Ketogenic Diet for Obesity: Friend or Foe?

Abstract

Obesity is reaching epidemic proportions and is a strong risk factor for a number of cardiovascular and metabolic disorders such as hypertension, type 2 diabetes, dyslipidemia, atherosclerosis, and also certain types of cancers. Despite the constant recommendations of health care organizations regarding the importance of weight control, this goal often fails. Genetic predisposition in combination with inactive lifestyles and high caloric intake leads to excessive weight gain. Even though there may be agreement about the concept that lifestyle changes affecting dietary habits and physical activity are essential to promote weight loss and weight control, the ideal amount and type of exercise and also the ideal diet are still under debate. For many years, nutritional intervention studies have been focused on reducing dietary fat with little positive results over the long-term. One of the most studied strategies in the recent years for weight loss is the ketogenic diet. Many studies have shown that this kind of nutritional approach has a solid physiological and biochemical basis and is able to induce effective weight loss along with improvement in several cardiovascular risk parameters. This review discusses the physiological basis of ketogenic diets and the rationale for their use in obesity, discussing the strengths and the weaknesses of these diets together with cautions that should be used in obese patients.

A 1-week extension of a ketogenic diet provides a further decrease in myocardial 18F-FDG uptake and a high detectability of myocarditis with FDG-PET

“…7 These observations are in agreement with the previous knowledge that drastic carbohydrate reduction, prolonged at least 3-5 days, are required to definitely enter into a state of ketosis. 15 After this delay-time, the glucose reserves become insufficient, both for normal fat oxidation via the supply of oxaloacetate in the Krebs cycle and for the supply of glucose, even in the central nervous system. 15,16 The present experimental study is the first in which the impact of such a drastic diet, leading to an increase in circulating ketone bodies at a very high level and equivalent to that reached by a prolonged 18-hour fasting period, could be monitored by serial 18 F-FDG-PET during a 7-day period.…”

“…15 After this delay-time, the glucose reserves become insufficient, both for normal fat oxidation via the supply of oxaloacetate in the Krebs cycle and for the supply of glucose, even in the central nervous system. 15,16 The present experimental study is the first in which the impact of such a drastic diet, leading to an increase in circulating ketone bodies at a very high level and equivalent to that reached by a prolonged 18-hour fasting period, could be monitored by serial 18 F-FDG-PET during a 7-day period. In these conditions, cardiac -FDG-PET in a vertical long-axis orientation in a myocarditis rat (B) and in a normal rat (A) both following the initial 18-hour fasting period and at the end of the 7-day ketogenic diet.…”

“…Such protocols have previously been shown to be well tolerated, even when prolonged several weeks or months in various diseases, including with an established efficacy in pediatric pharmaco-resistant epilepsy. [13][14][15] Ketogenic diet may also be prescribed in diabetic patients without significant risk and at the condition of adapting the antidiabetic treatment to the improvement in blood glucose levels and to the reduction of the need for insulin, which are currently induced by such diets. 30 In addition, low-carbohydrate diets have shown a significant albeit variable effectiveness for decreasing myocardial 18 F-FDG uptake in a number of 18 F-FDG-PET studies conducted in humans 4,[8][9][10] or animals.…”

“…This study was aimed at determining whether a drastic ketogenic diet provides a further decrease in physiological myocardial 18 F-FDG uptake and a high detectability of myocarditis by 18 F-FDG-PET in rats, when this diet is prolonged up to 1 week, as compared with a standard 18-hour fasting conditioning. Such diet can be prescribed at a much longer term than fasting, [13][14][15] leading to metabolic changes that are known to progressively suppress the metabolic use of glucose, even in the brain, within at least a 3-to 5-day period. [15][16][17][18] …”

“…Such diet can be prescribed at a much longer term than fasting, [13][14][15] leading to metabolic changes that are known to progressively suppress the metabolic use of glucose, even in the brain, within at least a 3-to 5-day period. [15][16][17][18] …”