Is the KETO diet a lifelong diet

Ketogenic Diet - Use and Implementation

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Ketogenic diets (KD) are very high-fat, low-carbohydrate diets. The goal is the state of ketosis, a metabolic state modeled on fasting. Here, instead of glucose, the body uses ketone bodies as an alternative source of energy. Ketogenic diets are used for various diseases such as therapy-resistant epilepsy in children and adolescents. This form of nutrition is increasingly establishing itself in a broader segment of the population.

Principles and effects / effects

In the ketogenic diet, instead of glucose, the body uses ketone bodies as an alternative source of energy. This is achieved by greatly reducing carbohydrates in favor of fat.

Ketone bodies are created when fats are broken down (beta oxidation) in the liver and can be used by organs (e.g. brain, muscles) for energy supply (if there is not enough glucose). Acetone, acetoacetate and beta-hydroxybutyric acid (ß-OH-butyrate) are the relevant representatives.

The fat breakdown products are believed to have a neuroprotective effect. Increased energy availability in the brain is said to improve the resistance of neurons, reduce the number of reactive oxygen species and decrease inflammatory activity [S1 guideline 2014].

With ketogenic diets, ketone body concentrations between 3 and 7 mmol / l are achieved (= target values).

Influence on hunger and satiety

After weight loss, on the one hand, appetite or hunger can increase and, on the other hand, the feeling of satiety or fullness can decrease. This can be explained by increased concentrations of the so-called hunger hormone ghrelin and lower concentrations of various satiety and digestive hormones (e.g. cholecystokinin) [DeB 2020].

The observed effects represent an adaptation of the body to a lower body weight and persist over a certain period of time. This period in turn depends on the initial weight and the strength or duration of the weight loss and can last up to 62 weeks [Fes 2021].

The effects seem to vary depending on the diet chosen. Studies show that the ketogenic diet does not lead to rising ghrelin levels during weight loss and does not trigger increased appetite or hunger. This could be due to the effect of ketone bodies such as beta-hydroxybutyric acid [Dee 2020].

Preventive and therapeutic potential

The ketogenic diet is used in certain forms of epilepsy as well as in some rare metabolic diseases and must be carried out under professional supervision. Further fields of application are currently being intensively researched and tested.

Pharmaco-resistant epilepsy (confirmed indication)

The ketogenic diet is a recognized therapy for drug-resistant epilepsy in children and adolescents [Lev 2012] [Mar 2016].

The exact mechanisms of action are still being researched. Presumably, chronic ketosis raises the cerebral energy level and releases more soothing / relaxing neurotransmitters such as gamma-aminobutyric acid (GABA). The formation of free oxygen radicals is also inhibited. An anticonvulsant effect of carbohydrate restriction and the ketone bodies themselves are also discussed [S1 guideline 2014]. A cumulative effect of the individual factors is likely, which lowers the tendency to cramp in the brain [Bou 2007].

Effects: Duration and frequency of seizures ↓, vigilance (alertness, attention) and quality of life ↑ [Hal 2012]

Duration: The diet should be carried out for about 2 years. The anticonvulsant effect can persist even after the diet has been discontinued [Fre 1998].

Defects in the cerebral energy metabolism (Therapy of choice)

Possible indications are the GLUT1 defect and the pyruvate dehydrogenase deficiency. Ketone bodies can cross the blood-brain barrier and be used as an alternative source of energy if the glucose transport is reduced [Kle 2008].

Duration: The diet must be adhered to for life.

Further (increasingly successful application)

There are also increasingly good experiences with:

  • West Syndrome [Kan 2011]
  • Dravet Syndrome [Veg 2011]
  • FIRES (febrile infection-related epilepsy syndrome) [Nab 2010]
  • Doose Syndrome [Ber 2012]
  • focal drug-resistant epilepsy to bridge epilepsy surgery [Lev 2012]
  • Mitochondrial disease with an isolated complex I defect in the respiratory chain [Fin 2010]

Positive individual reports can be found at:

Chronic headaches / migraines

Studies show promising effects on neurological diseases such as ADHD and migraines - especially because of the effect on brain metabolism, the release of neurotransmitters and neuronal inflammation.

