The metabolic syndrome is a group of disorders that are now thought to be a major contributory factor in the development of obesity, cardiovascular disease and type 2 diabetes. Metabolic syndrome, also called syndrome X, is characterised by changes to normal lipoprotein metabolism, elevated blood glucose and insulin levels, insulin resistance, abdominal body fat and non-alcoholic fatty liver disease. That fructose and refined carbohydrates are a major driver of the metabolic syndrome has been suggested. This is based on strong evidence that high intakes of crystalline fructose and carbohydrates refined from their fibre causes liver overload syndrome. As fructose can only be metabolised by the liver, and because refined carbohydrates cause such rapid increases in blood sugar, the combination overloads the liver with nutrients which are then pushed down the de novo lipogenesis pathway to form fatty acids. These fatty acids accumulate in skeletal muscle and the liver where they cause the insulin resistance that drives metabolic syndrome.
A number of studies have investigated the de novo lipogenesis pathway and its products in order to assess it role in the development of metabolic syndrome. One method that can be used to investigate its contribution to the disease is to measure the fatty acids that are a product of its flux. The de novo lipogenesis produces a number of specific fatty acids and these acids would be expected to be higher in individuals with a greater flux through the pathway. For example, in one study1, researchers measured the amount of myristic (C14:0), palmitic (c16:0), palmitoleic (c16:1 (N-7)), hexadecenoic (c16:1 (n-9)), stearic (C18:)), vaccenic (C19:1 (n-7)) and oleic (C18:1 (n-9)) acids in erythrocytes and determined their associations with the risk of metabolic syndrome in a Chinese population consuming over 60% of their energy as carbohydrate. The results confirmed that those subjects at the highest risk of metabolic syndrome did indeed have higher concentrations of fatty acids from the de novo lipogenesis pathways.
In particular, the fatty acids that are products of the de novo lipogenesis pathways were associated with a high ratio of carbohydrate to fat intake, less favourable lipid profiles and elevated liver enzymes (perhaps indicative of the development of non-alcoholic fatty liver disease). In addition the presence of palmitic (C16:0) and palmitoleic (C16:1 (n-7)) acids were associated with an increased risk of type 2 diabetes. Other studies have shown previously that palmitoleic acid, a primary product of the de novo lipogenesis pathways, is associated with an increased risk of metabolic syndrome. The elevated liver enzymes found in this study are interesting because they suggest that the metabolic dysfunction seen with the metabolic syndrome produces similar effects on the liver to excessive alcohol consumption. The similarities between alcoholic fatty liver caused by excessive alcohol consumption and non-alcoholic fatty liver cause by excessive fructose consumption have been identified previously.
Dr Robert Barrington’s Nutritional Recommendation: Crystalline fructose and refined carbohydrates are implicated as primary drivers of obesity and cardiovascular disease. Fructose should only be consumed in its original whole fruit form (and small quantities of honey) and refined carbohydrates should only be consumed within a 2 hour window of intense physical activity. Any foods with added crystalline fructose, sucrose or high fructose corn syrup should be avoided. Plant foods that maintain their original starch to fibre ratio are the only ones that should be consumed (except following exercise).
RdB
