Ketogenic Diet

Processed foods, pesticides, medications, and toxins damage the gut microbiome which in turn drives a range of digestive, autoimmune and neurological illness.  Various “Healing diets” work to heal the gut and calm the immune system and vary depending on the gut, genetics and environment.

Ketogenic Diet

The ketogenic diet was developed in 1924 by Dr. Russell Wilder at

the Mayo Clinic as a treatment for epilepsy. It was very popular in the 1920s and 1930s until the introduction of anticonvulsant medications. However, it is still utilized as a means of therapy for those who have a pharmacological resistance to epilepsy.

It is a high fat, low carbohydrate diet which induces a state that mimics carbohydrate starvation. By almost completely eliminating carbohydrates from the diet, the body resorts to burning fat and using ketone bodies as an energy source.

The diet is very strict and restrictive, and it doesn’t go without side effects. A systematic review noted that gastrointestinal disturbances were the most common adverse reaction, followed by hyperlipidemia. Weakness, mental ‘fog’, headaches and flu-like symptoms are also common side effects when first starting the ketogenic diet.

What are ketones?

The body’s preferred source of energy is glucose, which comes from dietary carbohydrates. Glycogen is the stored form of glucose in the body, and glycogen can also be broken down and converted back into glucose to use as energy if needed. When there is not enough glucose in the bloodstream due to a low carbohydrate intake, and glycogen stores are depleted, the body uses fat as an alternative source of energy.

The process of converting fat into energy occurs predominantly in the mitochondria of the liver. Fatty acids which are stored are broken down by specific enzymes, in a process called beta-oxidation, the metabolite formed is Acetyl-CoA and it is able to undergo metabolic processes to produce energy as ATP.

There are three types of ketones:

1. Acetoacetate

• Formed by fat breakdown
• First type of ketone body to be synthesized
• Converts into the other two ketones: acetone, or beta-hydroxybutyric acid
• Transports energy from liver cells to the entire body

2. Beta-hydroxybutyric acid

• From acetoacetate formation
• Transports energy from liver cells to the entire body

3. Acetone

• Created from acetoacetate
• If not used quickly for energy, it will be rapidly broken down and eliminated via detoxification channels (urine or respiration/breath)

A diet that induces ketosis should trigger this process, and testing for ketones can be done easily with a urine test.

Fasting, illnesses, vigorous exercise, and type 1 diabetes can also induce ketosis.

What conditions may benefit from the Ketogenic diet?

• Epilepsy

The ketogenic diet may significantly reduce seizure frequency, with studies demonstrating a reduction of up to 50% in a majority of child and adult patients.

The mechanism by which the ketogenic diet aids in epilepsy is still unclear, however it is hypothesized that ketones elicit an anticonvulsive effect. They influence excitatory and inhibitory neurotransmitters, in addition to cell excitability.

• Multiple Sclerosis

Due to altered and impaired glucose metabolism, increasing energy supply through ketosis could potentially be beneficial. There is also a lower uptake of glucose in the brain of MS sufferers, and providing the brain with an alternative source may reduce the rate of degeneration.

• Obesity

Fat is burned as a source of energy when ketosis is achieved.

• Alzheimer’s Disease (AD)

In AD, low glucose metabolism in the brain precedes cognitive decline and memory loss. The impaired glucose uptake present in AD may be supported by ketones, as beta-hydroxybutyrate and acetoacetate are the brain’s alternative energy sources to glucose. These ketones are able to act as energy sources for the brain, as the brain receives approximately 65% of its energy from ketone bodies when blood glucose levels are low.

• Parkinson’s Disease (PD)

It is hypothesized that the ketone body, beta-hydroxybutyrate elicits a protective action on neurons, and prevents neurodegeneration in PD.

Testing Ketones

By urinating on a urine strip, the colour detected will indicate the level of ketones in your urine.

It is advised to check ketones first thing in the morning, before breakfast, and in the afternoon, before dinner. If you are in ketosis in the morning, but the afternoon ketones show that you are no longer in ketosis, you need to reduce your carbohydrate intake.