Clinical data indicate that the high-fat and extremely low-carbohydrate diet has a positive effect on migraine disease in many ways [Bar2017] [Pao2013] [Jeo2011] [Goa2002]. For example, a ketogenic diet may prevent migraines from occurring by counteracting neural inflammation and improving mitochondrial energy metabolism.

In an observational study with 96 overweight migraine patients, the effect of a ketogenic diet was compared with that of a standardized low-calorie diet [DiL2015]. After the first month, in addition to weight loss, a significant reduction in headache frequency and medication intake could be determined. However, this temporarily worsened in the following months with the reintroduction of carbohydrates. Nevertheless, the test subjects continued to lose weight and, after the intervention, still showed better results in terms of headache frequency than at the time before the intervention.

In the other group of 51 migraineurs, no significant differences in headache were shown. The authors suspect that the positive effects on migraines are not due to weight loss in general, but primarily to the ketogenic diet.

The ketogenic diet has been reported to be a potent anti-inflammatory in some migraineurs. The observed effects can probably be explained by a low sugar and carbohydrate consumption, a high consumption of vegetables and herbs and the use of anti-inflammatory oils and fats, including fatty sea fish.

Experience from the therapy of other difficult to treat neurological diseases condenses the evidence that the macronutrient ratio in the diet has a decisive influence on the brain metabolism.

Due to the insulin resistance in the brain, which is prevalent in Alzheimer's disease, glucose uptake and utilization is restricted despite sufficient blood sugar supply. In this case, ketone bodies can serve as an alternative source of energy and continue to ensure the supply of ATP.

Using a ketogenic diet can lead to diabetes mellitus remission.

After 10 weeks, 48% of the participants achieved a functional remission (HbA 1c <6.5% without medication or only with metformin).

After 12 months there was a high level of adherence (89%); on average, body weight (-14 kg), HbA1c (-1.3%), fasting glucose (-22%) and fasting insulin (-43%) decreased. The use of medication has been significantly reduced. In addition, triglycerides (-24%) and CRP (-39%) decreased, while HDL cholesterol increased (+ 18%). The LDL cholesterol also rose somewhat overall [McK 2017].

On closer examination, however, it is found that the density of the LDL particles decreases (-23%) while the size (+29%) increases. Overall, the slight increase in LDL cholesterol is mainly due to larger cholesterol-rich LDL particles [Ath 2020].

Contraindications and possible side effects

But there are also absolute and relative contraindications to a ketogenic diet [S1 guideline 2014].

Absolute contraindications

  • Fatty acid oxidation disorders (impaired fatty acid breakdown inhibits the formation of ketone bodies)
  • Ketoneogenesis and ketolysis defects (impaired formation or impaired breakdown of ketone bodies)
  • Gluconeogenesis defects (life-threatening hypoglycaemia when starting the ketogenic diet)
  • Pyruvate carboxylase deficiency (impaired gluconeogenesis, see previous contraindication)
  • lack of compliance (insufficient treatment basis)

Relative contraindications

  • Respiratory chain defects (lactic acidosis increased by ketosis, deficient ATP synthesis)
  • Kidney stones (increased stone formation due to low urine pH in ketosis)
  • Liver, kidney and pancreatic diseases
  • Cardiomyopathy, cardiac arrhythmias (potential side effects on the ketogenic diet)
  • Osteoporosis and osteopenia (more common calcium deficiencies in ketogenic diets)
  • Disturbances of the fat metabolism (aggravating disturbance by high-fat diets possible)
  • Selenium deficiency (potentially promotes cardiac arrhythmias)
  • Carbonic anhydrase inhibitors (increase acidosis)

The recommendation to consume 90% of the total energy through fat means a severe restriction in the choice of food. Overall, the side effects are minor and usually easy to treat [Vin 2008].

short term

Vomiting, diarrhea, constipation, hunger and heartburn can occur at the beginning [Nea 2008]. Hypoglycaemia is also possible. Loss of fluid can occur, especially in the case of infections. Flu-like symptoms in the beginning are typical in adults. These subside after a few days.

medium to long term

Kidney stones, constipation and lipid metabolism disorders have been described in the medium to long term [Vin 2008]. Pancreatitis and disorders of the platelet and granulocyte functions are also possible [Ber 2001] [Woo 1989] [Ste 2001].

