The lipid hypothesis of cardiovascular disease states that atherosclerosis is caused by elevated levels of blood cholesterol, and that dietary cholesterol and saturated fatty acids can in turn influence blood cholesterol. According to this hypothesis, foods high in cholesterol and saturated fatty acids such as red meat can therefore increase the risk of atherosclerosis, which is in turn considered a cause of cardiovascular disease. There are a number of problems with the lipid theory of cardiovascular disease. The most notable of these problems is that dietary sources of cholesterol and saturated fatty acids do not consistently cause elevations in plasma cholesterol, and in most studies both are ineffective at raising plasma cholesterol levels in healthy individuals. Many feeding studies have been undertaken to investigate the effects of changes in the lipid content of the diet on blood cholesterol levels, and many of these have used red meat and eggs because of their high cholesterol and saturated fatty acid content.
One study1 published in 1980 was designed to test the then current recommendations with respect to reducing intakes of red meat and other cholesterol and saturated fatty acid containing foods in order to lower plasma cholesterol levels. The research study was designed to cause minimal changes to the diets of the subjects in order that they would be realistically related to the recommendations then in place. Twenty nine healthy men aged 31 to 61 years with mean plasma cholesterol levels below 240 mg/mL (6.21 mmol/L) and no metabolic symptoms were selects to consume the diets. Some of the subjects consumed either red meat, no fish or poultry with 3 eggs; red meat, no fish or poultry with no eggs; fish and poultry, no red meat and no eggs; fish and poultry, no red meat and 3 eggs, for 6 weeks each. Another group of subjects consumed the diets in the reverse order. The total cholesterol and high density lipoprotein levels (HDL) of the subjects were then measured at baseline and at 5 and 6 weeks into each diet.
The results of the study showed that in the group that consumed the diets in the forward direction, there was no significant changes to plasma cholesterol or HDL levels for any of the diets. Plasma cholesterol varied between 191 and 199 mg/mL and HDL varied between 43 and 47 mg/mL. However, in the group that consumed the diets in the reverse order, plasma cholesterol rose when eggs were added to either the fish and poultry or red meat diets. In this respect plasma total cholesterol levels were 198 and 216 mg/mL for the fish and poultry diet, with and without eggs, respectively; and 191 and 207 mg/mL in the red meat diet with and without eggs, respectively. However, the second group experienced no changes to HDL levels. Therefore the consumption of fish, poultry or red meat had no observable effects on total cholesterol or HDL cholesterol in these healthy subjects. However, the addition of eggs and the observed change to cholesterol levels in the second group deserves discussion.
Group 2 showed an increase in total cholesterol with addition of eggs to the diet. The inclusion of 3 eggs per day increased the cholesterol intake of the subjects by around 1000 mg per day. Other studies investigating the effects of dietary cholesterol have shown that this sort of increase in dietary cholesterol would have increased cholesterol absorption about 2 to 3 fold. However the mean values have been skewed by the inclusion of a single subjects who showed increases in total cholesterol to above 270 mg/mL (6.68 mmol/L) with addition of the three eggs. This subject accounts for much of the differences seen between the group in terms of the changes to plasma cholesterol from inclusion of the eggs. It is not known, but this subject could have a genetic defect such as familial hypercholesterolaemia (FH), that prevents the correct metabolism of cholesterol. In addition, the authors speculated that because the groups consumed the diets during different times of the year, that this could have influenced the plasma cholesterol levels.
The inclusion of subjects with FH is an interesting point and worthy also of further discussion. Many studies have not controlled for such subjects, and this may explain the detrimental effects of eggs seen in such studies. In this study the subjects were all metabolically healthy and had cholesterol levels within the normal range. This would likely exclude any subjects with genetic defects in cholesterol metabolism. However many studies recruit subjects with elevated levels of plasma cholesterol, and this can increase the chances of subjects possessing genetic defects in cholesterol metabolism such as FH. Certainly the Framingham study has been criticised for such selection bias. Unless subjects are screened to detect genetic defects and then these subjects excluded from the study, extrapolation to the population as a whole is problematic. As incidence of FH is about 1 in 500, inclusion of subjects with high cholesterol is quite likely to include some such individuals and therefore care needs to be taken interpreting the data.
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