Overweight and diabetes prevention: is a low-carbohydrate-high-fat diet recommendable?

Abstract

In the past, different types of diet with a generally low-carbohydrate content (< 50-< 20 g/day) have been promoted, for weight loss and diabetes, and the effectiveness of a very low dietary carbohydrate content has always been a matter of debate. A significant reduction in the amount of carbohydrates in the diet is usually accompanied by an increase in the amount of fat and to a lesser extent, also protein. Accordingly, using the term "low carb-high fat" (LCHF) diet is most appropriate. Low/very low intakes of carbohydrate food sources may impact on overall diet quality and long-term effects of such drastic diet changes remain at present unknown. This narrative review highlights recent metabolic and clinical outcomes of studies as well as practical feasibility of low LCHF diets. A few relevant observations are as follows: (1) any diet type resulting in reduced energy intake will result in weight loss and related favorable metabolic and functional changes; (2) short-term LCHF studies show both favorable and less desirable effects; (3) sustained adherence to a ketogenic LCHF diet appears to be difficult. A non-ketogenic diet supplying 100-150 g carbohydrate/day, under good control, may be more practical. (4) There is lack of data supporting long-term efficacy, safety and health benefits of LCHF diets. Any recommendation should be judged in this light. (5) Lifestyle intervention in people at high risk of developing type 2 diabetes, while maintaining a relative carbohydrate-rich diet, results in long-term prevention of progression to type 2 diabetes and is generally seen as safe.

Keywords: High-fat diet; Ketogenic diet; Low-carbohydrate diet; Obesity.; Type 2 diabetes.

Fig. 1

Gluconeogenesis (production of glucose) and glycolysis (breakdown of glucose) are processes that always take place simultaneously and are reciprocal (if one is high, the other is low, and vice versa). In cases of low-glucose availability from glycogen, glycolysis will be conducted at a low level and there will be a stimulus for gluconeogenesis

Fig. 2

In a high-carbohydrate diet, the glucose reserves in the liver and muscles are usually well stocked. In fasting conditions, blood glucose levels are kept steady by breakdown of glucose from the liver glycogen. This is regulated by the insulin/glucagon ratio. The low insulin levels ensure that relatively few fatty acids are stored in the adipose cells, while the secretion of fatty acids by the breakdown of stored lipid (lipolysis) ensures elevated blood plasma fatty acid levels. This leads to a high degree of fatty acids oxidation and relatively low oxidation of glucose. This is then expressed in a low respiratory quotient (RQ), usually 0.75–0.8

Fig. 3

Following a carbohydrate-rich meal, the blood glucose is elevated by the supply of glucose from the intestine, resulting in elevated insulin levels and a temporary decrease in glucagon levels. This combination results in a sharp decrease in glucose production from the liver glycogen. At the same time, the release of fatty acids from the adipose cells  is inhibited and the uptake of both glucose and fatty acids from the blood is stimulated. In this case, the burning of primarily fatty acids in a fasting condition shifts to a combination of elevated glucose- and reduced fat oxidation. This is expressed in an elevated respiratory quotient (RQ), depending on the carbohydrate intake and the magnitude of the insulin response, between 0.85 and 1.0. There is also a small contribution from amino acids, which are converted into glucose via gluconeogenesis. Under normal conditions, this amounts to approx. 1–3%, although in cases of acute or chronic carbohydrate restriction resulting in significant glycogen breakdown and depending on the degree of adaptation to the situation this can even rise to > 15% [–37]

Fig. 4

When following an LCHF diet, the amount of glucose that is taken up in the blood from the food each day is insufficient to maintain the glycogen stores in the liver and muscles. This results in an reduction of glycogen stores, reduced glucose release and consequently to reduced  blood glucose levels. The body experiences this as stress and will do everything it can to ensure it burns fatty acids as much as possible with the aim of preventing utilization of glucose, which is needed primarily for the central nervous system and the red blood cells, as much as possible. This is achieved by a sharp decrease in insulin and an increase of stress hormones. This results in an excess supply of fatty acids, leading to a partially incomplete metabolism in which ketones are produced (ketogenesis) from a part of the produced acetyl-CoA. These ketones can then be used by the brain and the muscles as an alternative fuel source instead of glucose. This is crucial to the brain, as fatty acids cannot pass through the blood–brain barrier, while glucose and ketones can. In the case of a shortage of glucose, the brain cells and neurons are able to use ketones as an alternative fuel source. There is also a small to medium contribution from amino acids, which are converted into glucose via gluconeogenesis

Fig. 5

Ketogenesis is a process that takes place entirely in the liver