The ability of humans to adapt to dietary changes is well reported in the nutritional literature. For example, in a recent study published in the American Journal of Clinical Nutrition1, researchers assessed the ability of humans subjects to adapt to consumption of a high fat diet. Subjects acted as their own controls and consumed both a high fat diet (37 % of energy from fat and 50 % of energy from carbohydrate) and a low fat diet (25 % of energy from fat and 63 % of energy from carbohydrate). After consuming the high fat diet for 3 days, plasma cholesterol, plasma low density (LDL) cholesterol and high density lipoprotein (HDL) cholesterol concentrations were significantly higher than when consuming the low fat diet. In addition, there was a significant increase in messenger RNA expression of key intestinal enzymes involved in lipoprotein metabolism. However, plasma triglycerides and apolipoprotein B-48 (a protein in chylomicrons) concentrations were significantly lower after the high fat diet.
These results are interesting because they follow a pattern seen during periods of increased fat intake. Firstly, plasma cholesterol increased during this time. Proponents of the cholesterol theory of cardiovascular disease will claim this shows that high fat diets are a driver of cardiovascular disease and that they are therefore detrimental to the health. However, many studies that have shown that high fat diets can raise plasma levels of cholesterol have generally been poorly designed. This is because high fat diets are also low fibre diets and decreasing the carbohydrate content of the diet also lowers the fibre content. As fibre is a plasma cholesterol modifying agent, it is not possible to say that the high fat content of the diet is the cause of the changes to plasma cholesterol concentrations in such cases. However, in this study the high and low fat diet were controlled to contain the same amount of fibre. Some other explanation is therefore required to explain the changes in plasma cholesterol levels.
If we look at the dietary content of the two diets we see that the high fat diet included 3.5 grams of trans fatty acids per day, whereas the trans fatty acid content of the low fat diet was too low to be detected. Because trans fatty acids are known to cause modifications to cholesterol levels, it is not possible to blame the high fat content of the diet as a whole, without singling out the role played by trans fats. In addition, the high fat diet contained fewer dietary plant sterols than the low fat diet (120 mg versus 180 mg, respectively). Plant sterols have been investigated for their ability to lower plasma cholesterol levels and so the assumption from this data is that the high fat diet may have caused increases in plasma cholesterol levels because the intake of plant sterols decreased. Interestingly, the researchers did not significantly increase the polyunsaturated fatty acid content of the ‘high fat diet’ which is strange as polyunsaturated fats have been shown to decrease plasma cholesterol levels. So were the researchers being disingenuous deliberately to vilify high fat diets?
High fat diets are well reported to lower plasma triglyceride levels in humans and this pattern was also seen in the results from this study. The ability of high fat diets to lower plasma triglyceride levels may relate to their higher content of polyunsaturated fatty acids. Some polyunsaturated fatty acids, particularly those found in fish oils, have been shown to significantly decrease plasma triglyceride levels. However, in this study the polyunsaturated fatty acids in the two diets were similar. Therefore another explanation is required. One possibility that may explain the lowering of plasma triglycerides by the high fat diet may relate to the role that refined carbohydrates, particularly fructose, play in the raising of plasma triglycerides. High intakes of fructose in the diet causes its metabolism in the liver to produce fatty acids, and these are packaged into very low density lipoprotein particles as triglycerides and exported to the plasma. Switching to a high fat diet can decrease intakes of fructose and this may lower plasma triglycerides.
The changes in the expression of RNA relating to lipoprotein metabolising enzymes are interesting because it suggests that enterocytes adapt to high fat diets within a few days. Although only enterocyte RNA was measured in this study (via biopsies of the intestinal tract), it is likely that other cells also adapt to high fat diets though up or down regulation of key metabolising and transporting genes. Switching to a high fat diet may therefore cause adaptation that prevents detrimental health effects. High fat diets such as the Atkins Diet have been criticised for being unhealthy as high fat diets have become synonymous with ill health. However, a high fat diet can be as healthy or as unhealthy as the individual desires. Food selection is therefore pivotal in maintaining health with a high fat diet. Incorporating processed and refined foods into a high fat diet is just as detrimental as including processed and refined foods into a low fat diet. If care is taken to select healthy foods, there is no reason that a high fat diet cannot be healthy.
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