketogenic diet, their body would consume
its own protein stores for fuel, leading to ketoacidosis, and eventually coma and
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death.[37]
Interactions
The ketogenic diet is usually initiated in combination with the patient's existing
anticonvulsant regimen, though patients may be weaned o anticonvulsants if the
diet is successful. There is some evidence of synergistic benets 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.[5]
Adverse eects
The ketogenic diet is not a benign, holistic or natural treatment for epilepsy; as
with any serious medical therapy, there may be complications. [29] These are
generally less severe and less frequent than with anticonvulsant medication or
surgery.[29] Common but easily treatable short-term side eects include
constipation, low-grade acidosis and hypoglycaemia if there is an initial fast.
Raised levels of lipids in the blood aect up to 60% of children[38] and cholesterol
levels may increase by around 30%.[29] This can be treated by changes to the fat
content of the diet, such as from saturated fats towards polyunsaturated fats, and,
if persistent, by lowering the ketogenic ratio.[38] Supplements are necessary to
counter the dietary deciency of many micronutrients.[5]
Long-term use of the ketogenic diet in children increases the risk of slowed or
stunted growth, bone fractures and kidney stones.[5] 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 eect on bone health.
Many factors may be involved such as acidosis and suppressed growth
hormone.[38] About 1 in 20 children on the ketogenic diet will 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 a sevenfold
decrease in 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]
Excess calcium in the urine (hypercalciuria) occurs due to increased bone
demineralisation with acidosis. Bones are mainly composed of calcium
phosphate. The phosphate reacts with the acid, and the calcium is excreted
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by the kidneys.[39]
Hypocitraturia: the urine has an abnormally low concentration of citrate,
which normally helps to dissolve free calcium.[39]
The urine has a low pH, which stops uric acid from dissolving, leading to
crystals that act as a nidus for calcium stone formation.[39]
Many institutions traditionally restricted the water intake of patients on the
diet to 80% of normal daily needs;[39] this practice is no longer
encouraged.[5]
In adults, common side eects include weight loss, constipation, raised
cholesterol levels and, in women, menstrual irregularities including
amenorrhoea.[41]
Implementation
The ketogenic diet is a medical nutrition therapy that involves participants from
various disciplines. Team members include a registered paediatric dietitian who
coordinates the diet programme; a paediatric neurologist who is experienced in
oering the ketogenic diet; and a registered nurse who is familiar with childhood
epilepsy. Additional help may come from a medical social worker who works with
the family and a pharmacist who can advise on the carbohydrate content of
medicines. Lastly, the parents and other caregivers must be educated in many
aspects of the diet for it to be safely implemented.[3]
Implementing the diet can present diiculties for caregivers and the patient due
to the time commitment involved in measuring and planning meals. Since any
unplanned eating can potentially break the nutritional balance required, some
people nd the discipline needed to maintain the diet challenging and unpleasant.
Some people terminate the diet or switch to a less demanding diet, like the
modied Atkins diet (MAD) or the low-glycemic index treatment (LGIT) diet,
because they nd the diiculties too great.[42]
Initiation
The Johns Hopkins Hospital protocol for initiating the ketogenic diet has been
widely adopted.[43] It involves a consultation with the patient and their caregivers
and, later, a short hospital admission.[21] Because of the risk of complications
during ketogenic diet initiation, most centres begin the diet under close medical
supervision in hospital.[9]
At the initial consultation, patients are screened for conditions that may
contraindicate the diet. A dietary history is obtained and the parameters of the
diet selected: the ketogenic ratio of fat to combined protein and carbohydrate, the
calorie requirements and the uid intake.[21]
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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. [21]
On admission, only calorie- and caeine-free uids[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.[21]
When in the hospital, glucose levels are checked several times daily and the
patient is monitored for signs of symptomatic ketosis (which can be treated with a
small quantity of orange juice). Lack of energy and lethargy are common but
disappear within two weeks.[20] The parents attend classes over the rst three full
days, which cover nutrition, managing the diet, preparing meals, avoiding sugar
and handling illness.[21] The level of parental education and commitment required
is higher than with medication.[44]
Variations on the Johns Hopkins protocol are common. The initiation can be
performed using outpatient clinics rather than requiring a stay in hospital. Often
there is no initial fast (fasting increases the risk of acidosis and hypoglycaemia
and weight loss). Rather than increasing meal sizes over the three-day initiation,
some institutions maintain meal size but alter the ketogenic ratio from 2:1 to
4:1.[9]