In addition, growth disorders can occur in small children, so that adequate medical observation is required during the diet [Vin 2002]. For older children, adolescents and adults, such a strict diet is also difficult to adhere to, as it means a significant deviation from previous eating habits and an additional decrease in quality of life.

implementation

In nutritional therapy, the ketogenic diet is usually initiated on an inpatient basis in order to treat complications in metabolic changes quickly and effectively. It is not recommended to use it without professional support. Accompanying training for patients and their relatives (e.g. minors) is recommended.

In order to be able to achieve therapeutic success at all, the diet must be strictly adhered to over a longer period of time. This requires a high level of acceptance and the intensive cooperation of all those involved. The patients themselves or the parents must be informed in advance about the implementation, the benefits and possible side effects.

Since a ketogenic diet in epilepsy follows very strict criteria and the specified nutrient ratios must be adhered to at every meal if possible, this form of therapy should only be carried out in the company of a nutritionist who is experienced in this field. Patients should not start this diet on their own and without professional advice.

Inpatient induction, for example in children and adolescents, is usually 5-7 days. Initial fasting is not necessary (contraindicated in the case of pyruvate dehydrogenase deficiency), but it can bring about the state of ketosis more quickly [Ber 2005]. The side effects are usually more common and more serious here.

Since a ketogenic diet in epilepsy follows very strict criteria and the specified nutrient ratios must be adhered to at every meal if possible, this form of therapy should only be carried out in the company of a nutritionist who is experienced in this field. Patients should not start this diet on their own and without professional advice.

Aspects to consider

There are some essential aspects to consider when implementing.

  1. Good fat quality is important. With a fat content of 60-90% energy, the intake of saturated fatty acids from animal foods is high. It is therefore important to ensure that foods with a high proportion of polyunsaturated fatty acids are used regularly [Kos 2008].
  2. In order to avoid the formation of kidney stones, it is important to ensure sufficient fluid intake [Sam 2007].
  3. For stable ketosis, the desired nutrient ratio should be aimed for in each meal. The fat intake should be evenly distributed over all meals.
  4. Exercise can increase ketosis.

The success of the ketogenic diet in the safe indications can only be assessed after 3 months of stable ketosis at the earliest.

Prolonged ketosis should be ended gradually and slowly.

Implementation forms

In addition to the classic ketogenic diet, more practicable forms such as the modified Atkins diet and the low-glycemic index therapy (LGIT) developed.

In the classic ketogenic diet, the energy-supplying nutrients are in the ratio of 4: 1 (4 weight units of fat to 1 weight unit of carbohydrates and protein) or 3: 1 (3 weight units of fat to 1 weight unit of carbohydrates and protein) in the diet.

These are calculated individually, taking into account the energy and protein requirements determined for the patient. The fat content is usually between 82 and 90%.

This form is gradually ended by reducing the nutrient ratio (4: 1 → 3.5: 1 → 3: 1 → 2.5: 1 etc.) [Fre 1998].

implementation [S1 guideline 2014]

  • Energy: individually calculated according to age, weight and physical activity
  • Protein: according to reference values ​​for nutrient intake
  • Fat: according to calculation, focus on fat quality (polyunsaturated fatty acids)
  • Carbohydrates: according to calculation, focus on low glycemic index
  • Dietary fiber: Focus on high fiber foods (increase meal volume, increase satiety)
  • Micronutrients: Requirement according to reference values ​​for nutrient intake; often cannot be covered sufficiently
  • Supplements: individual supplementation after appropriate diagnostics and evaluation of the nutritional protocol
  • Drinking amount: Unlimited, low hydration puts you at risk of constipation and kidney stones
  • Ratio of energy-supplying nutrients fat to carbohydrates and protein: 4: 1 (<2 years) to 3: 1 (> 2 years, with severe ketosis and insufficient compliance)
  • Meals: Nutrient ratio must be observed in each meal, ≥3 meals
  • Medium chain (MCT) or long chain fatty acids (LCT): LCT, for constipation and weak ketosis, MCT can be used in low doses
  • Miscellaneous: Sweeteners for sweetening, sugar substitutes have to be calculated

