Evidence suggests that the cholesterol theory of cardiovascular disease is erroneous and that naturally occurring dietary lipids are not the cause of atherosclerosis. Instead, research has consistently shown that carbohydrate in the diet is the cause of cardiovascular disease. In particular, high fructose intakes are though to be responsible for the development of a group of biochemical abnormalities known as metabolic syndrome. These include changes to blood lipids, abdominal adiposity and systemic inflammation, which together cause a significant increased risk of cardiovascular disease. The reason that fructose is able to cause the metabolic abnormalities associated with metabolic syndrome relates to the way it can overload the metabolic pathways of the liver. This subsequently increases de novo lipogenesis and the storage of lipids in the liver and skeletal muscle, which may be a contributory factor in the development of insulin resistance.
The detrimental effects of fructose have been known for a long time in the scientific community. However, the permeation of this information into the public domain has been deliberately hampered by aggressive propaganda from the food industry and the mainstream medical establishment. One study published in the American Journal of Clinical Nutrition back in 19891 investigated the effects of fructose on a number of important metabolic parameters. Both hyperinsulinaemic and non-hyperinsulinaemic men were fed a traditional Western diet, with either 20 % of total calories as fructose or high amylose cornstarch. Subjects consumed the diets consecutively in a random order for 5 weeks each. Diets were identical apart from the fructose or high amylose cornstarch with intake providing 51 % of calories as carbohydrate, 13 % as protein and 36 % as fat. The researchers used biochemical tests to assess the effects of the diets.
In the hyperinsulinaemic men, fructose caused a significant increase in plasma triglycerides (very low density lipoproteins (VLDL)), total cholesterol, apolipoprotein B-100 (a component of VDLD, intermediate density lipoprotein (IDL) and low density lipoproteins (LDL)), C-II (a components of VLDL and chylomicrons) and C-III (a component of VLDL) and uric acid. In the non-hyperinsulinaemic men, significant increases in plasma triglycerides (VLDL), total cholesterol, LDL and uric acid were reported. These results therefore support the theory that fructose in the diet at around 20 % of total calories is able to cause detrimental lipoprotein changes that are associated with an increased risk of cardiovascular disease. Although 20 % of calories as fructose seems large, estimates suggest that Western diets rich in soft drinks and other sucrose sweetened beverages may provide more than this amount. It is looking increasingly likely that fructose is the cause of the cardiovascular epidemic in recent decades.
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