Evidence suggests that high fructose intakes are a cause of insulin resistance in mammals. High intakes of fructose in laboratory mammals such as rats can cause the development of insulin resistance in just a few short weeks. While initially dismissed as being nutritionally irrelevant due to the high amounts of fructose used in such studies, nutritional surveys analysing the intakes of fructose have confirmed that many humans do in fact obtain equivalent levels of fructose to the rats (up to 70 grams per day). This fructose comes mainly from fruit juices, sugar sweetened beverages and other sugar containing products. Therefore fructose is a likely causative factor in the development of insulin resistance in humans, something that has been confirmed in clinical trials. The association of insulin resistance with weight gain, non-alcoholic fatty liver disease, abdominal obesity and blood lipid changes therefore suggests that fructose is a primary driver of the metabolic changes that lead to the development of the metabolic syndrome.
The ability of fructose to cause changes in blood lipid levels is interesting because the role of carbohydrates in the aetiology of cardiovascular disease has been totally overlooked by the vast majority of so called nutritional and medical experts. Despite protestations to the contrary made by informed and intelligent mavericks, the mainstream is still stuck in their lipid theory of cardiovascular disease. However, evidence dating back many decades has shown quite convincingly that refined carbohydrates such as crystalline sucrose and fructose are able to cause significant detrimental changes to the blood lipids of certain individuals. For example, a paper published in 1983 investigated the effects of varying concentrations of fructose (0, 7.5 or 15 % energy as fructose) in the diets of human subjects for 5 weeks periods1. The diets contained 43 % of energy as carbohydrate, 42 % as fat and 15 % as protein and so were similar to diets that the typical Westerner would have consumed in terms of macronutrient ratios.
The results of the study showed that total cholesterol and low density lipoprotein (LDL) cholesterol were significantly higher after the consumption of the 7.5 and 15 % fructose diets compared to the control diet (0 % fructose). Further the triglyceride levels of the subjects, actually a measure of the very low density lipoprotein (VLDL) cholesterol, rose in a dose response as a result of increasing intakes of fructose. Such lipoprotein changes are associated with cardiovascular disease and as such the consumption of fructose in these subjects put them at increased risk of developing the disease. This supports the many animals and human studies performed since this time that show that dietary refined crystalline fructose to be a disease causing agent and a likely driver of metabolic syndrome, obesity and cardiovascular disease. Fructose can cause detrimental lipoprotein changes because it is a metabolic poison that detrimentally affects the liver by shifting its metabolism to one of fatty acid synthesis.
Dr Robert Barrington’s Nutritional Recommendation: Evidence in the nutritional literature suggests that fructose is a primary driver of disease. However, not all fructose is detrimental. Fructose in its natural fruit form does not show the same detrimental health effects as refined crystalline fructose because the fibre and high water content of the fruit lessen the amount and rate of fructose delivered to the liver. Only fructose refined into a crystalline powder and added to foods as a sweetener in the absence of fibre appears to have these effects. The subjects in this study were selected because they were carbohydrate sensitive, meaning they likely already had some degree of insulin resistance. However, other studies have shown fructose has similar effects in healthy non-insulin resistant individuals.
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