Life-threatening complications of the Atkins diet? The Case Report concerning lifethreatening complications in a follower of the Atkins diet (March 18, p 958)1 could be misleading. First, it is of critical relevance to characterise and describe the baseline weight and body-mass index (BMI) as well as other potential confounding factors such as comorbidity or concomitant medication, previous weight-lowering attempts, and current physical activity patterns. Second, a more in-depth description of dietary compliance should have been reported, with emphasis on actual energy intake rather than just the characteristics of the average Atkins diet. These issues are of importance to the adequate interpretation of the situation and the validity of the outcome. Third, low-carbohydrate, high-fat diets have many diﬀerent versions, but some dietary approaches based on this macronutrient distribution have produced valid and eﬀective weight loss.2 Fourth, the publication of case reports helps in understanding the features of complex clinical syndromes and treatments, but we should not forget that randomised controlled trials based on ketogenic diets have shown weight loss over 6 months and improvement in other metabolicrelated problems such as hypertension, lipid proﬁle disturbances, or insulin resistance.3 Fifth, a systematic review of the safety of Atkins-related diets concluded that there is not enough evidence to make recommendations for or against the use of lowcarbohydrate, high-fat diets. This conclusion was later conﬁrmed by a Rapid Review in The Lancet.4 Sixth, ketogenesis was indeed the mechanism originally proposed to explain the Atkins diet’s eﬃcacy, but www.thelancet.com Vol 368 July 1, 2006
nowadays reduced caloric intake due to the limited food choice is regarded as the main factor promoting weight loss by this kind of diet.5 The case report should have taken all these issues into consideration.
*J Alfredo Martínez, M Dolores Parra [email protected]
Department of Physiology and Nutrition, University of Navarra, 31008 Pamplona, Spain. 1
Chen TY, Smith W, Rosenstock JL, Lessnau KD. A life-threatening complication of Atkins diet. Lancet 2006; 367: 958. Bravata DM, Sanders L, Huang J, et al. Eﬃcacy and safety of low-carbohydrate diets: a systematic review. JAMA 2003; 289: 1837–50. Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004; 140: 769–77. Astrup A, Meinert Larsen T, Harper A. Atkins and other low-carbohydrate diets: hoax or an eﬀective tool for weight loss? Lancet 2004; 364: 897–99. Abete I, Parra MD, Zulet MA, Martínez JA. Diﬀerent dietary strategies for weight loss in obesity: role of energy and macronutrient content. Nutr Res Rev (in press).
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.
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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.
Anssi H Manninen [email protected]
Advanced Research Press, Setauket, NY 11733, USA 1
Chen TY, Smith W, Rosenstock JL, Lessnau KD. A life-threatening complication of Atkins diet. Lancet 2006; 367: 958. Manninen AH. Very-low-carbohydrate diets and preservation of muscle mass. Nutr Metab 2006; 3: 9.
Tsuh-Yin Chen and colleagues1 describe profound metabolic acidosis with evidence of ketoacidosis as a life-threatening complication of the Atkins diet. Assuming that the blood sample taken for the determination of β-hydroxybutyrate was simultaneous with that used for other analyses, both the anion gap and base deﬁcit are greater than that predicted if β-hydroxybutyric acid at a concentration of 390 μg/mL (3·8 mmol/L) was the sole cause of the acidosis. Acetoacetate occurs at lower concentrations than β-hydroxybutyrate in ketoacidosis and cannot account for the missing anions. This raises the interesting question as to the nature of these anions.
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