The lipid theory of cardiovascular disease states that dietary cholesterol and saturated fat are the cause of elevated levels of blood cholesterol. Proponents claim further that these increases in blood cholesterol then cause atherosclerosis, which drives cardiovascular disease. Many studies have shown that increasing the saturated fat and cholesterol content of the diet does increase the plasma levels of cholesterol. However, increasing the dietary content of saturated fat and cholesterol necessitates in most cases reductions in other components of the diet, particularly carbohydrate. As dietary carbohydrate is the only sources of dietary fibre, what these studies often do inadvertently, is lower dietary intakes of fibre. Now this is problematic, because dietary fibre has been shown to be an effective modifier of blood cholesterol levels in the human diet. From such studies it is therefore not possible to conclude that the increases in cholesterol levels are due to the increases in dietary lipid intakes, as confounding variables exist.
The efficacy of dietary fibre to influence cholesterol metabolism has been shown in numerous well designed studies. Dietary fibre can influence blood cholesterol levels because the fibre binds to bile acids, themselves synthesised from cholesterol, and increase their excretion. Fibre therefore flushes a product of cholesterol metabolism from the gut. Replacement of the excreted bile acids, then necessitate a diversion of newly synthesised cholesterol to replace these biles acids, thus lowering the cholesterol available to be transported in the blood. For example, one study1 investigated the effects of high or low fibre intakes in young healthy subjects. In a random order, subject consumed either 59 grams of fibre or 21 grams of fibre for 4 days, before switching to the other fibre intake after a 9 day rest period. Sampling of faecal matter during the study showed that primary bile acid excretion, including chenodeoxycholic and cholic acid, increased from 4 to 32 % of total bile acids by switching from the control to high fibre diet.
Therefore the high fibre diet caused a significant increase in the excretion of primary bile acids. At the same time secondary bile acid excretion, including lithocholic and deoxycholic acid, showed concomitant decreases in excretion. Secondary bile acids are formed in the gut from the action of bacteria on primary bile acids, and the authors suggested that the decrease in secondary bile acids may have resulted from an inhibitory effect of the fibre on secondary bile acid synthesis by the bacteria in the colon. However, the reason for this is not exactly clear and other possibilities may explain this observation. Coprostanol, a metabolite of cholesterol synthesis, decreased from 76 % on the control diet to 64 % on the low fibre diet to 45 % on the high fibre diet, when calculated as a percentage of total neutral sterols. This suggests that the conversion of cholesterol to coprostanol may have decreased, perhaps because of the increased bile acid excretion limited the availability of the substrate for synthesis.
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