For patients who benet, half achieve a seizure reduction within ve days (if the
diet starts with an initial fast of one to two days), three-quarters achieve a
reduction within two weeks, and 90% achieve a reduction within 23 days. If the
diet does not begin with a fast, the time for half of the patients to achieve an
improvement is longer (two weeks) but the long-term seizure reduction rates are
unaected.[44] Parents are encouraged to persist with the diet for at least three
months before any nal consideration is made regarding eicacy.[9]
Maintenance
After initiation, the child regularly visits the hospital outpatient clinic where he or
she is seen by the dietitian and neurologist, and various tests and examinations
are performed. These are held every three months for the rst year and then
every six months thereafter. Infants under one year old are seen more frequently,
with the initial visit held after just two to four weeks. [9] A period of minor
adjustments is necessary to ensure consistent ketosis is maintained and to better
adapt the meal plans to the patient. This ne-tuning is typically done over the
telephone with the hospital dietitian[21] and includes changing the number of
calories, altering the ketogenic ratio, or adding some MCT or coconut oils to a
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classic diet.[5] Urinary ketone levels are checked daily to detect whether ketosis
has been achieved and to conrm that the patient is following the diet, though the
level of ketones does not correlate with an anticonvulsant eect. [21] This is
performed using ketone test strips containing nitroprusside, which change colour
from bu-pink to maroon in the presence of acetoacetate (one of the three ketone
bodies).[45]
A short-lived increase in seizure frequency may occur during illness or if ketone
levels uctuate. The diet may be modied if seizure frequency remains high, or
the child is losing weight.[21] Loss of seizure-control may come from unexpected
sources. Even "sugar-free" food can contain carbohydrates such as maltodextrin,
sorbitol, starch and fructose. The sorbitol content of suntan lotion and other
skincare products may be high enough for some to be absorbed through the skin
and thus negate ketosis.[32]
Discontinuation
About 20% of children on the ketogenic diet achieve freedom from seizures, and
many are able to reduce the use of anticonvulsant drugs or eliminate them
altogether.[5] Commonly, at around two years on the diet, or after six months of
being seizure-free, the diet may be gradually discontinued over two or three
months. This is done by lowering the ketogenic ratio until urinary ketosis is no
longer detected, and then lifting all calorie restrictions.[46] This timing and
method of discontinuation mimics that of anticonvulsant drug therapy in children,
where the child has become seizure free. When the diet is required to treat
certain metabolic diseases, the duration will be longer. The total diet duration is
up to the treating ketogenic diet team and parents; durations up to 12 years have
been studied and found benecial.[9]
Children who discontinue the diet after achieving seizure freedom have about a
20% risk of seizures returning. The length of time until recurrence is highly
variable but averages two years. This risk of recurrence compares with 10% for
resective surgery (where part of the brain is removed) and 3050% for
anticonvulsant therapy. Of those that have a recurrence, just over half can regain
freedom from seizures either with anticonvulsants or by returning to the
ketogenic diet. Recurrence is more likely if, despite seizure freedom, an
electroencephalogram (EEG) shows epileptiform spikes, which indicate epileptic
activity in the brain but are below the level that will cause a seizure. Recurrence
is also likely if an MRI scan shows focal abnormalities (for example, as in children
with tuberous sclerosis). Such children may remain on the diet longer than
average, and it has been suggested that children with tuberous sclerosis who
achieve seizure freedom could remain on the ketogenic diet indenitely. [46]
Variants
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Classic
The ketogenic diet is calculated by a dietitian for
each child. Age, weight, activity levels, culture and
food preferences all aect the meal plan. First, the
energy requirements are set at 8090% of the
recommended daily amounts (RDA) for the child's
age (the high-fat diet requires less energy to
process than a typical high-carbohydrate diet).
Highly active children or those with muscle
spasticity require more calories than this;
immobile children require less. The ketogenic ratio
of the diet compares the weight of fat to the
combined weight of carbohydrate and protein. This
is typically 4:1, but children who are younger than
18months, older than 12years, or who are obese
may be started on a 3:1 ratio. Fat is energy-rich,
with 9kcal/g (38kJ/g) compared to 4kcal/g
(17kJ/g) for carbohydrate or protein, so portions
on the ketogenic diet are smaller than normal. The
quantity of fat in the diet can be calculated from
the overall energy requirements and the chosen
ketogenic ratio. Next, the protein levels are set to
allow for growth and body maintenance, and are
around 1g protein for each kg of body weight.
Lastly, the amount of carbohydrate is set according
to what allowance is left while maintaining the
chosen ratio. Any carbohydrate in medications or
supplements must be subtracted from this
allowance. The total daily amount of fat, protein
and carbohydrate is then evenly divided across the
meals.[37]
The ratio of caloric

