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But beyond that, experts aren't convinced that the keto diet has any other scientifically proven health benefits. In fact, it may have some distinct downsides. If you follow the keto diet incorrectly, for example (like by eating lots of saturated fats, versus healthy unsaturated fats), you're at risk of raising your cholesterol levels. “The best strategy to keep your heart healthy is to get as much fat as possible from unsaturated sources such as olive, avocado and canola oils, nuts, seeds, avocados, and olives," says Ansel. For some people, it's possible to actually improve cholesterol if the fats in their diet are from varied and healthy sources, says Harvey.
You’ll quickly find that salads are your friend when in ketosis, and for a good reason: they provide lots of food to fill you up, but they’re not going to bog you down. A bed of spinach with some red onion, bacon, a little tomato, and a hot sauce vinaigrette is quick and delicious. Add in some protein – perhaps that leftover salmon from day 1 – and you’ve got a complete, healthy lunch.
The confusion between ketosis and ketoacidosis is a prominent reason why many individuals, particularly doctors, steer clear of the keto diet for beginners. It’s important to understand that these are two very DIFFERENT metabolic states. Ketoacidosis may occur in uncontrolled type 1 diabetics (DKA; diabetic ketoacidosis) due to insulin deficiencies. DKA is associated with both elevated blood glucose and ketone levels; due to little to no insulin production, blood glucose cannot enter insulin-dependent cells to be used for energy, and as such, cells become hungry, resulting in uncontrolled ketone production. In turn, a highly acidic environment is created that can have detrimental effects on an individual’s health, possibly resulting in death. It must be echoed that the ketogenic diet, which induces “nutritional” ketosis, is vastly different and should never be confused with DKA. To put this in perspective, a normal state of ketosis, as achieved via the keto diet for beginners may elevate ketones anywhere from 0.3–5mM, while DKA results in ketone levels of about 15mM or higher.
Note: Because you'll be excluding some major food groups on the keto diet (grains, many fruits) you should definitely think about taking a multivitamin—especially one that contains folic acid, which helps your body make new cells and is often found in enriched breads, cereals, and other grain products, says Julie Upton, R.D., cofounder of nutrition website Appetite for Health.
Because people with type 2 diabetes are at an increased risk for cardiovascular disease, there’s a specific concern that the saturated fat in the diet may drive up LDL, or “bad,” cholesterol levels, and further increase the odds of heart problems. If you have type 2 diabetes, talk to your doctor before attempting a ketogenic diet. They may recommend a different weight-loss diet for you, like a reduced-calorie diet, to manage diabetes. Those with epilepsy should also consult their doctor before using this as part of their treatment plan.
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]

Blood Ketone Meter: Measuring ketone levels in the blood more accurately measures and indicates an individual’s metabolic state of ketosis. Similar to measuring blood glucose levels, this method also uses a blood meter and a chemo-sensitive strip made specifically to measure ketones in the blood called beta‑hydroxybutyrate (βHB). As with blood glucose measurements, a blood sample can be acquired from a finger prick. The ketone level displays on the meter within a few seconds of a sample placement on the strip.
In the 1960s, medium-chain triglycerides (MCTs) were found to produce more ketone bodies per unit of energy than normal dietary fats (which are mostly long-chain triglycerides).[15] MCTs are more efficiently absorbed and are rapidly transported to the liver via the hepatic portal system rather than the lymphatic system.[16] The severe carbohydrate restrictions of the classic ketogenic diet made it difficult 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 12 children and adolescents with intractable seizures. 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.[15] The MCT diet replaced the classic ketogenic diet in many hospitals, though some devised diets that were a combination of the two.[10]
It is possible to combine the results of several small studies to produce evidence that is stronger than that available from each study alone—a 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.[23] It concluded that a third achieved an excellent reduction in seizure frequency and half the patients achieved a good reduction.[18]
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 flow; decreased inhibitory neurotransmitter synthesis; ineffective receptors for inhibitory neurotransmitters; insufficient breakdown of excitatory neurotransmitters leading to excess; immature synapse development; and impaired function of ionic channels.[7]
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