Sudden Cardiac Death of an Adolescent During Dieting

Amy Stevens, MD, D. Paul Robinson, MD, Julie Turpin, RD, Ted Groshong, MD, Joseph D. Tobias, MD


South Med J. 2002;95(9) 

In This Article


Low-carbohydrate/high-protein diets have fallen in and out of popularity since the 1960s, resurfacing in various forms including the Stillman diet, the Scarsdale diet, the Zone diet, the carbohydrate addicts' diet, and the Atkins diet. The Atkins diet was developed by Robert C. Atkins, MD, in 1970 and has gained recent popularity once again with the release of the revised and updated book Dr. Atkins' New Diet Revolution.[2]

Low-carbohydrate/high-protein plans seem attractive to many dieters because these diets set no limit on the amount of certain types of foods one can eat, exclude hunger from the dieting experience, reduce appetite, and at times, produce steady weight loss, even after dramatic failures or weight gain on other diets.

With a high-protein/high-fat intake, there is the release of cholecystokinin, a known appetite suppressant. The lack of glucose in the diet also avoids the 1-hour postprandial insulin surge associated with stimulation of neurogenic feeding centers. Additionally, the increased reliance on fat to meet the metabolic demands results in the production of ketone bodies and systemic ketosis, which may also suppress the appetite and curb feelings of hunger.

However, low-carbohydrate/high-protein diets are not without the potential for adverse biochemical and physiologic consequences. Ketone bodies compete with uric acid for renal tubular excretion, which can exacerbate disease in patients with gouty diathesis. Bloom and Azar[3] reported that postural hypotension can develop in subjects on low-carbohydrate diets. Using an isolated, perfused rat heart model, Russell and Taegtmeyer[4] showed that the beating heart loses contractile function (more than 50% in 60 minutes) when oxidizing acetoacetate alone.

Although results are contradictory, some studies have linked these diets to increases in serum triglycerides and low-density lipoprotein cholesterol.[5,6] Elevated levels of free fatty acids may promote both vascular thrombosis and cardiac arrhythmias.[7,8] Plasma lipolysis and infusion of albumin-bound free fatty acids have been associated with the development of serious arrhythmias in dogs, possibly through a detergent effect on mitochondrial and cell membranes.[7] These diets have also been associated with hypothyroidism characterized by a decrease in thyrotropin and a marked decrease in triiodothyronine, as well as alterations in the metabolism of diuretics and cholesterol medications.[9]

More importantly, deaths associated with other specialized diets have been reported. In the 1960s and 1970s, liquid protein diets were associated with several deaths.[10] Some of these deaths were related to QT prolongation with pathologic findings of myocardial atrophy and myocarditis. Other findings in patients who had sudden cardiac death related to liquid protein diets included electrolyte disturbances such as hypokalemia, hypocalcemia, and hypomagnesemia.[10] Restriction of caloric intake to less than the basal needs results in the catabolism of protein and glycogen stores, which have a high water content, leading to a diuretic effect with the loss of free water and electrolytes. Ketone bodies undergo urinary excretion with a cation to maintain electrical neutrality, resulting in the additional loss of cations, including calcium, magnesium, and potassium.[11] When compounded by inadequate intake, deficiencies of these cations may ensue. Caloric restriction is not generally recommended on most low carbohydrate diets, including the Atkins diet, further emphasizing the dangers of using these diets without strict adherence to their recommendations.

Our patient's sudden onset of cardiorespiratory arrest occurred without an underlying cause identified by history or on postmortem examination. Initial electrocardiogram revealed ventricular fibrillation, an unusual presenting arrythmia in a 16-year-old adolescent without underlying cardiac disease or electrolyte disturbance. During resuscitation, with a pH of 6.89, the serum potassium level was 3.8 mEq/L, suggesting profound hypokalemia if corrected for the pH. The ionized calcium level was 1.12 mEq/L (normal, 1.10 to 1.22 mEq/L). As with serum potassium, correction for the pH would indicate significant hypocalcemia. Serum magnesium level was not measured. Because potassium and magnesium undergo similar handling mechanisms in the renal tubules, hypomagnesemia is another potential cause of our patient's cardiorespiratory arrest. When considering the potential causes of these electrolyte disturbances in an otherwise healthy female adolescent, questions arise regarding the potential role of the low-carbohydrate/high-protein diet compounded by a period of inadequate caloric intake and the resultant catabolic state. It is also possible, although no such history was obtained in this case, that associated problems such as bulimia, anorexia, and diuretic or laxative abuse can cause or potentiate electrolyte losses in such patients.

In light of the previous reports of mortality related to liquid protein diets and the lack of information on electrolyte and physiologic changes during low-carbohydrate, high-protein diets, we do not recommend such dieting regimens. We continue to suggest moderate caloric restriction with a balanced macronutrient and micronutrient intake and increased physical activity under a physician's guidance. While it is possible that the patient's dietary regimen had nothing to do with her sudden cardiovascular collapse, continued surveillance for similar cases is suggested.


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