contributions from food
components of four diets, by
weight
A computer program such as KetoCalculator may be used to help generate

recipes.[47] The meals often have four components: heavy whipping cream, a
protein-rich food (typically meat), a fruit or vegetable and a fat such as butter,
vegetable oil or mayonnaise. Only low-carbohydrate fruits and vegetables are
allowed, which excludes bananas, potatoes, peas and corn. Suitable fruits are
divided into two groups based on the amount of carbohydrate they contain, and
vegetables are similarly divided into two groups. Foods within each of these four
groups may be freely substituted to allow for variation without needing to
recalculate portion sizes. For example, cooked broccoli, Brussels sprouts,
cauliower and green beans are all equivalent. Fresh, canned or frozen foods are
equivalent, but raw and cooked vegetables dier, and processed foods are an
additional complication. Parents are required to be precise when measuring food
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quantities on an electronic scale accurate to 1g. The child must eat the whole
meal and cannot have extra portions; any snacks must be incorporated into the
meal plan. A small amount of MCT oil may be used to help with constipation or to
increase ketosis.[37]
The classic ketogenic diet is not a balanced diet and only contains tiny portions of
fresh fruit and vegetables, fortied cereals and calcium-rich foods. In particular,
the B vitamins, calcium and vitamin D must be articially supplemented. This is
achieved by taking two sugar-free supplements designed for the patient's age: a
multivitamin with minerals and calcium with vitamin D.[5] A typical day of food for
a child on a 4:1 ratio, 1,500kcal (6,300kJ) ketogenic diet comprises: [29]
Breakfast: egg with bacon
28g egg, 11g bacon, 37g of 36% heavy whipping cream, 23g butter and
9g apple.
Snack: peanut butter ball
6g peanut butter and 9g butter.
Lunch: tuna salad
28g tuna sh, 30g mayonnaise, 10g celery, 36g of 36% heavy whipping
cream and 15g lettuce.
Snack: keto yogurt
18g of 36% heavy whipping cream, 17g sour cream, 4g strawberries and
articial sweetener.
Dinner: cheeseburger (no bun)
22g minced (ground) beef, 10g American cheese, 26g butter, 38g cream,
10g lettuce and 11g green beans.
Snack: keto custard
25g of 36% heavy whipping cream, 9g egg and pure vanilla avouring.
MCT oil
Normal dietary fat contains mostly long-chain triglycerides (LCT). Medium-chain
triglycerides are more ketogenic than LCTs because they generate more ketones
per unit of energy when metabolised. Their use allows for a diet with a lower
proportion of fat and a greater proportion of protein and carbohydrate,[5] leading
to more food choices and larger portion sizes.[2] The original MCT diet developed
by Peter Huttenlocher in the 1970s derived 60% of its calories from MCT oil. [18]
Consuming that quantity of MCT oil caused abdominal cramps, diarrhoea and
vomiting in some children. A gure of 45% is regarded as a balance between
achieving good ketosis and minimising gastrointestinal complaints. The classical
and modied MCT ketogenic diets are equally eective and dierences in
tolerability are not statistically signicant.[9] The MCT diet is less popular in the
United States; MCT oil is more expensive than other dietary fats and is not
covered by insurance companies.[5]
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Modied Atkins
First reported in 2003, the idea of using a form of the Atkins diet to treat epilepsy
came about after parents and patients discovered that the induction phase of the
Atkins diet controlled seizures. The ketogenic diet team at Johns Hopkins Hospital
modied the Atkins diet by removing the aim of achieving weight loss, extending
the induction phase indenitely, and specically encouraging fat consumption.
Compared with the ketogenic diet, the modied Atkins diet (MAD) places no limit
on calories or protein, and the lower overall ketogenic ratio (approximately 1:1)
does not need to be consistently maintained by all meals of the day. The MAD
does not begin with a fast or with a stay in hospital and requires less dietitian
support than the ketogenic diet. Carbohydrates are initially limited to 10g per
day in children or 20g per day in adults, and are increased to 2030g per day
after a month or so, depending on the eect on seizure control or tolerance of the
restrictions. Like the ketogenic diet, the MAD requires vitamin and mineral
supplements and children are carefully and periodically monitored at outpatient
clinics.[48]
The modied Atkins diet reduces seizure frequency by more than 50% in 43% of
patients who try it and by more than 90% in 27% of patients.[5] Few adverse
eects have been reported, though cholesterol is increased and the diet has not
been studied long term.[48] Although based on a smaller data set (126 adults and
children from 11 studies over ve centres), these results from 2009 compare
favourably with the traditional ketogenic diet.[5]
Low glycemic index treatment