Negative ketone levels: <0.6 mmol

Low-moderate ketones: Between 0.6-1.5mmol

High ketones: 1.6-3.0mmol

Very high ketones: >3.0mmol

Eating to induce ketosis

In order to induce a ketogenic state and remain in ketosis, it usually means eating approximately 20-50 grams of carbohydrates daily. This is an individual number, and the limit of carbohydrates will be different for everyone.

Significantly reduce or eliminate the following foods:

• Bread
• Grains (Wheat, barley, oats, rye, rice, buckwheat, sorghum, millet, spelt)
• Pasta
• Starchy vegetables (potatoes, sweet potatoes, corn,
• Most fruit (Bananas, grapes, canned fruit, dried fruit, melons)
• Lollies and desserts
• Fruit juice, soft drinks
• Legumes and beans (chickpeas, lentils, kidney beans, soybeans)
• Processed meats, crumbed meats
• Condiments and sauces with added sugar. Honey, sucralose, table sugar

Include the following foods:

• High fat (butter, coconut oil, olive oil, ghee, lard, avocado, nuts and seeds)
• Low carbohydrate vegetables (greens, onion, garlic, capsicum, celery, cucumber, zucchini, cauliflower, Konjac root or Shirataki noodles, also marketed as ‘Slendier Pasta’)
• Protein (eggs, beef, poultry, pork, fish, organ meats, lamb, shellfish)
• Fruit in small amounts (berries, lemon, cherries, grapefruit, kiwi)
• Sweeteners (if needed- stevia, monk fruit, erythritol)
• Dairy products (full-fat yoghurt, cottage cheese, hard and soft cheeses)

Meal Options for the Ketogenic Diet

Below is a sample menu of various meal options for the ketogenic diet:

References:

Cappello G, Franceschelli A, Cappello A, De Luca P, 2012, ‘Ketogenic enteral nutrition as a treatment for obesity: short term and long term results from 19,000 patients’, Nutr Metab (London), 9:96.

Cai QY, Zhou ZJ, Luo R, Gan J, Li SP, Mu DZ, Wan CM, 2017, ‘Safety and tolerability of the ketogenic diet used for the treatment of refractory childhood epilepsy: a systematic review of published prospective studies’, World J Pediatr.

Cunnane SC, Courchesne-Loyer A, St Pierre V, Vandenberghe C, Pierotti T, Fortier M, Croteau E, Castellano CA, 2016, ‘Can ketones compensate for deteriorating brain glucose uptake during ageing? Implications for risk and treatment of Alzheimer’s disease’, Ann N Y Acad Sci, 1367(1): 12-20

Pawlosky RJ, Kemper MF, Kashiwaya Y, King MT, Mattson MP, Veech RL, 2017, ‘Effects of a dietary ketone ester on hippocampal glycolytic and tricarboxylic acid cycle intermediates and amino acids in a 3xTgAD mouse model of Alzheimer’s disease’, J Neurochem, 141(2): 195-207

Paoli A, Bianco A, Damiani E, Bosco G, 2014, ‘Ketogenic Diet in Neuromuscular and Neurodegenerative Diseases’, Biomed Research International, 474296

Porta N, Vallee L, Boutry E, Auvin S, 2009, ‘The ketogenic diet and its variants: state of the art”, Rev Neurol (paris), 165(5): 430-439

Storoni M, Plant GT, 2015, ‘The therapeutic potential of the ketogenic diet in treating progressive Multiple Sclerosis’, Mult Scler Int, 681289

Swidinski A, Dorffel Y, Loening-Baucke V, Gille C, Gocktas O, Reibhauer A, Neuhaus J, Weylandt KH, Guschin A, Bock M, 2017, ‘Reduced mass and diversity of the colonic microbiome in patients with Multiple Sclerosis and their improvement with ketogenic diet’, Front Microbiol, 8:1141.

Walczyk T, Wick JY, 2017, ‘The Ketogenic Diet: Making a Comeback’, Consult Pharm, 32(7): 388-396

Diet Profile Research and Writing: Kimberly Kushner BHSc (Nutritional Medicine), BHSc (Naturopathy) for MINDD