The diet, named after the American cardiologist Robert Atkins, is characterized by a high fat and protein content and a low carbohydrate content. The diet originally developed for weight reduction also leads to the formation of ketone bodies, but compared to the classic ketogenic diet it is more varied, easier to carry out at home and does not require fasting or weighing certain food rations.

The fat percentage in the modified Atkins diet is 60-65% energy. Energy and protein components are not calculated. The daily carbohydrate intake is 10-20 g (children) and 30-40 g (adults).

This form is easier to implement, increases compliance and reduces the time required for training.

The modified Atkins diet is ended by increasing the amount of carbohydrates by 5 g every other day [Kos 2008].

implementation [S1 guideline 2014]

  • Energy: not calculated
  • Protein: not calculated
  • Fat: 60-65% energy; Focus on fat quality (polyunsaturated fatty acids)
  • Carbohydrates: 10-20 g / day (children), adults proportionally more
  • Dietary fiber: Focus on high fiber foods (increase meal volume, increase satiety)
  • Micronutrients: Requirement according to reference values ​​for nutrient intake; often cannot be covered sufficiently
  • Supplements: individual supplementation after appropriate diagnostics and evaluation of the nutritional protocol
  • Drinking amount: unlimited, low hydration puts you at risk of constipation and kidney stones
  • Meals: ≥3 meals
  • MCT or LCT: LCT, for constipation and weak ketosis, MCT can be used in low doses
  • Miscellaneous: Sweeteners for sweetening, sugar substitutes have to be calculated
Low Glycemic Index Therapy (LGIT)

The LGIT is based on the selection of foods containing carbohydrates with a glycemic index below 50. The daily amount is 40-60 g. This is combined with high-fat foods and the addition of high-fat ingredients to the dishes (e.g. cream, mascarpone, etc.).The fat is distributed as evenly as possible over all meals.

In addition to the larger selection of foods and the easier implementation in contrast to the classic ketogenic diet, the advantage of this form of nutrition is clearly the almost unlimited intake of vegetables. An undersupply of certain vitamins is not to be expected here.

Choosing foods with a glycemic index below 50% resulted in a reduction in seizures of over 90% in 10 out of 20 patients [Pfe 2005]. A somewhat larger study on 76 children showed a seizure reduction of more than 50% in 42% after one month, in 50% after 3 months and in 66% after one year [Muz 2009].

Break up: This form is ended by gradually introducing foods with a GI> 50 [Pfe 2008].

implementation [S1 guideline 2014]

  • Energy: not calculated
  • Protein: not calculated
  • Fat: High-fat foods and the addition of high-fat ingredients to every meal
  • Carbohydrates: 40-60 g / day, choosing foods with a GI <50
  • Dietary fiber: Focus on high fiber foods (increase meal volume, increase satiety)
  • Micronutrients: Requirement according to reference values ​​for nutrient intake; often cannot be covered sufficiently
  • Supplements: individual supplementation after appropriate diagnostics and evaluation of the nutritional protocol
  • Drinking amount: unlimited, low hydration puts you at risk of constipation and kidney stones
  • Meals: ≥3 meals with as evenly distributed fat as possible
  • Medium chain (MCT) or long chain fatty acids (LCT): LCT, for constipation and weak ketosis, MCT can be used in low doses
  • Miscellaneous: Sweeteners for sweetening, sugar substitutes have to be calculated

Relevant foods, specialty products and kitchen management

Depending on the form of implementation, the appropriate choice of food differs. Therefore, only “rough” recommendations are presented below: ↑ for suitable foods, ↓ for unsuitable foods

