**7. Mechanisms for weight loss on the LCHF eating plan**

Increased satiety, allowing a lower energy intake without hunger and a specific metabolic advantage have been proposed to explain how LCHF diets produce weight loss, despite an increased consumption of energy-dense 'fatty' foods.

A recent systematic review compared weight loss between participants on 'LCHF diets' and 'low fat balanced diets' [64] but excluded all trials that were not isoenergetic. Although the original study did not find any differences in weight loss between the different diets, a reanalysis [64] of the same data found a small but significantly great weight loss on the lower carbohydrate diet.

Greater satiety on LCHF diets in persons responding to the diet may result from a number of mechanisms, including increased protein intake, which promotes satiety [65]; ketogenesis, which suppresses appetite [66] and fewer instances of rebound hypoglycaemia.

**9. LCHF diets and cardiovascular risk factors**

82, 83] low glycaemic index [84] and many other diets.

be especially beneficial for those with insulin resistance.

particles [3, 81, 85, 90–92].

An understandable concern with any increased dietary fat intake on the LCHF diet is the increased risk of future cardiovascular disease. This is largely based on the Ancel Keys' original seven countries study [20], which led to the development of traditional LFHC dietary guidance. However, there is good evidence emerging now that LCHF diets significantly alter cardiovascular risk more so than LFHC diets, especially in those with T2DM and metabolic syndrome.

Low-Carbohydrate High-Fat (LCHF) Diet: Evidence of Its Benefits

http://dx.doi.org/10.5772/intechopen.73138

79

Many RCTs show that LCHF diets lower blood triglyceride [77] and blood apoprotein B concentrations significantly more than do LFHC diets [3, 78–81]. Furthermore, no other diet increases HDL-C concentrations as effectively as do LCHF diets, which outperform LFHC [79,

Tay et al. [79] compared a very LCHF with an LFHC diet over a 1-year period—despite similar weight loss, there was significantly more lowering of blood TG concentrations (−0.58 vs. −0.22 mmol/L) and greater increase in HDL-C concentrations (+0.30 vs. +0.07 mmol/L) with the LCHF diet. This has huge connotations for reducing coronary artery disease and would

A contentious issue regarding the LCHF diet is the variable LDL-C response to the increase in dietary fat intake. Some trials show a decrease or non-significant change in LDL-C concentrations [38, 85], whereas others report a more marked increase in LDL-C levels [86]. Tay et al. [79], in their study, have demonstrated that both LDL-C (+0.6 vs. +0.1 mmol/L) and total cholesterol (+0.7 vs. +0.1 mmol/L) concentrations increased significantly more in those following the LCHF diet.

Many other systematic reviews [87] and trials [88] have confirmed similar positive effects on overall lipid profile. However, one needs to remember that LDL-C concentrations predicted by the Friedewald equation becoming increasingly inaccurate at low blood TG concentrations [89] as seen with the LCHF diet. It has been shown that LCHF diets consistently reduce the proportion of small, dense LDL particles while increasing the number of large, buoyant LDL

Additionally, LCHF diets have been associated with improvements in flow-mediated arteriolar dilation [80], decreased inflammatory biomarkers [14], lower systolic and diastolic blood pressures [3], improved glycaemic control with reduced HbA1c, plasma glucose and insulin concentrations [87] and preferential reduction in visceral and liver fat—changes in these sur-

Non-alcoholic fatty liver disease (NAFLD) is characterised by elevated TG and low HDL-C concentrations with overproduction of VLDL and impaired clearance of TG-rich lipoproteins

rogate markers would be expected to reduce cardiovascular risk significantly [3, 93].

**10. LCHF and non-alcoholic fatty liver disease (NAFLD)**

Although still controversial, it has been suggested that LCHF diets may provide a metabolic 'advantage' favouring greater weight loss, despite the ingestion of an equal number of calories. This metabolic advantage could be related to thermogenic effects of protein intake, greater protein turnover for gluconeogenesis and loss of energy through excretion of ketones in sweat or urine [67, 68]. This state of increased lipolysis with reduced lipogenesis contributes to a metabolic milieu theoretically favouring fat loss. This effect is dependent on reduced blood insulin concentrations, uniquely produced by the LCHF diet.
