Low carbohydrates diets appear to be effective in treating obesity. This may relate to the ability of such diets to improve insulin sensitivity. If this hypothesis is correct, it would be expected that such diets would be effective because they lower the cause of insulin resistance which is the raised levels of plasma triglycerides. Such raised levels of triglycerides, thought to be caused by increases fatty acid production in the liver through the de novo lipogenesis pathway, are observed in subject with the insulin resistant state that characterises the metabolic syndrome. The cause of this lipid production is likely to be a combination of fructose in the diet along with refined carbohydrates, that can overload the liver and peripheral cells with nutrients and then causes the development of insulin resistance. Feeding animals and humans high fructose diets has been shown to increase plasma levels of fasting triglycerides in just a few weeks. Avoiding carbohydrates through low carbohydrate diets therefore may reverse this process.
Studies have observed triglyceride lowering effects from low carbohydrates diets. For example, one study investigated the effects of a low fat energy restricted diet against a low carbohydrate non-energy restricted diet over six months1. Obese subjects consuming the low fat diet experienced a 4 % decrease in fasting triglyceride levels, whilst obese subjects consuming the low carbohydrate non-energy restricted diet experienced a 20 % reduction in fasting triglycerides. Insulin sensitivity improved more in the low carbohydrate group compared to the low fat group (6 % versus 3 %, respectively), suggesting that insulin resistance was improved more through avoidance of carbohydrate than it had through energy or fat restriction. Another finding of this study was that the low carbohydrates diet was superior to the calorie and fat restricted diet at causing weight loss in the subjects. Subjects consuming the low carbohydrate diet lost 5.8 kg, whilst subjects consuming the low fat energy restricted diet lost only 1.9 kg.
The ability of low carbohydrate diets to improve plasma levels of triglycerides can be explained based on the conversion of glucose to fatty acids in the de novo lipogenesis pathway. Plasma triglycerides refers to fasting levels of the very low density lipoprotein (VLDL) particle, which contains high amounts of triglycerides within its lipid content. Fasting triglycerides as the VLDL particle are often either ignorantly or deliberately confused with postprandial triglycerides which are derived from intakes of fat in the diet that pass through the lymphatic system to the blood. Elevations in postprandial triglycerides are proportional to fat intake, and subside as the fat is stored and oxidised following absorption. In contrast raised levels of fasting triglycerides causes permanent elevations in VLDL particles and are a result of a disease process. The erroneous belief that fasting triglyceride levels are caused by dietary fat is therefore based on false logic, as it is carbohydrates that are implicated in this condition, not dietary fat.
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