While the medical establishment continues to spread its propaganda about the outdated and absurd cholesterol theory of cardiovascular disease, the rest of the World has come to its senses and moved on. This paradigm shift is based largely on evidence from the nutritional literature that is increasingly implicating fructose as the cause of the detrimental metabolic changes that result in obesity, type 2 diabetes and cardiovascular disease. Fructose is a metabolic poison because it can only be metabolised by hepatic tissue and in this regard fructose is similar to alcohol. High intakes of fructose, as are common in the Western diet, therefore place a burden on the liver tissue and may cause liver overload syndrome. This shifts metabolic pathways flux such that energy is diverted from glycogen synthesis to de novo lipogenesis, the result of which is the production of fatty acids. These endogenously synthesised fatty acids accumulate in hepatic and skeletal muscle where they interfere with insulin signalling and cause a reduction in insulin sensitivity.
One of the effects of the accumulated fatty acids in liver tissue is the development of abdominal obesity and non-alcoholic fatty liver. These conditions are thought to result in detrimental physiological changes to hepatic physiology, which ultimately causes a shift in metabolic pathway flux. Although the mechanisms are not fully understood, one of the consequences of this shift are deleterious changes to normal lipoprotein metabolism. Fructose therefore ultimately modifies normal levels of plasma lipoproteins, the changes to which are typically characterised by elevated levels of circulating very low density lipoprotein (VLDL) and depressed levels of circulating high density lipoprotein (HDL). Such lipoprotein changes are associated with an increased risk of cardiovascular disease, and have been used by many to implicate dietary cholesterol in the aetiology of cardiovascular disease. However, there is no mechanism by which dietary cholesterol can cause these changes, something which cannot be said for dietary fructose.
The main problem with fructose is the sheer volume of it consumed by many as part of their low quality ‘Western’ nutrition. Fructose is one of the monosaccharides in sucrose (table sugar) and as such makes up a large percentage of the modern Western diet. In addition, fructose is often consumed without the accompanying fibre that is present in all natural sources of fructose excluding honey. This fibre adds bulk to the foods and as such limits the rate at which they can be consumed. Because fruit contains fructose, but is not associated with obesity, researchers are interested in the ability of fibre to modulate the detrimental effects of fructose. For example, in one study1, researchers investigated the effects of low (<14 grams per day) and high (>34 grams per day) intakes of fibre on blood lipid changes caused by diets containing 0, 18, 36 and 54 % sucrose as a percentage of energy intake. As had been reported in animal experiments, consumption of the sucrose diets caused detrimental changes to the plasma lipoprotein profiles of the subjects.
For example, when the subjects swapped from their usual diet to the 0 % sucrose diets their plasma triglycerides declined significantly. For the 18 % sucrose diet plasma triglycerides showed a trend upwards that was prevented by an increase in dietary fibre. However, for the 36 and 52 % sucrose diets, plasma triglycerides rose significantly. This rise was only partially prevented by a higher fibre intake in the 36 % diet, but was not prevented by a greater intake of fibre in the 52 % sucrose diet. Therefore fibre may be able to prevent the detrimental changes to plasma triglycerides, but only at lower concentrations of sucrose. Compared to the control (0 % sucrose) all concentrations of sucrose caused a decrease in the plasma concentrations of HDL. However, these detrimental changes were not prevented by the addition of increased concentrations of fibre. There was no effect on total or LDL cholesterol at any concentration of sucrose, but as has been reported previously, higher intakes of fibre caused a lowering of plasma total cholesterol.
These data suggest that sucrose likely causes detrimental changes to plasma lipoprotein levels. In addition, these changes are not wholly prevented by the addition of higher intakes of fibre to the diet. This may suggest that there is a levels of sucrose in the diet above which no intake of fibre will be effective at preventing deleterious metabolic changes. Although it is not possible to implicate fructose in these changes just from data in this study, analysis of data from animals and other human studies suggests that the likely agent of change in the subjects was the fructose moiety of the sucrose molecule. Another caveat that should be considered from studies such as this relates to the inability to change one aspect of a subjects diets. By increasing the sucrose content of the diet, other components of the diet must decrease. Therefore the effects cannot definitively be attributed to sucrose. This ‘trick’ is often used by those wishing to show effects for increases in dietary cholesterol, that really should be attributed to reductions in dietary fibre.
RdB