The low glycemic index treatment (LGIT)[49] is an attempt to achieve the stable
blood glucose levels seen in children on the classic ketogenic diet while using a
much less restrictive regimen. The hypothesis is that stable blood glucose may be
one of the mechanisms of action involved in the ketogenic diet, [9] which occurs
because the absorption of the limited carbohydrates is slowed by the high fat
content.[3] Although it is also a high-fat diet (with approximately 60% calories
from fat),[3] the LGIT allows more carbohydrate than either the classic ketogenic
diet or the modied Atkins diet, approximately 4060g per day. [5] However, the
types of carbohydrates consumed are restricted to those that have a glycemic
index lower than 50. Like the modied Atkins diet, the LGIT is initiated and
maintained at outpatient clinics and does not require precise weighing of food or
intensive dietitian support. Both are oered at most centres that run ketogenic
diet programmes, and in some centres they are often the primary dietary therapy
for adolescents.[9]
Short-term results for the LGIT indicate that at one month approximately half of
the patients experience a greater than 50% reduction in seizure frequency, with
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overall gures approaching that of the ketogenic diet. The data (coming from one
centre's experience with 76 children up to the year 2009) also indicate fewer side
eects than the ketogenic diet and that it is better tolerated, with more palatable
meals.[5][50]
Prescribed formulations
Infants and patients fed via a gastrostomy tube can
also be given a ketogenic diet. Parents make up a
prescribed powdered formula, such as KetoCal,
into a liquid feed.[21] Gastrostomy feeding avoids
any issues with palatability, and bottle-fed infants
readily accept the ketogenic formula.[32] Some
studies have found this liquid feed to be more
eicacious and associated with lower total
cholesterol than a solid ketogenic diet.[5] KetoCal
is a nutritionally complete food containing milk
protein and is supplemented with amino acids, fat,
carbohydrate, vitamins, minerals and trace
elements. It is used to administer the 4:1 ratio
classic ketogenic diet in children over one year.
The formula is available in both 3:1 and 4:1 ratios,
either unavoured or in an articially sweetened
vanilla avour and is suitable for tube or oral
feeding.[51] Other formula products include
KetoVolve[52] and Ketonia.[53] Alternatively, a liquid
ketogenic diet may be produced by combining Ross
Carbohydrate Free soy formula with Microlipid
and Polycose.[53]
Measuring KetoCala
powdered formula for
administering the classic
ketogenic diet
Worldwide
There are theoretically no restrictions on where the ketogenic diet might be used,
and it can cost less than modern anticonvulsants. However, fasting and dietary
changes are aected by religious and cultural issues. A culture where food is
often prepared by grandparents or hired help means more people must be
educated about the diet. When families dine together, sharing the same meal, it
can be diicult to separate the child's meal. In many countries, food labelling is
not mandatory so calculating the proportions of fat, protein and carbohydrate is
diicult. In some countries, it may be hard to nd sugar-free forms of medicines
and supplements, to purchase an accurate electronic scale, or to aord MCT
oils.[54]
Jewish dietary laws prevent mixing meat and milk in one dish. In Asia, the normal
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diet includes rice and noodles as the main energy source, making their
elimination diicult. Therefore, the MCT-oil form of the diet, which allows more
carbohydrate, has proved useful. In India, religious beliefs commonly aect the
diet: some patients are vegetarians, will not eat root vegetables or avoid beef. The
Indian ketogenic diet is started without a fast due to cultural opposition towards
fasting in children. The low-fat, high-carbohydrate nature of the normal Indian
and Asian diet means that their ketogenic diets typically have a lower ketogenic
ratio (1:1) than in America and Europe. However, they appear to be just as
eective.[54]
In many developing countries, the ketogenic diet is expensive because dairy fats
and meat are more expensive than grain, fruit and vegetables. The modied
Atkins diet has been proposed as a lower-cost alternative for those countries; the
slightly more expensive food bill can be oset by a reduction in pharmaceutical
costs if the diet is successful. The modied Atkins diet is less complex to explain
and prepare and requires less support from a dietitian.[55]
Mechanism of action
Seizure pathology
The brain is composed of a network of neurons that
transmit signals by propagating nerve impulses. The
propagation of this impulse from one neuron's synapse to
another is typically controlled by neurotransmitters,
though there are also electrical pathways between some
neurons. Neurotransmitters can inhibit impulse ring
(primarily done by -aminobutyric acid, or GABA) or they
can excite the neuron into ring (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
signicantly 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 eect on neurons.[11]
Ketone bodies
-hydroxybutyrate
acetoacetic acid
acetone
The nerve impulse is characterised by a great inux of

