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KETOGENIC DIET THERAPY: WHAT’S ALL THE FUSS ABOUT? Susan Wood Specialist Dietitian; Ketogenic Therapies, Matthew's Friends Clinics and Charity
The referral of a young adult for ketogenic dietary therapy (KDT) certainly sent shivers of uncertainty down my spine in 2008 and nine years on, I still get a sense that many dietetic colleagues, particularly those in adult practice, are ill at ease when ketogenic diets (KD) are mentioned. However, the basic biochemical premise of a KD is simple . . .
Susan works full time for Matthew's Friends Clinics and Charity as a specialist Ketogenic Dietitian, treating children and adults with drug resistant epilepsy and adults with brain tumours.
When the body goes from the fed to the fasted state, the liver switches from an organ of carbohydrate utilisation and fatty acid synthesis to one of fatty acid oxidation and ketone body production.1 Ketones are circulated as an alternative energy source to glucose, ensuring uninterrupted fuelling of essential tissues with high energy demand (e.g. brain and heart muscle). A low carbohydrate KD mimics this fasting state and shifts us into fat burning mode, using fats consumed in the diet, supplemented with fats taken from body stores if the dietary fat intake is insufficient. It results in a sustained presence of ketones and a flattening of post-meal glucose and insulin peaks, with levels tending toward the mid to lower end of the normal ranges. The benign ketosis associated with a low carbohydrate KD must not be confused with ketoacidosis (Table 1).2 Beyond the changes in circulating ketones, glucose and insulin, a myriad of biochemical pathways and the gut
microbiota are altered, leading to many possible mechanisms of action by which the KD exerts a range of therapeutic effects. Almost a century on from its creation as a treatment for epilepsy, scientists still struggle to pin down ‘the ketogenic effect’. Nevertheless, its utility continues to deliver profound changes in around half the children and adults undergoing supervised KDT for drug resistant epilepsy and it remains the only treatment for Glucose transporter type-1 deficiency and Pyruvate Dehydrogenase Deficiency (PDHD). The potential for KD metabolism to influence the aberrant cellular function underpinning a broad range of medical conditions is creating significant research interest too, meaning that KDT is not going away anytime soon (Table 2 overleaf).3-6 KETOGENIC DIET BASICS
The most powerful, over simplified and misguided nutrition message to reach the UK population over the last few decades has been that; ‘fat is
Table 1: Ketosis is NOT Ketoacidosis The difference between the two conditions is a matter of volume and flow rate: Ketosis: benign nutritional ketosis is a controlled, insulin regulated process that results in a mild release of fatty acids and ketone body production in response to either a fast from food, or a reduction in carbohydrate intake. Ketoacidosis is driven by a lack of insulin in the body. Without insulin, blood glucose rises to high levels and stored fat streams from fat cells. This excess amount of fat metabolism results in the production of abnormal quantities of ketones. The combination of high blood glucose and high ketone levels can upset the normal acid/base balance in the blood and become dangerous. In order to reach a state of ketoacidosis, insulin levels must be so low that the regulation of blood sugar and fatty acid flow is impaired.
www.NHDmag.com November 2017 - Issue 129
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