Pirjo halusi nähdä tunnetussa The Lancet -tiedelehdessä julkaistun kommenttini koskien tapausselotusta, jossa Atkins-dieetin väitettiin aiheuttaneen ketoasidoosin. Kyseessä oli siis uutisankka, sillä hyvin niukkahiilihydraattinen dieetti ei voi aiheuttaa ketoasidoosia terveillä ihmisillä ilman lääkkeiden ja/tai alkoholin väärinkäyttöä.
The Lancet 2006; 368:23DOI:10.1016/S0140-6736(06)68954-X
Life-threatening complications of the Atkins diet?
In a Case Report,1 Tsuh-Yin Chen and colleagues describe a 40-year-old woman who was vomiting as often as six times daily and had difficulty breathing after strictly following the Atkins diet for a month. According to the report, “Serum was positive for acetone, and β-hydroxybutyrate [a major ketone body] was high at 390 μg/mL (normal 0–44 μg/mL), consistent with ketoacidosis.”
When the rate of mobilisation of fatty acids from fat tissue is accelerated, as, for example, during a very-low-carbohydrate diet (eg, the Atkins diet), the liver produces ketone bodies. The liver cannot use ketone bodies and therefore they flow from the liver to extrahepatic tissues (eg, brain, muscle) for use as a fuel. Simply stated, ketone body metabolism by the brain displaces glucose use and thus spares muscle mass.2 Dietary ketosis is a harmless physiological state; however, many health-care professionals and even some scientists have confused dietary ketosis with diabetic ketoacidosis.
All diabetic patients know that the detection in their urine of ketone bodies is a danger signal that their diabetes is poorly controlled. In severely uncontrolled diabetes, if the ketone bodies are produced in massive supranormal quantities, they are associated with ketoacidosis. In this life-threatening complication of diabetes mellitus, ketone bodies are produced rapidly, and overwhelm the body's acid-base buffering system. However, a very-low-carbohydrate diet cannot lead to dangerous ketoacidosis in healthy individuals (without alcohol or drug abuse) because ketone bodies have effects on insulin and glucagon secretions that contribute to the control of their own formation. The ketones present in Chen and colleagues' patient (390 μg/mL) are not sufficient to have caused the acidosis. In fact, they are less than half of the ketoacidosis seen in untreated type 1 diabetes.
I declare that I have no conflict of interest.
1. A life-threatening complication of Atkins diet. Lancet 2006; 367: 958.
2. Very-low-carbohydrate diets and preservation of muscle mass. Nutr Metab 2006; 3: 9.