sodium ions through channels in the neuron's cell membrane followed by an eux
of potassium ions through other channels. The neuron is unable to re again for a
short time (known as the refractory period), which is mediated by another
potassium channel. The ow through these ion channels is governed by a "gate"
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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.[11]
There are many ways in which epilepsy occurs. Examples of pathological
physiology include: unusual excitatory connections within the neuronal network of
the brain; abnormal neuron structure leading to altered current ow; decreased
inhibitory neurotransmitter synthesis; ineective receptors for inhibitory
neurotransmitters; insuicient breakdown of excitatory neurotransmitters leading
to excess; immature synapse development; and impaired function of ionic
channels.[11]
Seizure control
Although many hypotheses have been put forward to explain how the ketogenic
diet works, it remains a mystery. Disproven hypotheses include systemic acidosis
(high levels of acid in the blood), electrolyte changes and hypoglycaemia (low
blood glucose).[21] Although many biochemical changes are known to occur in the
brain of a patient on the ketogenic diet, it is not known which of these has an
anticonvulsant eect. The lack of understanding in this area is similar to the
situation with many anticonvulsant drugs.[56]
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 for 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 bloodbrain barrier. Fortunately, the liver
can use long-chain fatty acids to synthesise the three ketone bodies
-hydroxybutyrate, acetoacetate and acetone. These ketone bodies enter the brain
and substitute for glucose.[56] Medium-chain fatty acids octonoic and heptanoic
acids can cross the barrier and be used by the brain.[58][59][60]
The ketone bodies are possibly anticonvulsant in themselves; in animal models,
acetoacetate and acetone protect against seizures. The ketogenic diet results in
adaptive changes to brain energy metabolism that increase the energy reserves;
ketone bodies are a more eicient fuel than glucose, and the number of
mitochondria is increased. This may help the neurons to remain stable in the face
of increased energy demand during a seizure, and may confer a neuroprotective
eect.[56]
The ketogenic diet has been studied in at least 14 rodent animal models of
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seizures. It is protective in many of these models and has a dierent protection

