Kristin Parker is an American temporarily living in South Korea. Her role with Team Diet Doctor is customer service. If you have a question or a comment on our social media platforms, website or our Facebook group, she will likely be the one to answer you back! Kristin cooks for a family of four, including two hungry teenage sons. Her keto meal plan yields generous servings of substantial, hearty meals that they all like.
Be choosy about carbs. You can decide which ones you eat, and how much. Look for those that are low on the glycemic index (for instance, asparagus is lower on the glycemic index than a potato) or lower in carbs per serving than others. Whole grains are better choices than processed items, because processing removes key nutrients such as fiber, iron, and B vitamins. They may be added back, such as in “enriched” bread.
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]
In a state of ketosis, your body breaks fat down in the liver and converts it into ketones to be used for energy. Fat doesn't generate an insulin response, so insulin levels remain stable. This makes it much harder to store excess fat, and easier to tap into body fat stores for energy. Not only will this allow you to maintain your weight, but it will greatly encourage weight loss.
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]
I never set out to lose a certain amount of weight when I started, I just wanted to be healthy for myself and my kids. In the beginning it was tough, I was used to eating a whole large pizza with ranch for dinner, or 3 grilled cheese sandwiches dipped in barbecue sauce. Veggies were eschewed unless they were a topping on my cheeseburger. I remember my first week I packed a salad with chicken and bacon and blue cheese dressing, and that was pretty good. Then I made some brats and sauerkraut and mustard with a side of broccoli. Hey this isn't so bad. I got in to the habit of picking a protein and a veggie and mix and matching for variety. Chicken, pork chops, brats, steak, and broccoli, Brussels sprouts, asparagus, green beans were my staples. I didn't weigh or count macros, I just avoided the bad carbs and focused on the good.

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 (a retrospective study) and selected patients who had successfully maintained the dietary restrictions. However, these studies are difficult to compare to modern trials. One reason is that these older trials suffered 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).[19]
^ Freeman JM, Vining EP, Pillas DJ, Pyzik PL, Casey JC, Kelly LM. The efficacy of the ketogenic diet—1998: a prospective evaluation of intervention in 150 children. Pediatrics. 1998 Dec;102(6):1358–63. doi:10.1542/peds.102.6.1358. PMID 9832569. https://web.archive.org/web/20040629224858/http://www.hopkinsmedicine.org/press/1998/DECEMBER/981207.HTM Lay summary]—JHMI Office of Communications and Public Affairs. Updated 7 December 1998. Cited 6 March 2008.

Another difference between older and newer studies is that the type of patients treated with the ketogenic diet has changed over time. When first 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 difficult-to-treat epilepsy. Early and modern studies also differ because the treatment protocol has changed. In older protocols, the diet was initiated with a prolonged fast, designed to lose 5–10% body weight, and heavily restricted the calorie intake. Concerns over child health and growth led to a relaxation of the diet's restrictions.[19] 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 beneficial.[18]


In nutrition, diet is the sum of food consumed by a person or other organism.[1] The word diet often implies the use of specific intake of nutrition for health or weight-management reasons (with the two often being related). Although humans are omnivores, each culture and each person holds some food preferences or some food taboos. This may be due to personal tastes or ethical reasons. Individual dietary choices may be more or less healthy.
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]

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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]
^ Freeman JM, Vining EP, Pillas DJ, Pyzik PL, Casey JC, Kelly LM. The efficacy of the ketogenic diet—1998: a prospective evaluation of intervention in 150 children. Pediatrics. 1998 Dec;102(6):1358–63. doi:10.1542/peds.102.6.1358. PMID 9832569. https://web.archive.org/web/20040629224858/http://www.hopkinsmedicine.org/press/1998/DECEMBER/981207.HTM Lay summary]—JHMI Office of Communications and Public Affairs. Updated 7 December 1998. Cited 6 March 2008.
1 Reference for 5%: Blackburn G. (1995). Effect of degree of weight loss on health benefits. Obesity Research 3: 211S-216S. Reference for 10%: NIH, NHLBI Obesity Education Initiative. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. Available online: http://www.nhlbi.nih.gov/guidelines/obesity/ob_gdlns.pdf Cdc-pdf[PDF-1.25MB]External
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. Several possible explanations exist for this gap between evidence and clinical practice.[34] One major factor may be the lack of adequately trained dietitians who are needed to administer a ketogenic diet programme.[31]

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).[19] 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 effect. The lack of understanding in this area is similar to the situation with many anticonvulsant drugs.[56]
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 modified the Atkins diet by removing the aim of achieving weight loss, extending the induction phase indefinitely, and specifically encouraging fat consumption. Compared with the ketogenic diet, the modified Atkins diet (MAD) places no limit on calories or protein, and the lower overall ketogenic ratio (about 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 10 g per day in children or 20 g per day in adults, and are increased to 20–30 g per day after a month or so, depending on the effect 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]
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 overall figures 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 effects than the ketogenic diet and that it is better tolerated, with more palatable meals.[18][50]
One downside to a ketogenic diet for weight loss is the difficulty maintaining it. “Studies show that weight loss results from being on a low-carb diet for more than 12 months tend to be the same as being on a normal, healthy diet,” says Mattinson. While you may be eating more satiating fats (like peanut butter, regular butter, or avocado), you’re also way more limited in what’s allowed on the diet, which can make everyday situations, like eating dinner with family or going out with friends, far more difficult. Because people often find it tough to sustain, it’s easy to rely on it as a short-term diet rather than a long-term lifestyle.
Wondering what fits into a keto diet — and what doesn’t? “It’s so important to know what foods you’ll be eating before you start, and how to incorporate more fats into your diet,” says Kristen Mancinelli, RD, author of The Ketogenic Diet: A Scientifically Proven Approach to Fast, Healthy Weight Loss, who is based in New York City. We asked her for some guidelines.

Milestone 1: relearning what hunger feels like and what full feels like. In my old way of eating hunger came on like a screaming voice through a megaphone out of nowhere. Now it starts as a whisper, into a mumble, into a conversation. Learning when to eat and went to stop is the first milestone. You'll be tempted to start eating as soon as you hear that whisper of hunger, but eventually you'll realize you don't need to start until it turns into a conversation. Same with feeling full, you're used to stopping when you explode, but now you can stop at a comfortable level.


It is important to understand that weight is entirely a function of input and output. The input is the food you eat and the calories contained therein. The output is your energy output. To lose weight the output needs to be greater than the input. It is that simple. Do not believe any of the diet fads. If you are currently not gaining or losing weight then just burning 300 extra calories per week or eating/drinking 300 calories less per week (2 sodas for example or a small burger) WILL make you lose weight - in this case around 5 pounds of fat per year.
The word diet first appeared in English in the 13th century. Its original meaning was the same as in modern English, “habitually taken food and drink.” But diet was used in another sense too in the Middle and early modern English periods to mean “way of living.” This is, in fact, the original meaning of diet’s Greek ancestor diaita, which is derived from the verb diaitasthan, meaning “to lead one’s life.” In Greek, diaita, had already come to be used more specifically for a way of living prescribed by a physician, a diet, or other regimen.
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