↑ carbohydrate-free drinks ad libitum (water, tea, coffee), vegetable broth, "hot water" (garlic broth)

↓ sugary drinks (lemonades, wellness drinks, sweetened tea and coffee, juices, cocoa)

↑ Low-starch vegetables (fresh, frozen) without other additives such as cabbage, leafy vegetables, cucumber, tomatoes, avocado, artichoke

↓ Starch-rich vegetables (legumes, potatoes), canned vegetables and vegetable products with added sugar

↑ very small amounts of dark berry fruits

↓ almost all types of fruit (fresh, frozen), canned fruit, jam and other fruit products

Grains / products, pseudograins, rice

↑ Wheat germ

↓ almost all grain / pseudo-grain varieties and products as well as rice in large quantities

↑ high-fat dairy products without additional additives such as cheese, cream cheese, cream, quark and yoghurt with a high fat level

↓ Milk and low-fat milk products (quark, cottage cheese, low-fat yogurt)

↑ Meat and meat products (if possible from organic production) and eggs in moderate quantities (protein content!)

↓ Large quantities of highly processed sausage products with added sugar

↑ high-fat sea fish (tuna, salmon, mackerel, herring, sardines / anchovies), in moderate amounts seafood and low-fat fish

↓ sophisticated canned fish with added sugar

Ingredients rich in fat in every meal increase the percentage of fat. These include, for example:

  • Mascarpone, cream, crème fraîche in sauces, dips
  • Butter in vegetables
  • vegetable oils (e.g. linseed oil) in quark

Number of meals depends on the need. At least 3 meals a day are recommended. The recommended distribution of nutrients must be observed at every meal.

Diagnostics, supplements, influence on medication

Detection of ketone bodies (urine)

The term ketone bodies summarizes substances that are formed as an intermediate product in the breakdown of fat in the event of a lack of carbohydrates and which, in addition to glucose, serve the body as an energy supplier. In medical parlance, these compounds are referred to as acetoacetate, beta-hydroxybutyrate, and acetone. From a chemical point of view, beta-hydroxybutyrate is not a ketone, but due to its similar physiological properties it belongs to this group and represents the most important representative in terms of quantity. It is converted from acetoacetate by enzymes.

An increased concentration of ketone bodies is usually due to increased fat loss. This can occur in phases of hunger, with a strongly reduced carbohydrate / ketogenic diet, extreme physical stress or as a result of impaired sugar utilization or insulin deficiency (diabetes mellitus). But alcoholism, severe vomiting, severe diarrhea and infectious diseases can also result in increased concentrations. In newborns, ketone bodies in the urine can also be a sign of a congenital metabolic disease. Ketone bodies are excreted in the lungs with the exhaled air (acetone) or in the urine (ketonuria).

The determination of ketone bodies is usually carried out to clarify metabolic imbalances and greatly increased blood sugar levels, as an aid for the detection of hunger states or for the detection of rare congenital diseases. Detection of ketone bodies is possible both in urine and in serum / plasma.

The most common measurement is the so-called nitroprusside method, in which the ketone body concentration in the urine is determined. The test strips used here have a purple color after the reaction between ketones and nitroprusside (sodium nitroferricyanide). The sensitivity is 5 mg / dl, so that physiological increases of up to 2 mg / dl are not recorded. In addition, not all ketone bodies are measured with this method, but only acetoacetate and in some cases acetone. Beta-hydroxybutyrate is not recorded. This is particularly important if this method is used to detect ketone bodies. Enzymatic tests are used for the quantitative determination of beta-hydroxybutyrate and acetoacetate in serum / plasma.

The micronutrients calcium and carnitine are often insufficiently absorbed. The substitution of calcium should be considered from the start [Nea 2012]. Carnitine deficiencies are less common. However, the substance is necessary for the fatty acid metabolism and should therefore be checked regularly for diagnostics [Ber 2001] [Kos 2009].

Anticonvulsants are used for epilepsy. The classic ketogenic diet probably has only a minor impact on the effectiveness of anticonvulsants. A reduction in the dose is only considered after a successful diet.

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