prole than any known anticonvulsant. Conversely, fenobrate, not used clinically
as an antiepileptic, exhibits experimental anticonvulsant properties in adult rats
comparable to the ketogenic diet.[61] This, together with studies showing its
eicacy in patients who have failed to achieve seizure control on half a dozen
drugs, suggests a unique mechanism of action.[56]
Anticonvulsants suppress epileptic seizures, but they neither cure nor prevent the
development of seizure susceptibility. The development of epilepsy
(epileptogenesis) is a process that is poorly understood. A few anticonvulsants
(valproate, levetiracetam and benzodiazepines) have shown antiepileptogenic
properties in animal models of epileptogenesis. However, no anticonvulsant has
ever achieved this in a clinical trial in humans. The ketogenic diet has been found
to have antiepileptogenic properties in rats.[56]
Recently, a saturated medium-chain fatty acid called decanoic acid (C10) has
shown promise in both the control of seizures and of neurodegeneration.
Decanoic acid is a major constituent of the MCT ketogenic diet, and the authors
suggest its action may be through inducing mitochondrial biogenesis and helping
provide more ATP to maintain the resting membrane potential of the neuron. [62]
Other applications
The ketogenic diet may be a successful treatment for several rare metabolic
diseases. Case reports of two children indicate that it may be a possible treatment
for astrocytomas, a type of brain tumour. Autism, depression, migraine
headaches, polycystic ovary syndrome and diabetes mellitus type 2 have also been
shown to improve in small case studies.[21] There is evidence from uncontrolled
clinical trials and studies in animal models that the ketogenic diet can provide
symptomatic and disease-modifying activity in a broad range of
neurodegenerative disorders including amyotrophic lateral sclerosis, Alzheimer's
disease and Parkinson's disease,[21][63] and may be protective in traumatic brain
injury and stroke.[7][8]
Because tumor cells are ineicient in processing ketone bodies for energy, the
ketogenic diet has also been suggested as a treatment for cancer,[64][65] including
glioma,[66] as well as multiple sclerosis and other neurological disorders.[67][68]
A 2013 review said that there is enough suggestion of potential benet from
ketogenic diets in cancer therapy that establishing clinical trials is probably
warranted.[69] At present the only evidence of benet is anecdotal, but designing
eective trials to measure the eect of adopting a ketogenic diet could prove
challenging.[70]
In March 2009, Axona was approved as a medical food by the US Food and Drug
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Administration for the "dietary management of the metabolic processes and

nutritional requirements associated with mild to moderate Alzheimer's disease".
Glucose metabolism by the brain is impaired in Alzheimer's disease, and it is
proposed that ketone bodies may provide an alternative energy source.
Caprylidene is a powdered form of a medium-chain triglyceride, specically
caprylic triglyceride.[71]
See also
Low-carbohydrate diet
No-carbohydrate diet
Notes
1. In this article, kcal stands for calories as a unit of measure (4.1868kJ), and calories
stands for "energy" from food.
2. Unless otherwise stated, the term fasting in this article refers to going without food
while maintaining calorie-free uid intake.
3. Hippocrates, On the Sacred Disease, ch. 18; vol. 6.
4. Hippocrates, Epidemics, VII, 46; vol. 5.
5. Galen, De venae sect. adv. Erasistrateos Romae degentes, c. 8; vol. 11.
6. Galen, De victu attenuante, c. 1.
7. A good reduction is dened here to mean a 5090% decrease in seizure frequency. An
excellent reduction is a 9099% decrease.
8. Ketogenic "eggnog" is used during induction and is a drink with the required
ketogenic ratio. For example, a 4:1 ratio eggnog would contain 60g of 36% heavy
whipping cream, 25g pasteurised raw egg, saccharin and vanilla avour. This
contains 245kcal (1,025kJ), 4g protein, 2g carbohydrate and 24g fat (24:6 =
4:1).[20] The eggnog may also be cooked to make a custard, or frozen to make ice
cream.[37]
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Archived 2 March 2012.
Further reading
Freeman JM, Kosso EH, Freeman JB, Kelly MT. The Ketogenic Diet: A
Treatment for Children and Others with Epilepsy. 4th ed. New York: Demos;
2007. ISBN 1-932603-18-2.
External links
Matthew's Friends. (http://www.matthewsfriends.org/)
A UK charity and
information resource.
Ketogenic diet (https://www.dmoz.org/Health/Conditions_and_Diseases
/Neurological_Disorders/Epilepsy/Treatment/Ketogenic_Diet/)
at DMOZ
The Charlie Foundation. (http://www.charliefoundation.org/)
A US charity
and information resource, set up by Jim Abrahams.
epilepsy.com: Dietary Therapies & Ketogenic News. (http://www.epilepsy.com
/EPILEPSY/dietary_therapies)
Information and regular research news
27 of 28
16-07-09 01:29 AM
updates.
A Talk with John Freeman: Tending the Flame. (https://web.archive.org
/web/20120401230600/http://www.hopkinsmedicine.org
/neurology_neurosurgery/brainwaves/talk_with_john_freeman.html)
An
interview discussing the ketogenic diet that appeared in BrainWaves, Fall
2003, Volume 16, Number 2.
Lurie Children's Hospital: How the Ketogenic Diet Works
(https://www.luriechildrens.org/en-us/care-services/specialties-services
/epilepsy/programs/Pages/ketogenic-diet.aspx) .
Retrieved from "https://en.wikipedia.org/w/index.php?title=Ketogenic_diet&
oldid=724397178"
Categories: Diets Epilepsy Low-carbohydrate diets High-fat diets
This page was last modied on 9 June 2016, at 00:38.
Text is available under the Creative Commons Attribution-ShareAlike License
; additional terms may apply. By using this site, you agree to the Terms of
Use and Privacy Policy. Wikipedia is a registered trademark of the
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Ketogenic diet - Wikipedia, the free encyclopedia

The ketogenic diet is a high-fat, adequateprotein, low-carbohydrate diet that in medicine is

Testing for ketone bodies in

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

9.2 Seizure control

Ketogenic diet - Wikipedia, the free encyclopedia

that dietary therapy had a rational and physical

Ketogenic diet - Wikipedia, the free encyclopedia

research undertaken by neurologist Stanley Cobb and his assistant William G.

Anticonvulsants and decline

Ketogenic diet - Wikipedia, the free encyclopedia

In the 1960s, it was discovered that medium-chain

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

A study with an intent-to-treat prospective design was published in 1998 by a

Indications and contra-indications

Ketogenic diet - Wikipedia, the free encyclopedia

likely to become seizure-free with surgery than

Experts on the ketogenic diet

A survey in 2005 of 88 paediatric neurologists in the US found that 36% regularly

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

The ratio of caloric

A computer program such as KetoCalculator may be used to help generate

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

Low glycemic index treatment

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

The nerve impulse is characterised by a great inux of

Ketogenic diet - Wikipedia, the free encyclopedia

which is opened by either a voltage change or a chemical messenger known as a

Ketogenic diet - Wikipedia, the free encyclopedia

seizures. It is protective in many of these models and has a dierent protection

Ketogenic diet - Wikipedia, the free encyclopedia

Administration for the "dietary management of the metabolic processes and

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

28. Scottish Intercollegiate Guidelines Network. Guideline 81, Diagnosis and

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

53. Kosso EH. The Ketogenic Diet ... in a bottle? (http://www.epilepsy.com/epilepsy

Ketogenic diet - Wikipedia, the free encyclopedia

Ketogenic diet - Wikipedia, the free encyclopedia

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